PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 17563058-2 2007 In patients with type 2 diabetes, insulin resistance in skeletal muscle is associated with abnormalities in insulin signaling, fatty acid metabolism, and mitochondrial oxidative phosphorylation (OXPHOS). Fatty Acids 127-137 insulin Homo sapiens 34-41 17650308-11 2007 Meanwhile, it releases abundant fatty acid products (e.g. diacylglycerol, ceramides) that impair insulin actions via signal transduction, thereby causing MIR. Fatty Acids 32-42 insulin Homo sapiens 97-104 17671740-10 2007 Further studies will be needed to clarify how fatty acid synthesis is increased by SREBP-1c, which is under the control of insulin and AMP-activated protein kinase. Fatty Acids 46-56 insulin Homo sapiens 123-130 17785696-6 2007 The roles of increased circulating fatty acids in conditions of insulin resistance and the typical pro-inflammatory milieu of specific obesity patterns are provided. Fatty Acids 35-46 insulin Homo sapiens 64-71 17637087-5 2007 The role of fatty acids is central to the insulin sensitivity hypothesis. Fatty Acids 12-23 insulin Homo sapiens 42-49 17637087-10 2007 The insulin-sensitising effects of high-fibre diets are also related to changes in AT function and fatty acid metabolism, but manipulating colonic tissue in situ allows the mechanisms to be elucidated. Fatty Acids 99-109 insulin Homo sapiens 4-11 17663761-11 2007 While no experiment exists that measures all relevant variables, the model is supported by evidence in the literature that 1) dietary carbohydrate, via its effect on hormone levels controls fatty acid flux and oxidation, 2) the rate of lipolysis is a primary target of insulin, postprandial, and 3) chronic carbohydrate-restricted diets reduce the levels of plasma TAG in response to a single meal. Fatty Acids 190-200 insulin Homo sapiens 269-276 17878672-0 2007 Relationship between serum concentrations of saturated fatty acids and unsaturated fatty acids and the homeostasis model insulin resistance index in Japanese patients with type 2 diabetes mellitus. Fatty Acids 45-66 insulin Homo sapiens 121-128 17878672-2 2007 Exact relationship between saturated fatty acids (SFA) or PUFA and the insulin resistance of diabetics are unknown. Fatty Acids 27-48 insulin Homo sapiens 71-78 17878672-2 2007 Exact relationship between saturated fatty acids (SFA) or PUFA and the insulin resistance of diabetics are unknown. Fatty Acids 50-53 insulin Homo sapiens 71-78 17628546-5 2007 There is much evidence supporting that detrimental effects of glucose, fatty acids, hormones and cytokines leading to insulin resistance can be exerted via such a common pathway. Fatty Acids 71-82 insulin Homo sapiens 118-125 17431009-0 2007 Insulin protects liver cells from saturated fatty acid-induced apoptosis via inhibition of c-Jun NH2 terminal kinase activity. Fatty Acids 34-54 insulin Homo sapiens 0-7 17431009-3 2007 The present study examined insulin-mediated protection against saturated fatty acid-induced apoptosis in the rat hepatoma cell line, H4IIE, and primary rat hepatocytes. Fatty Acids 63-83 insulin Homo sapiens 27-34 17431009-11 2007 These data suggest that insulin is an important determinant of saturated fatty acid-induced apoptosis in liver cells and may have implications for fatty acid-mediated liver cell injury in insulin-deficient and/or -resistant states. Fatty Acids 63-83 insulin Homo sapiens 24-31 17431009-11 2007 These data suggest that insulin is an important determinant of saturated fatty acid-induced apoptosis in liver cells and may have implications for fatty acid-mediated liver cell injury in insulin-deficient and/or -resistant states. Fatty Acids 73-83 insulin Homo sapiens 24-31 17510709-0 2007 Acute exercise increases triglyceride synthesis in skeletal muscle and prevents fatty acid-induced insulin resistance. Fatty Acids 80-90 insulin Homo sapiens 99-106 17510709-4 2007 Prevention of fatty acid-induced insulin resistance after exercise accompanied enhanced skeletal muscle protein expression of key lipogenic enzymes and an increase in muscle triglyceride synthesis. Fatty Acids 14-24 insulin Homo sapiens 33-40 17510709-6 2007 We believe this is the first study to demonstrate that 1 session of exercise completely reverses fatty acid-induced insulin resistance in humans. Fatty Acids 97-107 insulin Homo sapiens 116-123 17339414-19 2007 adipose tissue from corn-fed steers to insulin resulted in a 165% increase in glucose incorporation into fatty acids. Fatty Acids 105-116 insulin Homo sapiens 39-46 17983553-6 2007 The insulin resistance which is concomitant with type 2 diabetes and obesity is linked to an increased intracellular availability of fatty acids which are precursors of lipid mediators inducing a decreased efficiency of insulin signal transmission. Fatty Acids 133-144 insulin Homo sapiens 4-11 17983553-6 2007 The insulin resistance which is concomitant with type 2 diabetes and obesity is linked to an increased intracellular availability of fatty acids which are precursors of lipid mediators inducing a decreased efficiency of insulin signal transmission. Fatty Acids 133-144 insulin Homo sapiens 220-227 17983553-7 2007 Therapies aimed at improving insulin sensitivity could then target proteins involved in the regulation of intacellular fatty acid availibility. Fatty Acids 119-129 insulin Homo sapiens 29-36 17510695-3 2007 The mechanisms of insulin resistance involve conditions leading to an increased supply of fatty acids (e.g., high energy intake, obesity) and conditions in which the degradation/oxidation of muscular fatty acids is impaired. Fatty Acids 90-101 insulin Homo sapiens 18-25 17510695-3 2007 The mechanisms of insulin resistance involve conditions leading to an increased supply of fatty acids (e.g., high energy intake, obesity) and conditions in which the degradation/oxidation of muscular fatty acids is impaired. Fatty Acids 200-211 insulin Homo sapiens 18-25 17510709-7 2007 Reversal of insulin resistance accompanied enhanced lipogenic capacity within skeletal muscle, reduced accumulation of highly bioactive fatty acid metabolites, and suppressed activation of proinflammatory pathways known to impair insulin action. Fatty Acids 136-146 insulin Homo sapiens 12-19 17510709-2 2007 Herein, we demonstrate that fatty acid-induced insulin resistance in humans is completely prevented the day after 1 session of endurance exercise. Fatty Acids 28-38 insulin Homo sapiens 47-54 17287462-7 2007 These data support the hypothesis that insulin resistance in skeletal muscle of insulin-resistant offspring is associated with dysregulation of intramyocellular fatty acid metabolism, possibly because of an inherited defect in the activity of mitochondrial oxidative phosphorylation. Fatty Acids 161-171 insulin Homo sapiens 39-46 17287462-7 2007 These data support the hypothesis that insulin resistance in skeletal muscle of insulin-resistant offspring is associated with dysregulation of intramyocellular fatty acid metabolism, possibly because of an inherited defect in the activity of mitochondrial oxidative phosphorylation. Fatty Acids 161-171 insulin Homo sapiens 80-87 17642443-2 2007 Recent studies have given a great deal of attention to the influence of the entry of fatty acids into muscles and steatosis in skeletal muscles during the onset and development of insulin resistance. Fatty Acids 85-96 insulin Homo sapiens 180-187 17337731-1 2007 Elevated non-esterified fatty acids, triglyceride, diacylglycerol, and ceramide have all been associated with insulin resistance in muscle. Fatty Acids 24-35 insulin Homo sapiens 110-117 17219404-0 2007 Fatty acid-induced defects in insulin signalling, in myotubes derived from children, are related to ceramide production from palmitate rather than the accumulation of intramyocellular lipid. Fatty Acids 0-10 insulin Homo sapiens 30-37 21179778-6 2007 CONCLUSION: Our study demonstrated that decrease of lipogenesis along with increase of fatty acids oxidation of adipose tissue could be a common cause of insulin resistance in obesity and type 2 diabetes, while functional changes of other genes, such as immune regulation genes,might also be involved in the pathogenesis of obesity and type 2 diabetes. Fatty Acids 87-98 insulin Homo sapiens 154-161 17444965-5 2007 Insulin action on Na,K-ATPase, in vivo, might be mediated by the high level of non-esterified fatty acids, which are circulating enzyme inhibitors and increase in obesity, diabetes and hypertension. Fatty Acids 94-105 insulin Homo sapiens 0-7 17438370-5 2007 (1) These data identify a novel mechanism by which inflammation in obesity is a precursor to defects in skeletal muscle fatty acid oxidation that generates a vicious cycle exacerbating the development of insulin resistance. Fatty Acids 120-130 insulin Homo sapiens 204-211 17429039-2 2007 Here we review recent human studies exploring the mechanistic links between disorders of fatty acid/lipid metabolism and insulin resistance. Fatty Acids 89-99 insulin Homo sapiens 121-128 17565412-3 2007 Several mechanisms have been proposed to be responsible for insulin resistance, including increased non-esterified fatty acids, inflammatory cytokines, adipokines, and mitochondrial dysfunction, as well as glucotoxicity, lipotoxicity, and amyloid formation for beta-cell dysfunction. Fatty Acids 115-126 insulin Homo sapiens 60-67 17339025-5 2007 First, they indicate that different fatty acids induce insulin resistance by distinct mechanisms discerned by their reliance on sphingolipid synthesis. Fatty Acids 36-47 insulin Homo sapiens 55-62 17344486-3 2007 The excess fatty acids are esterified and either stored or metabolized to various molecules that may participate or interfere with normal cellular signaling, particularly insulin-mediated signal transduction, thus altering cellular and, subsequently, whole-body glucose metabolism. Fatty Acids 11-22 insulin Homo sapiens 171-178 17435330-2 2007 PDK1-independent phosphorylation of PKC(eta) causes this reduction in insulin receptor gene expression.One of the pathways through which fatty acid can induce insulin resistance in insulin target cells is suggested by these studies.We provide an overview of this important area,emphasizing the current status. Fatty Acids 137-147 insulin Homo sapiens 70-77 17327442-1 2007 Insulin resistance is associated with metabolic inflexibility, impaired switching of substrate oxidation from fatty acids to glucose in response to insulin. Fatty Acids 110-121 insulin Homo sapiens 0-7 17327442-1 2007 Insulin resistance is associated with metabolic inflexibility, impaired switching of substrate oxidation from fatty acids to glucose in response to insulin. Fatty Acids 110-121 insulin Homo sapiens 148-155 17285001-2 2007 According to the glucose-fatty acid cycle of Randle, preferential oxidation of free fatty acids over glucose plays a major role in insulin sensitivity and the metabolic disturbances of diabetes mellitus. Fatty Acids 25-35 insulin Homo sapiens 131-138 17435330-2 2007 PDK1-independent phosphorylation of PKC(eta) causes this reduction in insulin receptor gene expression.One of the pathways through which fatty acid can induce insulin resistance in insulin target cells is suggested by these studies.We provide an overview of this important area,emphasizing the current status. Fatty Acids 137-147 insulin Homo sapiens 159-166 17172644-1 2007 Hepatic lipogenesis is the principal route to convert excess carbohydrates into fatty acids and is mainly regulated by two opposing hormones, insulin and glucagon. Fatty Acids 80-91 insulin Homo sapiens 142-149 17262885-1 2007 The human acyl-CoA-binding protein (ACBP) is a potential candidate gene of type 2 diabetes (T2D), since it plays a central role in determining the intracellular concentration of activated fatty acids which contribute to insulin resistance. Fatty Acids 188-199 insulin Homo sapiens 220-227 18025824-1 2007 BACKGROUND: Fatty acids can modulate lipid metabolism, this is related to insulin resistance (IR). Fatty Acids 12-23 insulin Homo sapiens 74-81 17554973-1 2007 BACKGROUND: Composition of the nonesterified fatty acids in plasma in metabolic syndrome patients and in other syndromes of insulin resistance is altered. Fatty Acids 45-56 insulin Homo sapiens 124-131 17554973-3 2007 The aim of the work was to study the fatty acid composition in the major plasma lipid classes in relation to the insulin resistance, to some polymorphisms of candidate genes with activity related to insulin resistance, and to the lipoprotein composition and parameters of lipid peroxidation. Fatty Acids 37-47 insulin Homo sapiens 113-120 17051236-0 2007 Non-esterified fatty acids and blood pressure elevation: a mechanism for hypertension in subjects with obesity/insulin resistance? Fatty Acids 4-26 insulin Homo sapiens 111-118 17051236-2 2007 Increased levels of non-esterified fatty acids (NEFAs) in abdominally obese subjects were reported to contribute in the development of various disturbances related to the metabolic syndrome, such as hepatic and peripheral insulin resistance (IR), dyslipidaemia, beta-cell apoptosis, endothelial dysfunction and others. Fatty Acids 35-46 insulin Homo sapiens 222-229 17204958-1 2007 BACKGROUND: The fatty acid composition of membrane structural lipids, which is partly dependent on dietary intake, is associated with insulin action. Fatty Acids 16-26 insulin Homo sapiens 134-141 17204958-2 2007 AIM: To examine the association between fatty acid composition of adipose tissue and skeletal muscle phospholipids with insulin resistance markers in a healthy pediatric population. Fatty Acids 40-50 insulin Homo sapiens 120-127 16497094-4 2007 The decreased fat oxidation results into the accumulation of intermediates of fatty acid metabolism that are supposed to interfere with the insulin signaling cascade and in consequence negatively influence the glucose utilization. Fatty Acids 78-88 insulin Homo sapiens 140-147 17130640-0 2006 Fatty acid signaling in the beta-cell and insulin secretion. Fatty Acids 0-10 insulin Homo sapiens 42-49 17211560-1 2006 Insulin resistance is a major factor in the pathogenesis of type 2 diabetes mellitus (T2DM) and is related to the fatty acid profile of the plasma membranes. Fatty Acids 114-124 insulin Homo sapiens 0-7 18333368-2 2007 Evidence has been provided that increased levels of non esterified fatty acids (NEFA) in the portal flow would produce insulin resistance and would also stimulate the hepatic protein synthesis, thereby explaining the increased plasma levels not only of apolipoprotein B, but also of other liver-derived enzymes and proteins occurring in overweight and hypertriglyceridemic patients. Fatty Acids 67-78 insulin Homo sapiens 119-126 17167471-2 2006 In obese individuals, adipose tissue releases increased amounts of non-esterified fatty acids, glycerol, hormones, pro-inflammatory cytokines and other factors that are involved in the development of insulin resistance. Fatty Acids 82-93 insulin Homo sapiens 200-207 17130640-2 2006 For the pancreatic beta-cell, while the presence of some FAs is essential for glucose-stimulated insulin secretion, FAs have enormous capacity to amplify glucose-stimulated insulin secretion, which is particularly operative in situations of beta-cell compensation for insulin resistance. Fatty Acids 57-60 insulin Homo sapiens 97-104 17130640-2 2006 For the pancreatic beta-cell, while the presence of some FAs is essential for glucose-stimulated insulin secretion, FAs have enormous capacity to amplify glucose-stimulated insulin secretion, which is particularly operative in situations of beta-cell compensation for insulin resistance. Fatty Acids 116-119 insulin Homo sapiens 173-180 17130640-2 2006 For the pancreatic beta-cell, while the presence of some FAs is essential for glucose-stimulated insulin secretion, FAs have enormous capacity to amplify glucose-stimulated insulin secretion, which is particularly operative in situations of beta-cell compensation for insulin resistance. Fatty Acids 116-119 insulin Homo sapiens 173-180 17052206-9 2006 In common Type 2 (non-insulin-dependent) diabetes, which is generally associated with obesity, a decline in mitochondrial function in adipose cells seems to result in an inappropriate scavenging of fatty acids by beta-oxidation. Fatty Acids 198-209 insulin Homo sapiens 22-29 17142140-8 2006 However, marked insulin hypersecretion can compensate for impaired insulin action, resulting in normal glucose and fatty acid metabolism during basal conditions. Fatty Acids 115-125 insulin Homo sapiens 16-23 16788709-1 2006 OBJECTIVE: Proteins involved in cellular fatty acid (FA) uptake and metabolism may be of relevance in the context of disturbed FA metabolism associated with insulin resistance. Fatty Acids 41-51 insulin Homo sapiens 157-164 17053832-0 2006 TLR4 links innate immunity and fatty acid-induced insulin resistance. Fatty Acids 31-41 insulin Homo sapiens 50-57 17052194-6 2006 GPR40, activated by medium and long-chain fatty acids, has been shown to potentiate insulin secretion at the beta-cell, and has been hypothesized to participate in the detrimental effects of chronic fatty acid exposure on beta-cell function. Fatty Acids 42-52 insulin Homo sapiens 84-91 16981831-0 2006 The fatty acid oxidation pathway as a therapeutic target for insulin resistance. Fatty Acids 4-14 insulin Homo sapiens 61-68 16896932-7 2006 CONCLUSIONS/INTERPRETATION: Lifestyle-induced changes in fatty acid profile of cholesteryl esters and desaturase activities were independently related to changes in insulin sensitivity in subjects at risk of type 2 diabetes. Fatty Acids 57-67 insulin Homo sapiens 165-172 16896932-1 2006 AIMS/HYPOTHESIS: The aim of this study was to investigate whether lifestyle intervention-induced changes in serum fatty acid profile of cholesteryl esters and estimated desaturase activities are related to improvements in insulin sensitivity in subjects at risk of type 2 diabetes. Fatty Acids 114-124 insulin Homo sapiens 222-229 16478780-0 2006 Metformin counters the insulin-induced suppression of fatty acid oxidation and stimulation of triacylglycerol storage in rodent skeletal muscle. Fatty Acids 54-64 insulin Homo sapiens 23-30 17125591-3 2006 beta-Cells are responsible for insulin production, storage and secretion in accordance to the demanding concentrations of glucose and fatty acids. Fatty Acids 134-145 insulin Homo sapiens 31-38 16938460-4 2006 Tumor necrosis factor alpha stimulates triglyceride hydrolysis by multiple intracellular pathways acting on insulin signaling, G proteins and perilipins, and might contribute to enhanced plasma fatty acid levels in obesity. Fatty Acids 194-204 insulin Homo sapiens 108-115 16897074-1 2006 Defective fatty acid oxidation in skeletal muscle is one of the possible causes of insulin resistance. Fatty Acids 10-20 insulin Homo sapiens 83-90 16897074-3 2006 The aim of this study was to verify whether activation of fatty acid oxidation by PPARbeta agonists in human skeletal muscle cells prepared from type 2 diabetic patients could improve the reduced responses to insulin that characterized this cell model. Fatty Acids 58-68 insulin Homo sapiens 209-216 16897074-9 2006 This suggests that additional studies are needed to better characterize the link between fatty acid oxidation and insulin sensitivity in humans. Fatty Acids 89-99 insulin Homo sapiens 114-121 16464906-1 2006 Muscle fatty acid (FA) metabolism is impaired in obesity and insulin resistance, reflected by reduced rates of FA oxidation and accumulation of lipids. Fatty Acids 7-17 insulin Homo sapiens 61-68 16958313-3 2006 Insulin resistance may be partly modified by the specific types of dietary fatty acids. Fatty Acids 75-86 insulin Homo sapiens 0-7 16865295-2 2006 The aim of this study was to determine whether an abnormality in membrane fatty acid composition was related to a weakening of insulin"s inhibitory effect on agonist-stimulated intracellular free calcium elevation. Fatty Acids 74-84 insulin Homo sapiens 127-134 16305809-6 2006 The early phase of obesity-related insulin resistance has 2 components: (a) interruption of lipid homeostasis leading to the increased plasma concentration of fatty acids that is normally suppressed by the activation of PPAR-gamma, and (b) activation of factors such as cytokines depressed by PPAR-gamma that cause insulin resistance. Fatty Acids 159-170 insulin Homo sapiens 35-42 16838661-5 2006 Although the mechanism how insulin resistance develops is not fully understood, dysregulation of fatty acid metabolism, abnormalities of the function and the secretion of adipokines, as well as the increase in stress signaling might contribute to the development of insulin resistance. Fatty Acids 97-107 insulin Homo sapiens 266-273 16709632-10 2006 Since fatty acids have a key role in insulin resistance, especially in muscles, activating AMPK in adipose tissue might be found to be beneficial in insulin-resistant states, particularly as AMPK activation also reduces cytokine secretion in adipocytes. Fatty Acids 6-17 insulin Homo sapiens 37-44 16570163-2 2006 Among conventional insulin analogues, which are usually created by amino acid exchange, insulin detemir is the first analogue to be acylated with a fatty acid to enable reversible albumin binding. Fatty Acids 148-158 insulin Homo sapiens 19-26 16570163-2 2006 Among conventional insulin analogues, which are usually created by amino acid exchange, insulin detemir is the first analogue to be acylated with a fatty acid to enable reversible albumin binding. Fatty Acids 148-158 insulin Homo sapiens 88-95 16680032-7 2006 SUMMARY: Altered fatty acid metabolism and the accumulation of triacylglycerol and lipid metabolites has been strongly associated with insulin resistance and diabetes, but we do not fully understand how the entry of fatty acids into cells is regulated. Fatty Acids 17-27 insulin Homo sapiens 135-142 16732014-14 2006 CONCLUSIONS: PLIN 11482G-->A/14995A-->T polymorphisms modulate the association between SFAs/carbohydrate in diet and insulin resistance in Asian women. Fatty Acids 93-97 insulin Homo sapiens 123-130 16680032-7 2006 SUMMARY: Altered fatty acid metabolism and the accumulation of triacylglycerol and lipid metabolites has been strongly associated with insulin resistance and diabetes, but we do not fully understand how the entry of fatty acids into cells is regulated. Fatty Acids 216-227 insulin Homo sapiens 135-142 16596361-1 2006 AIMS/HYPOTHESIS: Prolonged elevation of plasma specific fatty acids may exert differential effects on glucose-stimulated insulin secretion (GSIS), insulin sensitivity and clearance. Fatty Acids 56-67 insulin Homo sapiens 121-128 16596361-1 2006 AIMS/HYPOTHESIS: Prolonged elevation of plasma specific fatty acids may exert differential effects on glucose-stimulated insulin secretion (GSIS), insulin sensitivity and clearance. Fatty Acids 56-67 insulin Homo sapiens 147-154 16713711-6 2006 In particular, the fact that fatty acid oxidation and energy dissipation in skeletal muscle and adipose tissue by PPARdelta agonists lead to improved lipid profile, reduced adiposity and insulin sensitivity is a breakthrough. Fatty Acids 29-39 insulin Homo sapiens 187-194 16463046-8 2006 CONCLUSIONS/INTERPRETATION: We propose that the metabolic effect of insulin resistance, partly mediated by depressed plasma adiponectin levels, increases fatty acid flux from adipose tissue to the liver and induces the accumulation of fat in the liver. Fatty Acids 154-164 insulin Homo sapiens 68-75 16327015-4 2006 Insulin-induced changes in glucose oxidation (GLUox) and fatty acid (FA) oxidation (FAox) were measured in isolated hearts from control and diabetic mice, perfused with both low as well as high concentration of glucose and FA: 10 mM glucose/0.5 mM palmitate and 28 mM glucose/1.1 mM palmitate. Fatty Acids 57-67 insulin Homo sapiens 0-7 16611988-3 2006 Here we show that insulin-stimulated fatty acid uptake is completely abolished in FATP1-null adipocytes and greatly reduced in skeletal muscle of FATP1-knockout animals while basal LCFA uptake by both tissues was unaffected. Fatty Acids 37-47 insulin Homo sapiens 18-25 16524879-1 2006 Control of fatty acid homeostasis is crucial to prevent insulin resistance. Fatty Acids 11-21 insulin Homo sapiens 56-63 16361853-3 2006 Aberrant fatty acid metabolism has been associated with a number of cellular abnormalities such as increased mitochondrial permeability (a promoter of apoptosis), insulin resistance, and enhanced generation of free radicals. Fatty Acids 9-19 insulin Homo sapiens 163-170 16549443-0 2006 Regulation of the insulin gene by glucose and fatty acids. Fatty Acids 46-57 insulin Homo sapiens 18-25 16426829-4 2006 Obesity-induced insulin resistance leads to elevated levels of plasma insulin, glucose and fatty acids. Fatty Acids 91-102 insulin Homo sapiens 16-23 16430716-2 2006 OBJECTIVE: Cross-sectional studies suggest that the fatty acid (FA) composition of phospholipids in skeletal muscle cell membrane may modulate insulin sensitivity in humans. Fatty Acids 52-62 insulin Homo sapiens 143-150 16420480-5 2006 As a consequence, it can modulate insulin-stimulated glucose and fatty acid oxidation. Fatty Acids 65-75 insulin Homo sapiens 34-41 16436102-3 2006 Low-carbohydrate intakes result in a reduction of the circulating insulin level, which promotes high level of circulating fatty acids, used for oxidation and production of ketone bodies. Fatty Acids 122-133 insulin Homo sapiens 66-73 16528409-0 2006 Insulin resistance reduces arterial prostacyclin synthase and eNOS activities by increasing endothelial fatty acid oxidation. Fatty Acids 104-114 insulin Homo sapiens 0-7 16802531-10 2006 While in DKA the lack of insulin combined with increased catecholamines results in accelerated lipolysis and thus production of excess fatty acids, leading to beta-oxidation and ketogenesis, in HHS residual beta-cell function is adequate to prevent lipolysis but not hyperglycemia. Fatty Acids 135-146 insulin Homo sapiens 25-32 16463611-3 2006 Traditionally, the Randle cycle was used to explain the mechanism behind fatty acid-induced insulin resistance in skeletal muscle. Fatty Acids 73-83 insulin Homo sapiens 92-99 16463611-4 2006 An alternative explanation is that the increased supply of free fatty acids leads to the accumulation of IMTG and fatty-acid metabolites, which can induce defects in the insulin signalling cascade, causing insulin resistance in skeletal muscle. Fatty Acids 114-124 insulin Homo sapiens 170-177 16463611-4 2006 An alternative explanation is that the increased supply of free fatty acids leads to the accumulation of IMTG and fatty-acid metabolites, which can induce defects in the insulin signalling cascade, causing insulin resistance in skeletal muscle. Fatty Acids 114-124 insulin Homo sapiens 206-213 17144879-3 2006 Recent research has shown that fatty acids, derived from adipose tissue, can interfere with insulin signalling in muscle. Fatty Acids 31-42 insulin Homo sapiens 92-99 16445715-0 2006 Convergence of glucose- and fatty acid-induced abnormal myocardial excitation-contraction coupling and insulin signalling. Fatty Acids 28-38 insulin Homo sapiens 103-110 16028214-3 2006 Recent molecular evidence highlights the interaction between muscle fatty acid kinetics in dictating whole body insulin action. Fatty Acids 68-78 insulin Homo sapiens 112-119 17144879-10 2006 These observations, and others in severely obese individuals and type 2 diabetes patients, suggest that impaired rates of fatty acid oxidation are associated with insulin resistance. Fatty Acids 122-132 insulin Homo sapiens 163-170 17144879-12 2006 Thus, excess intracellular lipid metabolite accumulation, which interferes with insulin signalling, can occur as a result of impaired rates of fatty acid oxidation and/or increased rates of fatty acid transport into muscle. Fatty Acids 143-153 insulin Homo sapiens 80-87 16445986-4 2006 The sphingolipid ceramide is a putative intermediate linking both excess nutrients (i.e. saturated fatty acids) and inflammatory cytokines (e.g. tumor necrosis factor-alpha, TNFalpha) to the induction of insulin resistance. Fatty Acids 89-110 insulin Homo sapiens 204-211 16309849-1 2006 The molecular mechanism responsible for obesity-associated insulin resistance has been partially clarified: increased fatty acid levels in muscle fibers promote diacylglycerol synthesis, which activates certain isoforms of protein kinase C (PKC). Fatty Acids 118-128 insulin Homo sapiens 59-66 16820727-2 2006 It also refers to a clustering of specific cardiovascular disease risk factors whose underlying pathophysiology is thought to be related to insulin resistance with an excessive flux of fatty acids implicated. Fatty Acids 185-196 insulin Homo sapiens 140-147 16487789-6 2006 Although it is widely accepted that fatty acid (FA) metabolism (notably FA synthesis and/or formation of LC-acyl-CoA) is necessary for stimulation of insulin secretion, the key regulatory molecular mechanisms controlling the interplay between glucose and fatty acid metabolism and thus insulin secretion are not well understood but are now described in detail in this review. Fatty Acids 36-46 insulin Homo sapiens 150-157 16487789-6 2006 Although it is widely accepted that fatty acid (FA) metabolism (notably FA synthesis and/or formation of LC-acyl-CoA) is necessary for stimulation of insulin secretion, the key regulatory molecular mechanisms controlling the interplay between glucose and fatty acid metabolism and thus insulin secretion are not well understood but are now described in detail in this review. Fatty Acids 36-46 insulin Homo sapiens 286-293 16319806-6 2005 Higher levels of membrane saturated fatty acids seem to greatly impair the action of insulin, whereas the presence of polyunsaturated fatty acids, especially of the omega-3 and -6 families, in contrast, improves insulin sensitivity. Fatty Acids 26-47 insulin Homo sapiens 85-92 17326333-2 2006 Following subcutaneous injection, insulin detemir binds to albumin via fatty acid chain, thereby providing slow absorption and a prolonged metabolic effect. Fatty Acids 71-81 insulin Homo sapiens 34-41 16204368-10 2005 The direct energy-dissipating effects could be significant tools to treat obesity and to improve insulin resistance in type 2 diabetic patients by reduction of fat accumulation in adipocytes or by reprogramming fatty acid metabolism. Fatty Acids 211-221 insulin Homo sapiens 97-104 16319806-11 2005 Greater understanding of the role played by dietary fat and plasma fatty acids in pathogenesis of insulin resistance, will allow for more timely prevention and improved treatment in the future. Fatty Acids 67-78 insulin Homo sapiens 98-105 16007182-2 2005 It is also involved in mediating the effects of insulin, such as lipogenesis, glucose uptake and conversion of glucose into fatty acids and cholesterol. Fatty Acids 124-135 insulin Homo sapiens 48-55 16412956-2 2005 These cells are responsible for insulin production and secretion in response to increases in circulating concentrations of nutrients, such as glucose, fatty acids and amino acids. Fatty Acids 151-162 insulin Homo sapiens 32-39 16219010-3 2005 Methods of pro-tracting the time-action curve of injected insulin include complexing with proteins, insulin crystal formation, shifting the iso-electric point of the amino acid sequence or attaching a fatty-acid side chain to the molecule. Fatty Acids 201-211 insulin Homo sapiens 58-65 16044321-0 2005 Free fatty acid receptor 1 (FFA(1)R/GPR40) and its involvement in fatty-acid-stimulated insulin secretion. Fatty Acids 66-76 insulin Homo sapiens 88-95 16044321-2 2005 The recently de-orphanized G-protein coupled receptor, FFA(1)R/GPR40, has been shown to be essential for fatty-acid-stimulated insulin release in MIN6 mouse insulinoma cells. Fatty Acids 105-115 insulin Homo sapiens 127-134 16044321-10 2005 The results demonstrate that FFA(1)R/GPR40 is inhibited by the CPT-1 inhibitor, 2BrP, and confirm that FFA(1)R/GPR40 is indeed necessary, at least in part, for fatty-acid-stimulated insulin release. Fatty Acids 160-170 insulin Homo sapiens 182-189 16148539-10 2005 In addition to atherosclerosis, these fatty acid binding proteins also exert a dramatic impact on obesity, insulin resistance, type 2 diabetes and fatty liver disease. Fatty Acids 38-48 insulin Homo sapiens 107-114 16389895-4 2005 The most recent approach has been to acylate the insulin molecule with a fatty acid which provides the insulin molecule with a specific affinity for albumin. Fatty Acids 73-83 insulin Homo sapiens 49-56 16128592-0 2005 Submicromolar concentrations of palmitoyl-CoA specifically thioesterify cysteine 244 in glyceraldehyde-3-phosphate dehydrogenase inhibiting enzyme activity: a novel mechanism potentially underlying fatty acid induced insulin resistance. Fatty Acids 198-208 insulin Homo sapiens 217-224 16128592-1 2005 The accumulation of fatty acids and their metabolites results in insulin resistance and reduced glucose utilization through a variety of complex mechanisms that remain incompletely understood. Fatty Acids 20-31 insulin Homo sapiens 65-72 16128592-10 2005 Since the hallmark of lipotoxicity is the accumulation of fatty acids and their acyl-CoA metabolites in excess of a cell"s ability to appropriately metabolize them, these results identify a novel mechanism potentially contributing to the insulin resistance, reduced glucose utilization, and maladaptive metabolic alterations underlying the lipotoxic state. Fatty Acids 58-69 insulin Homo sapiens 238-245 16358671-2 2005 The fatty acid modification allows insulin detemir to reversibly bind to albumin, thereby providing slow absorption and a prolonged metabolic effect (up to 24 hours) with low variability. Fatty Acids 4-14 insulin Homo sapiens 35-42 16389895-4 2005 The most recent approach has been to acylate the insulin molecule with a fatty acid which provides the insulin molecule with a specific affinity for albumin. Fatty Acids 73-83 insulin Homo sapiens 103-110 15956083-9 2005 Insulin diminished spillover of both free fatty acids and amino acids, but these actions were not reversed by pancreastatin. Fatty Acids 42-53 insulin Homo sapiens 0-7 15929861-3 2005 In fact, they increase insulin precisely to the degree needed to compensate for the fatty acid-induced insulin resistance. Fatty Acids 84-94 insulin Homo sapiens 23-30 15955844-9 2005 In conclusion, the reversion of insulin resistance after BPD might allow reversal of leptin resistance, restoration of leptin pulsatility, and consequent inhibition of ACC2 mRNA expression, translating to a reduced synthesis of malonyl-CoA, which, in turn, results in increased fatty acid oxidation. Fatty Acids 278-288 insulin Homo sapiens 32-39 16129713-13 2005 Up-regulation of ADRP may act to sequester fatty acids as triglycerides in discrete lipid droplets that could protect muscle from the detrimental effects of fatty acids on insulin action and glucose tolerance. Fatty Acids 43-54 insulin Homo sapiens 172-179 16129713-13 2005 Up-regulation of ADRP may act to sequester fatty acids as triglycerides in discrete lipid droplets that could protect muscle from the detrimental effects of fatty acids on insulin action and glucose tolerance. Fatty Acids 157-168 insulin Homo sapiens 172-179 15727952-14 2005 Augmentation of fatty acid disposal in skeletal muscle, potentially reducing intramyocellular triglyceride content, may represent one mechanism for the lipid-lowering and insulin-sensitizing effects of thiazolidinediones. Fatty Acids 16-26 insulin Homo sapiens 171-178 15930971-4 2005 This is reflected in the modulation of lipolysis/lipogenesis, local insulin sensitivity of glucose and fatty acid uptake, the expression levels of several adipokines in adipose tissue, and the modulation of fat cell number. Fatty Acids 103-113 insulin Homo sapiens 68-75 16003131-2 2005 Insulin resistance is considered as having a central role in NAFLD pathogenesis, which is related with oxidative stress, abnormal production of cytokines and deregulation of fatty acid metabolism. Fatty Acids 174-184 insulin Homo sapiens 0-7 15929861-3 2005 In fact, they increase insulin precisely to the degree needed to compensate for the fatty acid-induced insulin resistance. Fatty Acids 84-94 insulin Homo sapiens 103-110 15929863-3 2005 Fatty acids appear to cause this defect in glucose transport by inhibiting insulin-stimulated tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1) and IRS-1-associated phosphatidylinositol 3-kinase activity. Fatty Acids 0-11 insulin Homo sapiens 75-82 15929863-3 2005 Fatty acids appear to cause this defect in glucose transport by inhibiting insulin-stimulated tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1) and IRS-1-associated phosphatidylinositol 3-kinase activity. Fatty Acids 0-11 insulin Homo sapiens 122-129 15919794-1 2005 Elevated circulating fatty acid concentration is a hallmark of insulin resistance and is at least in part attributed to the action of adipose tissue-derived tumor necrosis factor-alpha (TNF-alpha) on lipolysis. Fatty Acids 21-31 insulin Homo sapiens 63-70 15757684-7 2005 It is suggested that lifespan extension by reduced insulin/IGF signalling may also be mediated by changes in membrane fatty acid composition. Fatty Acids 118-128 insulin Homo sapiens 51-58 15769984-9 2005 The expression of mRNA for fatty acid synthase, a target gene for SREBP-1c, was increased by hCG (24-fold, P = 0.006) and insulin (19-fold, P = 0.024), which also increased the level of cellular, total fatty acid (1.34-fold; P = 0.03). Fatty Acids 27-37 insulin Homo sapiens 122-129 15769984-10 2005 Thus, hCG and insulin cause a switch toward expression of the SREBP-1c isoform with consequent effects on fatty acid synthesis. Fatty Acids 106-116 insulin Homo sapiens 14-21 15920645-6 2005 Insulin"s ability to reduce intracellular fatty acid metabolism may also reduce cellular membrane damage. Fatty Acids 42-52 insulin Homo sapiens 0-7 15955060-4 2005 Using a cultured human skeletal muscle cell model system, we found that expression of both PDK2 and PDK4 mRNA is upregulated in response to glucose deprivation and fatty acid supplementation, the effects of which are reversed by insulin treatment. Fatty Acids 164-174 insulin Homo sapiens 229-236 15774472-0 2005 Acid ceramidase overexpression prevents the inhibitory effects of saturated fatty acids on insulin signaling. Fatty Acids 66-87 insulin Homo sapiens 91-98 15824195-3 2005 Fatty acids appear to cause this defect in glucose transport by inhibiting insulin-stimulated tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1) and IRS-1 associated phosphatidylinositol 3-kinase activity. Fatty Acids 0-11 insulin Homo sapiens 75-82 15870679-1 2005 Fatty acids play an important role in regulating insulin secretion, but the mechanisms are unclear. Fatty Acids 0-11 insulin Homo sapiens 49-56 15824195-3 2005 Fatty acids appear to cause this defect in glucose transport by inhibiting insulin-stimulated tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1) and IRS-1 associated phosphatidylinositol 3-kinase activity. Fatty Acids 0-11 insulin Homo sapiens 122-129 15823385-3 2005 Several mechanisms have been proposed, including increased non-esterified fatty acids, inflammatory cytokines, adipokines, and mitochondrial dysfunction for insulin resistance, and glucotoxicity, lipotoxicity, and amyloid formation for beta-cell dysfunction. Fatty Acids 74-85 insulin Homo sapiens 157-164 15572652-7 2005 We conclude that the postprandial uptake of fatty acids by liver and skeletal muscle is increased in type 2 diabetes and may underlie the elevated tissue triglyceride stores and consequent insulin resistance. Fatty Acids 44-55 insulin Homo sapiens 189-196 15522993-1 2005 High plasma fatty acid availability and a positive energy balance in sedentary individuals reduce insulin sensitivity. Fatty Acids 12-22 insulin Homo sapiens 98-105 16207659-2 2005 Aberrant fatty-acid metabolism has been associated with the promotion of free-radical production, insulin resistance, and cellular apoptosis. Fatty Acids 9-19 insulin Homo sapiens 98-105 15959399-7 2005 Lipid metabolism is impaired in insulin resistant skeletal muscles, fatty acids role in the pathophysiology of insulin resistance generates several hypothesis we briefly describe. Fatty Acids 68-79 insulin Homo sapiens 32-39 15959399-7 2005 Lipid metabolism is impaired in insulin resistant skeletal muscles, fatty acids role in the pathophysiology of insulin resistance generates several hypothesis we briefly describe. Fatty Acids 68-79 insulin Homo sapiens 111-118 15522993-2 2005 This study"s purpose was to determine whether high plasma fatty acid availability and systemic caloric excess after exercise also impair insulin sensitivity. Fatty Acids 58-68 insulin Homo sapiens 137-144 15562033-9 2005 Circulating fatty acids, although closely correlated with central fat, independently predict insulin sensitivity. Fatty Acids 12-23 insulin Homo sapiens 93-100 15736105-2 2005 Recent studies suggest that GPR40 is highly expressed in pancreatic beta cells and insulin-secreting cell lines, and that fatty acids increase intracellular calcium concentration and amplify glucose-stimulated insulin secretion by activating GPR40. Fatty Acids 122-133 insulin Homo sapiens 83-90 15736105-2 2005 Recent studies suggest that GPR40 is highly expressed in pancreatic beta cells and insulin-secreting cell lines, and that fatty acids increase intracellular calcium concentration and amplify glucose-stimulated insulin secretion by activating GPR40. Fatty Acids 122-133 insulin Homo sapiens 210-217 15677505-0 2005 Fatty acid translocase (FAT/CD36) is localized on insulin-containing granules in human pancreatic beta-cells and mediates fatty acid effects on insulin secretion. Fatty Acids 0-10 insulin Homo sapiens 50-57 15677505-0 2005 Fatty acid translocase (FAT/CD36) is localized on insulin-containing granules in human pancreatic beta-cells and mediates fatty acid effects on insulin secretion. Fatty Acids 0-10 insulin Homo sapiens 144-151 15677505-0 2005 Fatty acid translocase (FAT/CD36) is localized on insulin-containing granules in human pancreatic beta-cells and mediates fatty acid effects on insulin secretion. Fatty Acids 122-132 insulin Homo sapiens 50-57 15677505-0 2005 Fatty acid translocase (FAT/CD36) is localized on insulin-containing granules in human pancreatic beta-cells and mediates fatty acid effects on insulin secretion. Fatty Acids 122-132 insulin Homo sapiens 144-151 15562033-0 2005 Circulating fatty acids, non-high density lipoprotein cholesterol, and insulin-infused fat oxidation acutely influence whole body insulin sensitivity in nondiabetic men. Fatty Acids 12-23 insulin Homo sapiens 130-137 15655035-8 2005 The primary mechanisms by which adiponectin enhance insulin sensitivity appears to be through increased fatty acid oxidation and inhibition of hepatic glucose production. Fatty Acids 104-114 insulin Homo sapiens 52-59 15671481-2 2005 Such homeostatic mechanisms can also be activated by excess nutrients or inducers of insulin resistance (such as fatty acids and proinflammatory cytokines) to produce an insulin-resistant state that often leads to the development of diabetes. Fatty Acids 113-124 insulin Homo sapiens 85-92 15671481-2 2005 Such homeostatic mechanisms can also be activated by excess nutrients or inducers of insulin resistance (such as fatty acids and proinflammatory cytokines) to produce an insulin-resistant state that often leads to the development of diabetes. Fatty Acids 113-124 insulin Homo sapiens 170-177 15638874-1 2005 OBJECTIVES: Elevations in non-esterified fatty acids (NEFA) have been shown to decrease insulin action and secretion, and are a risk factor for the development of Type 2 diabetes. Fatty Acids 30-52 insulin Homo sapiens 88-95 15654918-3 2005 Pre-treatment of myotubes with palmitate, chronic hyperglycaemia, and acute high concentrations of insulin changed fatty acid metabolism in favour of accumulation of intracellular lipids. Fatty Acids 115-125 insulin Homo sapiens 99-106 15691219-2 2005 The fatty acid modification allows insulin detemir to reversibly bind to albumin, thereby providing slow absorption and a prolonged and consistent metabolic effect of up to 24 hours in patients with type 1 or type 2 diabetes mellitus. Fatty Acids 4-14 insulin Homo sapiens 35-42 15922116-3 2005 Indeed, insulin resistance increases adipocyte lipolysis and subsequently elevates circulating free fatty acids, thus stimulating the accumulation of fatty acids in the liver (hepatic steatosis). Fatty Acids 100-111 insulin Homo sapiens 8-15 15607577-3 2005 Indeed, in subjects who are insulin resistant, diabetic, and/or obese, fatty acid oxidation by skeletal muscle tends to be inefficient, reflecting decreased expression of mitochondria and mitochondrial enzymes in muscle. Fatty Acids 71-81 insulin Homo sapiens 28-35 15666485-1 2004 There is a state of major stress during acute coronary syndromes with insulin resistance which results in cardiac cellular metabolism becoming almost completely dependant on fatty acids. Fatty Acids 174-185 insulin Homo sapiens 70-77 15776817-1 2005 The purpose of this study was to investigate the effect of chemical enhancers (fatty acids and limonene) and iontophoresis on the in vitro permeability enhancement of insulin through porcine epidermis. Fatty Acids 79-90 insulin Homo sapiens 167-174 15850231-4 2005 These marine fatty acids appear to be working at a number of sites to achieve an improvement in lipid metabolism and insulin sensitivity. Fatty Acids 13-24 insulin Homo sapiens 117-124 15448091-0 2004 Evidence against the involvement of oxidative stress in fatty acid inhibition of insulin secretion. Fatty Acids 56-66 insulin Homo sapiens 81-88 15479216-0 2004 Effects of dietary fatty acids on insulin sensitivity and secretion. Fatty Acids 19-30 insulin Homo sapiens 34-41 15684682-4 2004 In the current study, we investigated the effects of insulin preconditioning and amino acid supplementation on the gene expression profile of the urea cycle and fatty acid metabolism enzymes. Fatty Acids 161-171 insulin Homo sapiens 53-60 15591007-4 2004 A reduction of the fatty acid transport inside the mitochondria results in the cytosolic accumulation of triglycerides, which is implicated in the pathogenesis of insulin resistance. Fatty Acids 19-29 insulin Homo sapiens 163-170 15505010-7 2004 These results demonstrate that in humans, a primary in vivo impairment of insulin action affects glucose and fatty acid metabolism as previously shown and also protein/amino acid metabolism. Fatty Acids 109-119 insulin Homo sapiens 74-81 15448091-7 2004 These results indicate that fatty acid inhibition of insulin secretion 1) is not mediated by de novo ceramide synthesis, ROS, NO, or PGE(2), and 2) is likely to be caused by the generation of signals or metabolites downstream of diacylglycerol. Fatty Acids 28-38 insulin Homo sapiens 53-60 15448091-2 2004 Here we investigated 1) whether ceramide synthesis, which we reported to mediate fatty acid inhibition of insulin gene expression, also inhibits insulin secretion and 2) whether fatty acid inhibition of insulin secretion involves the generation of reactive oxygen species (ROS), nitric oxide (NO), or prostaglandin E(2) (PGE(2)). Fatty Acids 81-91 insulin Homo sapiens 106-113 15252018-0 2004 Fatty acid-induced insulin resistance in L6 myotubes is prevented by inhibition of activation and nuclear localization of nuclear factor kappa B. Fatty Acids 0-10 insulin Homo sapiens 19-26 15252018-1 2004 Recent studies have implicated inhibitor of kappaB kinase (IKK) in mediating fatty acid (FA)-induced insulin resistance. Fatty Acids 77-87 insulin Homo sapiens 101-108 15350011-11 2004 The key enzyme activities of the energy-consuming process of glycogen and fatty acid synthesis as well as lipoprotein metabolism were accelerated by insulin through the IRS-2 / SREBP-1c pathway. Fatty Acids 74-84 insulin Homo sapiens 149-156 15126243-1 2004 Muscle insulin resistance develops when plasma free fatty acids (FFAs) are acutely increased to supraphysiological levels (approximately 1,500-4,000 micromol/l). Fatty Acids 52-63 insulin Homo sapiens 7-14 15306834-3 2004 One recent approach that has met with success has been to acylate, the insulin molecule with a fatty acid, thereby enabling reversible albumin binding. Fatty Acids 95-105 insulin Homo sapiens 71-78 15243703-0 2004 Non-esterified fatty acids impair insulin-mediated glucose uptake and disposition in the liver. Fatty Acids 15-26 insulin Homo sapiens 34-41 15490412-13 2004 Many studies showed that carnitine allowed mitochondrial fatty acid usage to link to the rate of glucose usage, thus improving insulin resistance. Fatty Acids 57-67 insulin Homo sapiens 127-134 15309208-4 2004 Insulin resistance, whether present endogenously or produced experimentally through exposure to fatty acids, glucosamine or tumour necrosis factor alpha, is associated with impaired endothelium-dependent vasodilation and, specifically, with impaired insulin-stimulated vasodilation. Fatty Acids 96-107 insulin Homo sapiens 0-7 15277397-1 2004 Considerable data support adiponectin as an important adipose-derived insulin sensitizer that enhances fatty acid oxidation and alters hepatic gluconeogenesis. Fatty Acids 103-113 insulin Homo sapiens 70-77 15256315-0 2004 Fatty acid composition of erythrocyte phospholipids is related to insulin levels, secretion and resistance in obese type 2 diabetics on Metformin. Fatty Acids 0-10 insulin Homo sapiens 66-73 15256315-1 2004 BACKGROUND: Relationships between fatty acids in erythrocyte phospholipids and insulin parameters have been described in healthy and overweight individuals, but not in obese diabetics. Fatty Acids 34-45 insulin Homo sapiens 79-86 15256315-3 2004 METHODS: In 23 diabetics, the fractions of the different fatty acids in erythrocyte phospholipids were correlated with insulin levels, secretion, sensitivity, resistance and insulinemic response following a standardised breakfast. Fatty Acids 57-68 insulin Homo sapiens 119-126 15297079-7 2004 A recent multicenter study (KANWU) has shown that shifting from a diet rich in saturated fatty acids to one rich in monounsaturated fat improves insulin sensitivity in healthy people while a moderate alpha-3 fatty acids supplementation does not affect insulin sensitivity. Fatty Acids 79-100 insulin Homo sapiens 145-152 15297079-7 2004 A recent multicenter study (KANWU) has shown that shifting from a diet rich in saturated fatty acids to one rich in monounsaturated fat improves insulin sensitivity in healthy people while a moderate alpha-3 fatty acids supplementation does not affect insulin sensitivity. Fatty Acids 89-100 insulin Homo sapiens 145-152 15612519-9 2004 Finally, it shows the target genes activated by the different isoforms of PPARs, the metabolic integration between the different PPAR isoforms to maintain a balance between fatty acid synthesis and oxidation and the association with the development of obesity and insulin resistance. Fatty Acids 173-183 insulin Homo sapiens 264-271 15105415-0 2004 Increased beta-oxidation in muscle cells enhances insulin-stimulated glucose metabolism and protects against fatty acid-induced insulin resistance despite intramyocellular lipid accumulation. Fatty Acids 109-119 insulin Homo sapiens 128-135 15105415-1 2004 Skeletal muscle insulin resistance may be aggravated by intramyocellular accumulation of fatty acid-derived metabolites that inhibit insulin signaling. Fatty Acids 89-99 insulin Homo sapiens 16-23 15105415-2 2004 We tested the hypothesis that enhanced fatty acid oxidation in myocytes should protect against fatty acid-induced insulin resistance by limiting lipid accumulation. Fatty Acids 39-49 insulin Homo sapiens 114-121 15105415-2 2004 We tested the hypothesis that enhanced fatty acid oxidation in myocytes should protect against fatty acid-induced insulin resistance by limiting lipid accumulation. Fatty Acids 95-105 insulin Homo sapiens 114-121 15168018-2 2004 Obesity and insulin resistance are polygenic disorders, heavily influenced by environmental and life-style factors, and are virtually always associated with disturbed fatty acid metabolism in adipose and other tissues. Fatty Acids 167-177 insulin Homo sapiens 12-19 15168018-3 2004 The aim of this study was to investigate mRNA expression levels of fatty-acid-handling proteins in adipose tissue in relation to markers of genetic and acquired obesity and insulin resistance. Fatty Acids 67-77 insulin Homo sapiens 173-180 15168018-8 2004 CONCLUSIONS/INTERPRETATION: These findings indicate that expression of specific adipose tissue fatty-acid-handling proteins is related to obesity and insulin resistance, and that, in particular, FATP4 plays a role in acquired obesity. Fatty Acids 95-105 insulin Homo sapiens 150-157 15181027-6 2004 The insulin-resistant state that is so common in obesity probably reflects the effects of increased release of fatty acids from fat cells that are then stored in the liver or muscle. Fatty Acids 111-122 insulin Homo sapiens 4-11 15183629-3 2004 Insulin-sensitive organs, overburdened by high concentrations of non-esterified fatty acids, may develop resistance to insulin action. Fatty Acids 80-91 insulin Homo sapiens 0-7 15183629-3 2004 Insulin-sensitive organs, overburdened by high concentrations of non-esterified fatty acids, may develop resistance to insulin action. Fatty Acids 80-91 insulin Homo sapiens 119-126 15183629-4 2004 In addition, insulin secretion from pancreatic beta-cells may be impaired by long-standing elevation of concentrations of non-esterified fatty acid in plasma. Fatty Acids 137-147 insulin Homo sapiens 13-20 15168018-0 2004 Expression of fatty-acid-handling proteins in human adipose tissue in relation to obesity and insulin resistance. Fatty Acids 14-24 insulin Homo sapiens 94-101 15111489-2 2004 The aim of the present study was to examine the content and composition of fatty acids in ceramide and sphingomyelin in human muscle and to evaluate their relationships with insulin sensitivity. Fatty Acids 75-86 insulin Homo sapiens 174-181 15113941-6 2004 We also showed that linoleic acid, a representative PUFA, attenuated the actions of insulin and Dex on fatty acid and lipid synthesis as well as FAS activity and expression. Fatty Acids 103-113 insulin Homo sapiens 84-91 15026062-1 2004 The central role of adipose tissue hormone-sensitive lipase in regulating fatty acid metabolism makes it a potential pharmacological target for the prevention of peripheral insulin resistance in obese, prediabetic and diabetic individuals. Fatty Acids 74-84 insulin Homo sapiens 173-180 15131759-3 2004 In a further study (study 2), relationships between erythrocyte membrane fatty acid concentrations and insulin sensitivity, S(I), measured using the intravenous glucose tolerance test (IVGTT), were evaluated in 30 asymptomatic men. Fatty Acids 73-83 insulin Homo sapiens 103-110 15131759-6 2004 In study 2, highly insulin-sensitive individuals (n = 8) had significantly lower erythrocyte membrane fatty acid concentrations than those with low/normal S(I). Fatty Acids 102-112 insulin Homo sapiens 19-26 15294047-2 2004 It has been speculated that elevated NEFA delivery and/or impaired fatty acid (FA) oxidation result in intramyocellular accumulation of triacylglycerol and FA metabolites, which are likely to induce defects in the insulin signalling cascade, causing insulin resistance. Fatty Acids 67-77 insulin Homo sapiens 214-221 15163922-5 2004 Adiponectin improves insulin sensitivity in skeletal muscle and liver, through a stimulation of fatty acid oxidation and glucose utilization. Fatty Acids 96-106 insulin Homo sapiens 21-28 15223984-4 2004 In contrast, the B-oxidation of fatty acids can be either increased (as in insulin resistance-associated NASH) or decreased (as in drug-induced NASH). Fatty Acids 32-43 insulin Homo sapiens 75-82 15177133-0 2004 The role of the A54T polymorphism of the intestinal fatty acid binding protein for lipid levels, insulin sensitivity and carotid atherosclerosis. Fatty Acids 52-62 insulin Homo sapiens 97-104 14968298-5 2004 RESULTS: Non-esterified fatty acids decreased glucose-stimulated insulin secretion, insulin content and increased triglyceride content of human isolated islets, independently from the deleterious effect of glucose. Fatty Acids 24-35 insulin Homo sapiens 65-72 14968298-5 2004 RESULTS: Non-esterified fatty acids decreased glucose-stimulated insulin secretion, insulin content and increased triglyceride content of human isolated islets, independently from the deleterious effect of glucose. Fatty Acids 24-35 insulin Homo sapiens 84-91 14968298-9 2004 CONCLUSION/INTERPRETATION: In our model of isolated human islets, increased glucose and non-esterified fatty acids separately reproduced the two major beta-cell alterations observed in vivo, i.e. loss of glucose-stimulated insulin secretion and reduction in islet insulin content. Fatty Acids 103-114 insulin Homo sapiens 223-230 14968298-9 2004 CONCLUSION/INTERPRETATION: In our model of isolated human islets, increased glucose and non-esterified fatty acids separately reproduced the two major beta-cell alterations observed in vivo, i.e. loss of glucose-stimulated insulin secretion and reduction in islet insulin content. Fatty Acids 103-114 insulin Homo sapiens 264-271 15068229-2 2004 Because fatty acids modulate insulin-stimulated Akt signaling cascades in smooth muscle cells, we hypothesized that fatty acids would differentially regulate endothelial Akt signaling, eNOS phosphorylation, and NO production. Fatty Acids 8-19 insulin Homo sapiens 29-36 15068229-2 2004 Because fatty acids modulate insulin-stimulated Akt signaling cascades in smooth muscle cells, we hypothesized that fatty acids would differentially regulate endothelial Akt signaling, eNOS phosphorylation, and NO production. Fatty Acids 116-127 insulin Homo sapiens 29-36 14960743-8 2004 CONCLUSIONS: These data support the hypothesis that insulin resistance in the skeletal muscle of insulin-resistant offspring of patients with type 2 diabetes is associated with dysregulation of intramyocellular fatty acid metabolism, possibly because of an inherited defect in mitochondrial oxidative phosphorylation. Fatty Acids 211-221 insulin Homo sapiens 52-59 14960743-8 2004 CONCLUSIONS: These data support the hypothesis that insulin resistance in the skeletal muscle of insulin-resistant offspring of patients with type 2 diabetes is associated with dysregulation of intramyocellular fatty acid metabolism, possibly because of an inherited defect in mitochondrial oxidative phosphorylation. Fatty Acids 211-221 insulin Homo sapiens 97-104 15090211-1 2004 The modulation of fatty acid metabolism and especially the stimulation of fatty acid oxidation in liver or skeletal muscle are attractive therapeutic approaches for the treatment of obesity and the associated insulin resistance. Fatty Acids 18-28 insulin Homo sapiens 209-216 15090211-1 2004 The modulation of fatty acid metabolism and especially the stimulation of fatty acid oxidation in liver or skeletal muscle are attractive therapeutic approaches for the treatment of obesity and the associated insulin resistance. Fatty Acids 74-84 insulin Homo sapiens 209-216 14684613-8 2004 Although purely speculative, it is possible that higher levels of fatty acid translocase/CD36 in human female liver might contribute to the sexually dimorphic development of diseases resulting from or characterized by disturbances in lipid metabolism, such as arteriosclerosis, hyperlipidemia, and insulin resistance. Fatty Acids 66-76 insulin Homo sapiens 298-305 15068229-0 2004 Fatty acids differentially modulate insulin-stimulated endothelial nitric oxide production by an Akt-independent pathway. Fatty Acids 0-11 insulin Homo sapiens 36-43 15163922-2 2004 Insulin resistance in skeletal muscle is of a particular importance, and could be the consequence of an increase in intracellular and circulating fatty acids and triglycerides. Fatty Acids 146-157 insulin Homo sapiens 0-7 14634727-2 2004 Insulin resistance, a characteristic of gestational diabetes and obesity, is correlated with the fatty acids profile of the red cell and skeletal muscle membranes. Fatty Acids 97-108 insulin Homo sapiens 0-7 14749269-2 2004 We have attempted to analyze the role of PPAR-alpha-linked fatty acid metabolism in islet function in health and in insulin-resistant states linked to lifestyle factors, in particular pregnancy and a diet inappropriately high in saturated fat. Fatty Acids 59-69 insulin Homo sapiens 116-123 15029093-5 2004 Conversely, leptin and adiponectin both exert an insulin-sensitizing effect, at least in part, by favoring tIssue fatty-acId oxIdation through activation of AMP-activated kinase. Fatty Acids 114-124 insulin Homo sapiens 49-56 15030793-1 2004 Fatty acid metabolism is abnormal in insulin-resistant states that increase the risk of atherosclerosis such as type 2 diabetes and the metabolic syndrome. Fatty Acids 0-10 insulin Homo sapiens 37-44 15384826-1 2004 Failure of the pancreatic beta cells to produce insulin or development of defective molecular signaling of insulin to the peripheral tissue cells (insulin resistance) induces persistent hyperglycemia and accumulation of fatty acids in the blood of patients with diabetes. Fatty Acids 220-231 insulin Homo sapiens 48-55 15384826-1 2004 Failure of the pancreatic beta cells to produce insulin or development of defective molecular signaling of insulin to the peripheral tissue cells (insulin resistance) induces persistent hyperglycemia and accumulation of fatty acids in the blood of patients with diabetes. Fatty Acids 220-231 insulin Homo sapiens 107-114 15384826-1 2004 Failure of the pancreatic beta cells to produce insulin or development of defective molecular signaling of insulin to the peripheral tissue cells (insulin resistance) induces persistent hyperglycemia and accumulation of fatty acids in the blood of patients with diabetes. Fatty Acids 220-231 insulin Homo sapiens 107-114 14722654-7 2004 We review how circulating factors such as insulin itself, TNF-alpha, interleukins, fatty acids and glycation products influence insulin action through insulin signalling molecules themselves or through other pathways ultimately impinging on the insulin-signalling pathway. Fatty Acids 83-94 insulin Homo sapiens 128-135 14722654-7 2004 We review how circulating factors such as insulin itself, TNF-alpha, interleukins, fatty acids and glycation products influence insulin action through insulin signalling molecules themselves or through other pathways ultimately impinging on the insulin-signalling pathway. Fatty Acids 83-94 insulin Homo sapiens 128-135 14722654-7 2004 We review how circulating factors such as insulin itself, TNF-alpha, interleukins, fatty acids and glycation products influence insulin action through insulin signalling molecules themselves or through other pathways ultimately impinging on the insulin-signalling pathway. Fatty Acids 83-94 insulin Homo sapiens 128-135 15516157-2 2004 The fatty acid modification allows insulin detemir to reversibly bind to albumin, thereby providing slow absorption and a prolonged and consistent metabolic effect of up to 24 hours in patients with type 1 or type 2 diabetes mellitus. Fatty Acids 4-14 insulin Homo sapiens 35-42 14715877-1 2004 Disturbances in fatty acid metabolism are involved in the etiology of insulin resistance and the related dyslipidemia, hypertension, and procoagulant state. Fatty Acids 16-26 insulin Homo sapiens 70-77 14693719-12 2004 This finding suggests that mitochondrial fatty acid oxidation influences insulin secretion by a hitherto unknown mechanism. Fatty Acids 41-51 insulin Homo sapiens 73-80 15898827-5 2004 Insulin administration switches cell metabolism from fatty acids to carbohydrates and restores calcium fluxes, resulting in improvement in cardiac contractility. Fatty Acids 53-64 insulin Homo sapiens 0-7 14681835-3 2004 We have previously shown that in combination, the relationships with fasting insulin of dietary polyunsaturated to saturated fatty acid ratio (P:S ratio) and physical activity are additive. Fatty Acids 115-135 insulin Homo sapiens 77-84 14641007-5 2003 These include stimulation of hepatic glucose output by fatty acids, potentiation of glucose-stimulated insulin secretion by fatty acids, and the cellular mechanism whereby high glucose and insulin concentrations inhibit fatty acid oxidation via malonyl-CoA regulation of carnitine palmitoyltransferase-1. Fatty Acids 124-135 insulin Homo sapiens 103-110 14641017-5 2003 Conversely, leptin and adiponectin exert an insulin-sensitizing effect, at least in part by favouring tissue fatty-acid oxidation through AMP-activated kinase activation. Fatty Acids 109-119 insulin Homo sapiens 44-51 14641015-0 2003 Fatty acid-induced insulin resistance: role of insulin receptor substrate 1 serine phosphorylation in the retroregulation of insulin signalling. Fatty Acids 0-10 insulin Homo sapiens 19-26 14641015-0 2003 Fatty acid-induced insulin resistance: role of insulin receptor substrate 1 serine phosphorylation in the retroregulation of insulin signalling. Fatty Acids 0-10 insulin Homo sapiens 47-54 14641007-5 2003 These include stimulation of hepatic glucose output by fatty acids, potentiation of glucose-stimulated insulin secretion by fatty acids, and the cellular mechanism whereby high glucose and insulin concentrations inhibit fatty acid oxidation via malonyl-CoA regulation of carnitine palmitoyltransferase-1. Fatty Acids 124-135 insulin Homo sapiens 189-196 14641015-5 2003 Elevated plasma fatty acid concentrations are associated with reduced insulin-stimulated glucose transport activity as a consequence of altered insulin signalling through PI 3-kinase. Fatty Acids 16-26 insulin Homo sapiens 70-77 14708363-0 2003 [Insulin resistance as an inhibition of intake of the saturated fatty acids in form of triglycerides by myocyte receptors]. Fatty Acids 54-75 insulin Homo sapiens 1-8 14641015-5 2003 Elevated plasma fatty acid concentrations are associated with reduced insulin-stimulated glucose transport activity as a consequence of altered insulin signalling through PI 3-kinase. Fatty Acids 16-26 insulin Homo sapiens 144-151 14704736-6 2003 Using a similar (13)C/(31)P MRS approach, we have also demonstrated that fatty acids cause insulin resistance in humans due to a decrease in insulin-stimulated muscle glucose transport activity, which could be attributed to reduced insulin-stimulated IRS-1-associated phosphatidylinositol 3-kinase activity, a required step in insulin-stimulated glucose transport into muscle. Fatty Acids 73-84 insulin Homo sapiens 91-98 14704736-6 2003 Using a similar (13)C/(31)P MRS approach, we have also demonstrated that fatty acids cause insulin resistance in humans due to a decrease in insulin-stimulated muscle glucose transport activity, which could be attributed to reduced insulin-stimulated IRS-1-associated phosphatidylinositol 3-kinase activity, a required step in insulin-stimulated glucose transport into muscle. Fatty Acids 73-84 insulin Homo sapiens 141-148 14704736-6 2003 Using a similar (13)C/(31)P MRS approach, we have also demonstrated that fatty acids cause insulin resistance in humans due to a decrease in insulin-stimulated muscle glucose transport activity, which could be attributed to reduced insulin-stimulated IRS-1-associated phosphatidylinositol 3-kinase activity, a required step in insulin-stimulated glucose transport into muscle. Fatty Acids 73-84 insulin Homo sapiens 141-148 14704736-6 2003 Using a similar (13)C/(31)P MRS approach, we have also demonstrated that fatty acids cause insulin resistance in humans due to a decrease in insulin-stimulated muscle glucose transport activity, which could be attributed to reduced insulin-stimulated IRS-1-associated phosphatidylinositol 3-kinase activity, a required step in insulin-stimulated glucose transport into muscle. Fatty Acids 73-84 insulin Homo sapiens 141-148 14704736-8 2003 Finally, we propose that any perturbation that leads to an increase in intramyocellular lipid (fatty acid metabolites) content such as acquired or inherited defects in mitochondrial fatty acid oxidation, defects in adipocyte fat metabolism or simply increased fat delivery to muscle/liver due to increased energy intake will lead to insulin resistance through this final common pathway. Fatty Acids 95-105 insulin Homo sapiens 333-340 14605989-7 2003 In conclusion, our data provide preliminary evidence that insulin resistance of skeletal muscle does not necessarily involve primary defects in insulin action, but could represent susceptibility to the desensitizing effect of fatty acids and possibly other environmental or adipose tissue-derived factors. Fatty Acids 226-237 insulin Homo sapiens 58-65 14505485-4 2003 The importance of non-esterified fatty acids in the formation of the lipoproteins is discussed, as well as the effects of non-esterified fatty acids on insulin secretion and glucose transport, since the hallmark of Type II diabetes is insulin resistance. Fatty Acids 137-148 insulin Homo sapiens 152-159 14605989-2 2003 In the present study, we tested the hypothesis that treating cultured skeletal muscle cells with fatty acids has an effect on insulin action which differs between insulin-sensitive and insulin-resistant subjects. Fatty Acids 97-108 insulin Homo sapiens 126-133 14605989-2 2003 In the present study, we tested the hypothesis that treating cultured skeletal muscle cells with fatty acids has an effect on insulin action which differs between insulin-sensitive and insulin-resistant subjects. Fatty Acids 97-108 insulin Homo sapiens 163-170 14605989-2 2003 In the present study, we tested the hypothesis that treating cultured skeletal muscle cells with fatty acids has an effect on insulin action which differs between insulin-sensitive and insulin-resistant subjects. Fatty Acids 97-108 insulin Homo sapiens 163-170 12777469-6 2003 Metabolic profile changes in response to GLP-1-induced cell differentiation include selective increases in de novo fatty acid synthesis from glucose and consequent chain elongation, allowing increased membrane formation and greater insulin availability and release. Fatty Acids 115-125 insulin Homo sapiens 232-239 12939551-1 2003 The effect of insulin resistance (IR) on the fatty acid metabolism of myocardium, and therefore on the recovery of left ventricular (LV) wall motion, has not been established in patients with acute myocardial infarction (AMI). Fatty Acids 45-55 insulin Homo sapiens 14-21 14502097-5 2003 Reduced suppression of lipolysis by insulin in obese subjects is associated with increased levels of fatty acids that damage the arterial wall and promote atherosclerosis. Fatty Acids 101-112 insulin Homo sapiens 36-43 12684219-6 2003 It has been proposed that nutrient insulin secretagogues stimulate insulin release by increasing formation of malonyl-CoA, which, by blocking carnitine palmitoyltransferase 1 (CPT-1), switches fatty acid (FA) catabolism to synthesis of PKC-activating lipids. Fatty Acids 193-203 insulin Homo sapiens 35-42 12684219-6 2003 It has been proposed that nutrient insulin secretagogues stimulate insulin release by increasing formation of malonyl-CoA, which, by blocking carnitine palmitoyltransferase 1 (CPT-1), switches fatty acid (FA) catabolism to synthesis of PKC-activating lipids. Fatty Acids 193-203 insulin Homo sapiens 67-74 12826272-8 2003 Antagonizing the entry of fatty acids into the mitochondria, with either insulin or malonyl CoA, did not interfere with ALCAR protection against MPP(+). Fatty Acids 26-37 insulin Homo sapiens 73-80 14692611-5 2003 Furthermore, evidence is increasing that insulin-resistant muscle is characterised by a lowered ability to oxidise fatty acids. Fatty Acids 115-126 insulin Homo sapiens 41-48 14584587-9 2003 Emerging evidence indicates that "diabetogenic factors" associated with insulin resistance, such as TNFalpha and elevated circulating fatty acids, impact on insulin signalling at the level of IRS-1 serine/threonine phosphorylation. Fatty Acids 134-145 insulin Homo sapiens 72-79 14584587-9 2003 Emerging evidence indicates that "diabetogenic factors" associated with insulin resistance, such as TNFalpha and elevated circulating fatty acids, impact on insulin signalling at the level of IRS-1 serine/threonine phosphorylation. Fatty Acids 134-145 insulin Homo sapiens 157-164 12700337-7 2003 Together, these data are the first to implicate in vivo increases in Munc18c as a potential contributing mechanism to fatty acid-induced insulin resistance. Fatty Acids 118-128 insulin Homo sapiens 137-144 12888298-3 2003 The postprandial model of insulin resistance--the hypothesis that excessive postprandial free, fatty acid (FFA) flux plays a key role in the genesis of the insulin resistance syndrome--may help to rationalize this seemingly paradoxical observation. Fatty Acids 95-105 insulin Homo sapiens 26-33 12888298-7 2003 When circulating triglycerides are broken down by muscle or by insulin-sensitive subcutaneous adipocytes, the evolved fatty acids are apt to be stored immediately--whereas the fatty acids produced by chylomicron breakdown in the visceral depot are much more prone to escape to the circulation and contribute to high postprandial FFA flux. Fatty Acids 118-129 insulin Homo sapiens 63-70 12888298-7 2003 When circulating triglycerides are broken down by muscle or by insulin-sensitive subcutaneous adipocytes, the evolved fatty acids are apt to be stored immediately--whereas the fatty acids produced by chylomicron breakdown in the visceral depot are much more prone to escape to the circulation and contribute to high postprandial FFA flux. Fatty Acids 176-187 insulin Homo sapiens 63-70 12700337-1 2003 Fatty acids inhibit insulin-mediated glucose metabolism in skeletal muscle, an effect largely attributed to defects in insulin-mediated glucose transport. Fatty Acids 0-11 insulin Homo sapiens 20-27 12800094-0 2003 Nicotinic acid-induced insulin resistance is related to increased circulating fatty acids and fat oxidation but not muscle lipid content. Fatty Acids 78-89 insulin Homo sapiens 23-30 12800094-3 2003 We hypothesized that the reduction in insulin sensitivity occurs via elevation of circulating nonesterified fatty acids (NEFAs) and an increase in intramyocellular lipid (IMCL). Fatty Acids 108-119 insulin Homo sapiens 38-45 12761455-10 2003 Insulin sensitivity was negatively related to fasting plasma insulin (r=-0.67, p<0.001) and non-esterified fatty acids (r=-0.43, p<0.02). Fatty Acids 99-121 insulin Homo sapiens 0-7 12800094-12 2003 Therefore, induction of insulin resistance by NA occurs with increased availability of circulating fatty acids to muscle rather than with increased muscle lipid content. Fatty Acids 99-110 insulin Homo sapiens 24-31 12716789-1 2003 OBJECTIVE: Fatty acids (FAs) have been involved in the development of chronic inflammatory conditions such as insulin resistance and obesity. Fatty Acids 11-22 insulin Homo sapiens 110-117 12716789-1 2003 OBJECTIVE: Fatty acids (FAs) have been involved in the development of chronic inflammatory conditions such as insulin resistance and obesity. Fatty Acids 24-27 insulin Homo sapiens 110-117 12716789-15 2003 CONCLUSIONS: Dietary FAs (as inferred from plasma FA concentration) seem to be linked to inflammatory activity in overweight subjects and in subjects with insulin resistance. Fatty Acids 21-24 insulin Homo sapiens 155-162 12828082-1 2003 BACKGROUND/AIMS: The relationship between insulin resistance and the occurrence of fatty acid has been documented. Fatty Acids 83-93 insulin Homo sapiens 42-49 12747853-0 2003 Insulin secretion: fatty acid signalling via serpentine receptors. Fatty Acids 19-29 insulin Homo sapiens 0-7 12727983-1 2003 We compared metabolic effects as well as plasma and interstitial fluid kinetics of fatty acid-acylated insulin, Lys(B29)(N(epsilon)-omega-carboxynonadecanoyl)-des(B30) human insulin (O346), with previously determined kinetics of native insulin and insulin detemir. Fatty Acids 83-93 insulin Homo sapiens 103-110 12525490-0 2003 A role for ceramide, but not diacylglycerol, in the antagonism of insulin signal transduction by saturated fatty acids. Fatty Acids 97-118 insulin Homo sapiens 66-73 12663471-0 2003 Protein kinase C delta activation and translocation to the nucleus are required for fatty acid-induced apoptosis of insulin-secreting cells. Fatty Acids 84-94 insulin Homo sapiens 116-123 12601639-0 2003 Effect of obesity on susceptibility to fatty acid-induced peripheral tissue insulin resistance. Fatty Acids 39-49 insulin Homo sapiens 76-83 12793596-1 2003 Augmented release of non-esterified fatty acids (NEFA) from insulin-resistant adipocytes appears to be the main cause of the "atherogenic lipoprotein profile" associated with insulin resistance and type 2 diabetes. Fatty Acids 36-47 insulin Homo sapiens 60-67 12793596-1 2003 Augmented release of non-esterified fatty acids (NEFA) from insulin-resistant adipocytes appears to be the main cause of the "atherogenic lipoprotein profile" associated with insulin resistance and type 2 diabetes. Fatty Acids 36-47 insulin Homo sapiens 175-182 12540412-1 2003 BACKGROUND: Fatty acid concentrations are increased in patients with HIV and fat redistribution and may contribute to insulin resistance in this population. Fatty Acids 12-22 insulin Homo sapiens 118-125 12540412-8 2003 CONCLUSIONS: Acute inhibition of lipolysis and reduction in fatty acid concentrations are associated with improved insulin sensitivity in patients with HIV lipodystrophy and hyperinsulinemia. Fatty Acids 60-70 insulin Homo sapiens 115-122 12544656-6 2003 This review summarizes recent data on the relationships between fatty acid composition in plasma and insulin resistance, diabetes and other disorders related to the metabolic syndrome. Fatty Acids 64-74 insulin Homo sapiens 101-108 12544656-7 2003 RECENT FINDINGS: Insulin resistance and insulin resistant states are often associated with the fatty acid pattern in plasma, characterized by an increased proportion of palmitic (16 : 0) and a low proportion of linoleic (18 : 2 n-6) acids, with a distribution of other fatty acids indicating an increased activity of delta-9 and delta-6 desaturase. Fatty Acids 95-105 insulin Homo sapiens 17-24 12544656-7 2003 RECENT FINDINGS: Insulin resistance and insulin resistant states are often associated with the fatty acid pattern in plasma, characterized by an increased proportion of palmitic (16 : 0) and a low proportion of linoleic (18 : 2 n-6) acids, with a distribution of other fatty acids indicating an increased activity of delta-9 and delta-6 desaturase. Fatty Acids 95-105 insulin Homo sapiens 40-47 12544656-7 2003 RECENT FINDINGS: Insulin resistance and insulin resistant states are often associated with the fatty acid pattern in plasma, characterized by an increased proportion of palmitic (16 : 0) and a low proportion of linoleic (18 : 2 n-6) acids, with a distribution of other fatty acids indicating an increased activity of delta-9 and delta-6 desaturase. Fatty Acids 269-280 insulin Homo sapiens 17-24 12544656-7 2003 RECENT FINDINGS: Insulin resistance and insulin resistant states are often associated with the fatty acid pattern in plasma, characterized by an increased proportion of palmitic (16 : 0) and a low proportion of linoleic (18 : 2 n-6) acids, with a distribution of other fatty acids indicating an increased activity of delta-9 and delta-6 desaturase. Fatty Acids 269-280 insulin Homo sapiens 40-47 12485810-0 2003 Acute lowering of circulating fatty acids improves insulin secretion in a subset of type 2 diabetes subjects. Fatty Acids 30-41 insulin Homo sapiens 51-58 12674487-10 2002 In the linear regression analysis, saturated fatty acids were significantly related to waist circumference, fasting glucose, fasting insulin, and HOMA. Fatty Acids 35-56 insulin Homo sapiens 133-140 12447984-7 2003 Although, it has been accepted that fatty acid oxidation is necessary for its stimulation of insulin secretion, the possible mechanisms by which fatty acids (FA) affect insulin secretion are discussed in this review. Fatty Acids 36-46 insulin Homo sapiens 93-100 12447984-7 2003 Although, it has been accepted that fatty acid oxidation is necessary for its stimulation of insulin secretion, the possible mechanisms by which fatty acids (FA) affect insulin secretion are discussed in this review. Fatty Acids 145-156 insulin Homo sapiens 169-176 12546272-1 2002 The metabolic syndrome may be viewed as a state of insulin-counterregulatory overdrive: counterregulatory hormones and fatty acids chronically duel with insulin, causing a cascade of biochemical interactions resulting in insulin resistance, hypertension, and dyslipidemia. Fatty Acids 119-130 insulin Homo sapiens 51-58 12546272-1 2002 The metabolic syndrome may be viewed as a state of insulin-counterregulatory overdrive: counterregulatory hormones and fatty acids chronically duel with insulin, causing a cascade of biochemical interactions resulting in insulin resistance, hypertension, and dyslipidemia. Fatty Acids 119-130 insulin Homo sapiens 153-160 12546272-1 2002 The metabolic syndrome may be viewed as a state of insulin-counterregulatory overdrive: counterregulatory hormones and fatty acids chronically duel with insulin, causing a cascade of biochemical interactions resulting in insulin resistance, hypertension, and dyslipidemia. Fatty Acids 119-130 insulin Homo sapiens 153-160 12436337-0 2002 Interaction between specific fatty acids, GLP-1 and insulin secretion in humans. Fatty Acids 29-40 insulin Homo sapiens 52-59 12436337-1 2002 AIMS/HYPOTHESIS: Fatty acids affect insulin secretion in vivo, but little is known about the effects of specific fatty acids. Fatty Acids 17-28 insulin Homo sapiens 36-43 12580537-1 2002 To counteract insulin resistance, it is necessary to increase the utilization rate of fatty acids in blood and adipose tissue. Fatty Acids 86-97 insulin Homo sapiens 14-21 12685221-10 2002 We also review other approaches with novel insulin molecules attached to thyroxin or fatty acids in order to create a bridge for binding to plasmatic proteins. Fatty Acids 85-96 insulin Homo sapiens 43-50 12370214-0 2002 Supplementation with conjugated linoleic acid causes isomer-dependent oxidative stress and elevated C-reactive protein: a potential link to fatty acid-induced insulin resistance. Fatty Acids 140-150 insulin Homo sapiens 159-166 12370214-10 2002 The oxidative stress seems closely related to induced insulin resistance, suggesting a link between the fatty acid-induced lipid peroxidation seen in the present study and insulin resistance. Fatty Acids 104-114 insulin Homo sapiens 54-61 12370214-10 2002 The oxidative stress seems closely related to induced insulin resistance, suggesting a link between the fatty acid-induced lipid peroxidation seen in the present study and insulin resistance. Fatty Acids 104-114 insulin Homo sapiens 172-179 12231074-5 2002 These alterations in glucose transport activity are likely the result of dysregulation of intramyocellular fatty acid metabolism, whereby fatty acids cause insulin resistance by activation of a serine kinase cascade, leading to decreased insulin-stimulated insulin receptor substrate (IRS)-1 tyrosine phosphorylation and decreased IRS-1-associated phosphatidylinositol 3-kinase activity, a required step in insulin-stimulated glucose transport into muscle. Fatty Acids 107-117 insulin Homo sapiens 238-245 12231074-5 2002 These alterations in glucose transport activity are likely the result of dysregulation of intramyocellular fatty acid metabolism, whereby fatty acids cause insulin resistance by activation of a serine kinase cascade, leading to decreased insulin-stimulated insulin receptor substrate (IRS)-1 tyrosine phosphorylation and decreased IRS-1-associated phosphatidylinositol 3-kinase activity, a required step in insulin-stimulated glucose transport into muscle. Fatty Acids 107-117 insulin Homo sapiens 238-245 12231074-5 2002 These alterations in glucose transport activity are likely the result of dysregulation of intramyocellular fatty acid metabolism, whereby fatty acids cause insulin resistance by activation of a serine kinase cascade, leading to decreased insulin-stimulated insulin receptor substrate (IRS)-1 tyrosine phosphorylation and decreased IRS-1-associated phosphatidylinositol 3-kinase activity, a required step in insulin-stimulated glucose transport into muscle. Fatty Acids 107-117 insulin Homo sapiens 238-245 12231074-5 2002 These alterations in glucose transport activity are likely the result of dysregulation of intramyocellular fatty acid metabolism, whereby fatty acids cause insulin resistance by activation of a serine kinase cascade, leading to decreased insulin-stimulated insulin receptor substrate (IRS)-1 tyrosine phosphorylation and decreased IRS-1-associated phosphatidylinositol 3-kinase activity, a required step in insulin-stimulated glucose transport into muscle. Fatty Acids 138-149 insulin Homo sapiens 156-163 12231074-5 2002 These alterations in glucose transport activity are likely the result of dysregulation of intramyocellular fatty acid metabolism, whereby fatty acids cause insulin resistance by activation of a serine kinase cascade, leading to decreased insulin-stimulated insulin receptor substrate (IRS)-1 tyrosine phosphorylation and decreased IRS-1-associated phosphatidylinositol 3-kinase activity, a required step in insulin-stimulated glucose transport into muscle. Fatty Acids 138-149 insulin Homo sapiens 238-245 12231074-5 2002 These alterations in glucose transport activity are likely the result of dysregulation of intramyocellular fatty acid metabolism, whereby fatty acids cause insulin resistance by activation of a serine kinase cascade, leading to decreased insulin-stimulated insulin receptor substrate (IRS)-1 tyrosine phosphorylation and decreased IRS-1-associated phosphatidylinositol 3-kinase activity, a required step in insulin-stimulated glucose transport into muscle. Fatty Acids 138-149 insulin Homo sapiens 238-245 12231074-5 2002 These alterations in glucose transport activity are likely the result of dysregulation of intramyocellular fatty acid metabolism, whereby fatty acids cause insulin resistance by activation of a serine kinase cascade, leading to decreased insulin-stimulated insulin receptor substrate (IRS)-1 tyrosine phosphorylation and decreased IRS-1-associated phosphatidylinositol 3-kinase activity, a required step in insulin-stimulated glucose transport into muscle. Fatty Acids 138-149 insulin Homo sapiens 238-245 12209017-1 2002 The intestinal fatty acid binding protein (FABP2) gene is proposed as a candidate gene for diabetes because the protein it codes is involved in fatty acid (FA) absorption and metabolism and may, therefore, affect insulin sensitivity and glucose metabolism. Fatty Acids 15-25 insulin Homo sapiens 213-220 12209017-1 2002 The intestinal fatty acid binding protein (FABP2) gene is proposed as a candidate gene for diabetes because the protein it codes is involved in fatty acid (FA) absorption and metabolism and may, therefore, affect insulin sensitivity and glucose metabolism. Fatty Acids 144-154 insulin Homo sapiens 213-220 12207841-1 2002 The fasting concentration of non-esterified fatty acids (NEFA) and the degree to which it declines during an oral glucose tolerance test are closely associated with insulin resistance and glucose intolerance. Fatty Acids 44-55 insulin Homo sapiens 165-172 12493085-0 2002 Acute effects of meal fatty acid composition on insulin sensitivity in healthy post-menopausal women. Fatty Acids 22-32 insulin Homo sapiens 48-55 12493085-1 2002 Postprandial plasma insulin concentrations after a single high-fat meal may be modified by the presence of specific fatty acids although the effects of sequential meal ingestion are unknown. Fatty Acids 116-127 insulin Homo sapiens 20-27 12493085-6 2002 The plasma insulin response was significantly higher following the SFA meal than the other meals after both breakfast and lunch (P<0.006) although there was no effect of breakfast fatty acid composition on plasma glucose concentrations. Fatty Acids 67-70 insulin Homo sapiens 11-18 12221198-6 2002 The differences in response of inflammatory signals and of insulin resistance to different fatty acids indicate that not all fatty acids are the same. Fatty Acids 91-102 insulin Homo sapiens 59-66 12196420-12 2002 Considering the use of CLA-supplements among obese individuals, it is important to clarify the clinical consequences of these results, but they also provide physiological insights into the role of specific dietary fatty acids as modulators of insulin resistance in humans. Fatty Acids 214-225 insulin Homo sapiens 243-250 12079847-1 2002 Insulin resistance is characterized by specific changes of the composition of fatty acids in the serum lipids and in the skeletal muscle membranes. Fatty Acids 78-89 insulin Homo sapiens 0-7 12086926-8 2002 To evaluate whether the fatty acid-induced insulin activation of PKC was associated with a change in the IkB kinase (IKK)/nuclear factor (NF)-kappaB pathway, we determined the abundance in muscle of IkappaB-alpha, an inhibitor of NF-kappaB that is degraded after its phosphorylation by IKK. Fatty Acids 24-34 insulin Homo sapiens 43-50 12079892-1 2002 A summary of the Fourth International Smolenice Symposium on Lipids and Insulin Resistance focusing on "The Role of Fatty Acid Metabolism and Fuel Partitioning" is provided. Fatty Acids 116-126 insulin Homo sapiens 72-79 12079860-3 2002 A recent multicenter study (the Kanwu study) on humans has shown that shifting from a diet rich in saturated fatty acids to one rich in monounsaturated fat improved insulin sensitivity in healthy people, while a moderate omega(3) supplementation did not affect it; this second finding confirms previous results in type 2 diabetic patients with hypertriglyceridemia. Fatty Acids 99-120 insulin Homo sapiens 165-172 12079847-7 2002 The strong relationships between the Delta5 desaturase activity, a high content of long-chain polyunsaturated fatty acids in the skeletal muscle, and insulin sensitivity may be due to parallel effects of diet and/or physical activity on the fatty acid composition and on insulin sensitivity. Fatty Acids 110-120 insulin Homo sapiens 150-157 11978645-0 2002 Increased efficiency of fatty acid uptake contributes to lipid accumulation in skeletal muscle of high fat-fed insulin-resistant rats. Fatty Acids 24-34 insulin Homo sapiens 111-118 12643176-3 2002 Skeletal muscle"s ability to select substrate for fuel metabolism, a metabolic flexibility, is also lost in insulin resistance, and defects in fatty acid metabolism during fasting or postabsorptive conditions likely play an important role in lipid oversupply to insulin-resistant muscle. Fatty Acids 143-153 insulin Homo sapiens 262-269 12643176-4 2002 These impairments appear to be at least indirectly centered on the ability of mitochondria to oxidize fatty acids, possibly through mediation of lipid metabolite levels such as ceramide or diacylglycerol, which are known to directly attenuate insulin signaling. Fatty Acids 102-113 insulin Homo sapiens 243-250 12643176-7 2002 Defining mechanisms by which dysregulation of fatty acid metabolism and persistent lipid oversupply alter insulin action may help to target more effective strategies to prevent or treat type 2 diabetes. Fatty Acids 46-56 insulin Homo sapiens 106-113 12037735-2 2002 The plasma concentrations of fatty acids are principally regulated by insulin, which suppresses the release of fatty acids from lipid stores, and catecholamines, which increase their release from lipid stores. Fatty Acids 29-40 insulin Homo sapiens 70-77 12037735-2 2002 The plasma concentrations of fatty acids are principally regulated by insulin, which suppresses the release of fatty acids from lipid stores, and catecholamines, which increase their release from lipid stores. Fatty Acids 111-122 insulin Homo sapiens 70-77 12037735-10 2002 Baseline postabsorptive plasma fatty acid concentrations were significantly correlated to insulin sensitivity (M value) as measured during the euglycemic clamp. Fatty Acids 31-41 insulin Homo sapiens 90-97 12107742-8 2002 Raised non-esterified fatty acids impair insulin"s effect on glucose uptake in skeletal muscle and the vascular endothelium and thus could have detrimental effects on the vasculature, leading to premature cardiovascular disease. Fatty Acids 22-33 insulin Homo sapiens 41-48 12060056-9 2002 Baseline esterified fatty acid composition was also associated with changes in insulin. Fatty Acids 9-30 insulin Homo sapiens 79-86 12099395-1 2002 In diabetes mellitus (DM), increased fatty acids have negative effects on pancreatic beta-cell functions, in addition to enhanced mitochondrial transportation of fatty acids related to decreased insulin levels. Fatty Acids 162-173 insulin Homo sapiens 195-202 12037735-12 2002 These data demonstrate a sustained differential effect of insulin on the plasma fatty acid profile. Fatty Acids 80-90 insulin Homo sapiens 58-65 12021247-1 2002 Recent studies have implicated fatty acid-dependent activation of the serine kinase IKKbeta, which plays a key role in tissue inflammation, in the pathogenesis of insulin resistance. Fatty Acids 31-41 insulin Homo sapiens 163-170 11991847-0 2002 Decreased mitochondrial carnitine translocase in skeletal muscles impairs utilization of fatty acids in insulin-resistant patients. Fatty Acids 89-100 insulin Homo sapiens 104-111 11916926-3 2002 Skeletal muscle is a major site of insulin action, and insulin sensitivity may be related to the fatty acid composition of muscle lipids. Fatty Acids 97-107 insulin Homo sapiens 55-62 12189904-1 2002 BACKGROUND AND AIM: It has been suggested that the threonine (Thr) 54 allele of the intestinal fatty acid binding protein 2 (FABP2) gene is associated with insulin resistance and affects the fatty acid composition of serum lipids. Fatty Acids 95-105 insulin Homo sapiens 156-163 11927386-0 2002 Acute effects of fatty acids on insulin secretion from rat and human islets of Langerhans. Fatty Acids 17-28 insulin Homo sapiens 32-39 11927386-1 2002 Fatty acids have both stimulatory and inhibitory effects on insulin secretion. Fatty Acids 0-11 insulin Homo sapiens 60-67 11927386-2 2002 Long-term exposure to fatty acids results in impaired insulin secretion whilst acute exposure has generally been found to enhance insulin release. Fatty Acids 22-33 insulin Homo sapiens 54-61 11927386-5 2002 We have therefore studied the acute effects of a range of fatty acids on insulin secretion from rat and human islets of Langerhans at different glucose concentrations. Fatty Acids 58-69 insulin Homo sapiens 73-80 11927386-6 2002 Fatty acids (0.5 mM) acutely stimulated insulin release from rat islets of Langerhans in static incubations in a glucose-dependent manner. Fatty Acids 0-11 insulin Homo sapiens 40-47 11927386-10 2002 Stimulation of insulin secretion by fatty acids was also studied in perifused rat islets. Fatty Acids 36-47 insulin Homo sapiens 15-22 11927386-13 2002 The insulin secretory responses to fatty acids of human islets in static incubations were similar to those of rat islets. Fatty Acids 35-46 insulin Homo sapiens 4-11 11970897-0 2002 Insulin causes fatty acid transport protein translocation and enhanced fatty acid uptake in adipocytes. Fatty Acids 15-25 insulin Homo sapiens 0-7 11970897-0 2002 Insulin causes fatty acid transport protein translocation and enhanced fatty acid uptake in adipocytes. Fatty Acids 71-81 insulin Homo sapiens 0-7 11872653-2 2002 This study examined in vivo the interstitial appearance of insulin in hindlimb using the fatty acid acylated insulin analog Lys(B29)-tetradecanoyl des-(B30) human insulin, or NN304, as a marker for insulin transport. Fatty Acids 89-99 insulin Homo sapiens 109-116 11943835-3 2002 Because insulin resistance may be related to fatty acid release from adipose tissue, we hypothesized that the two SAT depots may have a different lipolytic activity. Fatty Acids 45-55 insulin Homo sapiens 8-15 11872653-2 2002 This study examined in vivo the interstitial appearance of insulin in hindlimb using the fatty acid acylated insulin analog Lys(B29)-tetradecanoyl des-(B30) human insulin, or NN304, as a marker for insulin transport. Fatty Acids 89-99 insulin Homo sapiens 109-116 11872660-1 2002 Cyclic nucleotide phosphodiesterase (PDE) 3B plays an important role in the antilipolytic action of insulin and, thereby, the release of fatty acids from adipocytes. Fatty Acids 137-148 insulin Homo sapiens 100-107 11872660-2 2002 Increased concentrations of circulating fatty acids as a result of elevated or unrestrained lipolysis cause insulin resistance. Fatty Acids 40-51 insulin Homo sapiens 108-115 11872653-2 2002 This study examined in vivo the interstitial appearance of insulin in hindlimb using the fatty acid acylated insulin analog Lys(B29)-tetradecanoyl des-(B30) human insulin, or NN304, as a marker for insulin transport. Fatty Acids 89-99 insulin Homo sapiens 109-116 11921432-0 2002 Insulin resistance in type 2 diabetes: role of fatty acids. Fatty Acids 47-58 insulin Homo sapiens 0-7 11914742-8 2002 Insulin sensitivity and plasma low density lipoprotein cholesterol concentrations improved with the diet rich in polyunsaturated fatty acids compared with the diet rich in saturated fatty acids. Fatty Acids 119-140 insulin Homo sapiens 0-7 11872682-6 2002 In conclusion, these results support the hypothesis that thiazolidinediones enhance insulin sensitivity in patients with type 2 diabetes by promoting increased insulin sensitivity in peripheral adipocytes, which results in lower plasma fatty acid concentrations and a redistribution of intracellular lipid from insulin responsive organs into peripheral adipocytes. Fatty Acids 236-246 insulin Homo sapiens 160-167 11872682-6 2002 In conclusion, these results support the hypothesis that thiazolidinediones enhance insulin sensitivity in patients with type 2 diabetes by promoting increased insulin sensitivity in peripheral adipocytes, which results in lower plasma fatty acid concentrations and a redistribution of intracellular lipid from insulin responsive organs into peripheral adipocytes. Fatty Acids 236-246 insulin Homo sapiens 160-167 11925664-1 2002 BACKGROUND: A direct relation has been found between the insulin sensitivity and fatty acid (FA) composition of serum and tissue lipids in adult humans. Fatty Acids 81-91 insulin Homo sapiens 57-64 11823113-3 2002 The pronounced increase in pp insulin levels during VPA treatment may indicate an effect of the fatty acid derivate VPA on pancreatic islet cells. Fatty Acids 96-106 insulin Homo sapiens 30-37 11833059-3 2002 Fatty acids are known to modulate insulin resistance in other disease states, but a comprehensive evaluation of fatty acids has not been undertaken among HIV-infected patients with fat redistribution. Fatty Acids 0-11 insulin Homo sapiens 34-41 11833043-0 2002 Thiazolidinediones enhance insulin-mediated suppression of fatty acid flux in type 2 diabetes mellitus. Fatty Acids 59-69 insulin Homo sapiens 27-34 11833043-3 2002 We evaluated the effect of the TZD troglitazone on insulin-mediated suppression of fatty acid and glycerol kinetics. Fatty Acids 83-93 insulin Homo sapiens 51-58 11739092-1 2002 Fatty acids are known to decrease insulin-mediated glucose utilization in humans, both at rest and during exercise. Fatty Acids 0-11 insulin Homo sapiens 34-41 12476925-0 2002 Effects of long-term fasting on insulin responses to fatty acids in man. Fatty Acids 53-64 insulin Homo sapiens 32-39 11788651-0 2002 Fatty acid-induced insulin resistance: decreased muscle PI3K activation but unchanged Akt phosphorylation. Fatty Acids 0-10 insulin Homo sapiens 19-26 11719829-0 2001 Effect of increased plasma non-esterified fatty acids (NEFAs) on arginine-stimulated insulin secretion in obese humans. Fatty Acids 42-53 insulin Homo sapiens 85-92 11944631-5 2002 The mechanisms that promote the transition from steatosis to nonalcoholic steatohepatitis appear to involve multiple cellular adaptations to the oxidative stress that occurs when fatty acid metabolism is deranged during insulin resistance. Fatty Acids 179-189 insulin Homo sapiens 220-227 11735096-1 2001 Relationships have been demonstrated between insulin sensitivity and the fatty acid (FA) composition of serum and tissue lipids in adult humans. Fatty Acids 73-83 insulin Homo sapiens 45-52 11719829-1 2001 AIMS/HYPOTHESIS: We have shown previously that the increase of plasma non-esterified fatty acids for 48 h results in decreased glucose-stimulated insulin secretion in lean and non-diabetic obese subjects. Fatty Acids 85-96 insulin Homo sapiens 146-153 11719836-10 2001 CONCLUSION/INTERPRETATION: Isocaloric substitution of carbohydrates and monounsaturated fatty acids for saturated fatty acids improved insulin sensitivity in vivo and in vitro, with an increase in glucose disposal. Fatty Acids 78-99 insulin Homo sapiens 135-142 11694656-6 2001 Many studies indicate that dietary patterns that stimulate insulin resistance or secretion, including high consumption of sucrose, various sources of starch, a high glycemic index and high saturated fatty acid intake, are associated with a higher risk of colon cancer. Fatty Acids 189-209 insulin Homo sapiens 59-66 11712400-4 2001 des-B30 human insulin(NN-304), which metabolic action is prolonged by association of the fatty acid residue to albumin in the blood and peripheral tissues, belongs to a new class of soluble long-acting insulin analogs. Fatty Acids 89-99 insulin Homo sapiens 14-28 11712400-4 2001 des-B30 human insulin(NN-304), which metabolic action is prolonged by association of the fatty acid residue to albumin in the blood and peripheral tissues, belongs to a new class of soluble long-acting insulin analogs. Fatty Acids 89-99 insulin Homo sapiens 14-21 11500316-4 2001 During muscle contraction, when total palmitate uptake was increased, insulin further enhanced uptake (+21%, P < 0.05) and esterification of fatty acids (FA) to PL (+73%, P < 0.05), DG (+19%, P < 0.05), and TG (+161%, P < 0.01). Fatty Acids 144-155 insulin Homo sapiens 70-77 11555841-2 2001 Both control and early growth-restricted animals fed a diet rich in saturated fatty acids showed a doubling of the plasma insulin levels as well as a reduced degree of unsaturation in liver and skeletal muscle membrane phospholipids compared with animals fed diets rich in unsaturated fatty acids. Fatty Acids 68-89 insulin Homo sapiens 122-129 11589678-1 2001 OBJECTIVE: High non-esterified fatty acid (NEFA) levels impair glucose-stimulated insulin secretion from islets derived from non-diabetic Zucker rats that are genetically predisposed to diabetes. Fatty Acids 31-41 insulin Homo sapiens 82-89 11831112-3 2001 An increased flux of fatty acids into muscle, liver and pancreas is probably a major cause of insulin resistance and possibly of pancreatic secretory disturbances. Fatty Acids 21-32 insulin Homo sapiens 94-101 11831112-4 2001 Liver exposure to fatty acid overload may also be the main reason for the atherogenic lipoprotein profile of insulin resistance and type 2 diabetes, which is characterised by prolonged post-prandial hypertriglyceridemia, high levels of large very low-density lipoproteins (VLDL) and small, dense low-density lipoproteins (LDL), and a reduced number of apoAl-containing high-density lipoproteins (HDL). Fatty Acids 18-28 insulin Homo sapiens 109-116 11831112-6 2001 The treatment of type 2 diabetes and insulin resistance in obese or non-obese subjects should therefore aim at normalising fatty acid fluxes because this can be expected to enhance insulin action and ameliorate the atherogenic lipoprotein abnormalities. Fatty Acids 123-133 insulin Homo sapiens 37-44 11831112-6 2001 The treatment of type 2 diabetes and insulin resistance in obese or non-obese subjects should therefore aim at normalising fatty acid fluxes because this can be expected to enhance insulin action and ameliorate the atherogenic lipoprotein abnormalities. Fatty Acids 123-133 insulin Homo sapiens 181-188 11423496-0 2001 Association of the Ala54-Thr polymorphism in the intestinal fatty acid-binding protein with 2-h postchallenge insulin levels in the Framingham Offspring Study. Fatty Acids 60-70 insulin Homo sapiens 110-117 11423482-12 2001 We propose that, during short-term caloric restriction, the reduced ability of insulin to inhibit lipids, despite a preserved antilipolytic effect of the hormone in adipose tissue, is caused by an augmented mobilization of fat from skeletal muscle, and that a physiological role of muscle lipolysis provides a local source of fatty acids. Fatty Acids 326-337 insulin Homo sapiens 79-86 11443187-0 2001 Gender factors affect fatty acids-induced insulin resistance in nonobese humans: effects of oral steroidal contraception. Fatty Acids 22-33 insulin Homo sapiens 42-49 11507681-10 2001 In conclusion, our results reveal a significant association between endothelial dysfunction and impaired non-esterified fatty acid suppression in insulin resistant subjects. Fatty Acids 120-130 insulin Homo sapiens 146-153 11479436-10 2001 Moreover, new fatty acid derivatives of insulin analogues are now under experimentation. Fatty Acids 14-24 insulin Homo sapiens 40-47 11440374-0 2001 --to: Bergman RN (2000) non-esterified fatty acids and the liver: why is insulin secreted into the portal vein? Fatty Acids 39-50 insulin Homo sapiens 73-80 11411746-5 2001 Fatty acids are elevated among abdominally obese individuals, are more resistant to suppression by insulin, and may contribute to hypertension. Fatty Acids 0-11 insulin Homo sapiens 99-106 11375335-0 2001 Decreased susceptibility to fatty acid-induced peripheral tissue insulin resistance in women. Fatty Acids 28-38 insulin Homo sapiens 65-72 11452220-10 2001 However deleterious effects of saturated fatty acids on insulin action and the beneficial effects of polyunsaturated fatty acids (PUFAs) could be suspected from animal studies, and from epidemiological or clinical studies in humans. Fatty Acids 31-52 insulin Homo sapiens 56-63 11347757-5 2001 These impairments in fatty acid metabolism during fasting conditions may be related to a metabolic inflexibility in insulin resistance that is not limited to defects in glucose metabolism during insulin-stimulated conditions. Fatty Acids 21-31 insulin Homo sapiens 116-123 11347757-6 2001 Thus, there is substantial evidence implicating perturbations in fatty acid metabolism during accumulation of skeletal muscle triglyceride and in the pathogenesis of insulin resistance. Fatty Acids 65-75 insulin Homo sapiens 166-173 11266382-2 2001 We tested the hypothesis that NASH is associated with 2 defects: (1) peripheral insulin resistance, which increases lipolysis, delivery of free fatty acids (FFA) to the liver, and hepatic fatty acid beta oxidation, thereby creating oxidative stress; and (2) an abnormality within the hepatocytes that might render them more susceptible to injury from oxidative stress. Fatty Acids 144-154 insulin Homo sapiens 80-87 11124961-3 2001 However, certain fatty acids and their derivatives can also act as endogenous ligands for peroxisome proliferator-activated receptor gamma (PPARgamma), a nuclear receptor that positively modulates insulin sensitivity. Fatty Acids 17-28 insulin Homo sapiens 197-204 11158925-0 2001 DAG accumulation from saturated fatty acids desensitizes insulin stimulation of glucose uptake in muscle cells. Fatty Acids 22-43 insulin Homo sapiens 57-64 11327119-3 2001 A few candidate genes, encoding proteins of glucose, insulin and lipid metabolism, lipolytic cascade, fatty acid intestinal absorption, glucocorticoid metabolism, haemostasis and blood pressure, have been associated with a clustering of metabolic abnormalities, although the functional significance of these associations remains to be established. Fatty Acids 102-112 insulin Homo sapiens 53-60 11317662-5 2001 RESULTS: Insulin sensitivity was significantly impaired on the saturated fatty acid diet (-10%, p = 0.03) but did not change on the monounsaturated fatty acid diet (+2%, NS) (p = 0.05 for difference between diets). Fatty Acids 63-83 insulin Homo sapiens 9-16 11317662-8 2001 The favourable effects of substituting a monounsaturated fatty acid diet for a saturated fatty acid diet on insulin sensitivity were only seen at a total fat intake below median (37E%). Fatty Acids 47-67 insulin Homo sapiens 108-115 11317662-9 2001 Here, insulin sensitivity was 12.5% lower and 8.8% higher on the saturated fatty acid diet and monounsaturated fatty acid diet respectively (p = 0.03). Fatty Acids 65-85 insulin Homo sapiens 6-13 11317662-11 2001 CONCLUSIONS/INTERPRETATION: A change of the proportions of dietary fatty acids, decreasing saturated fatty acid and increasing monounsaturated fatty acid, improves insulin sensitivity but has no effect on insulin secretion. Fatty Acids 67-78 insulin Homo sapiens 164-171 11224662-1 2001 In target organs, insulin switches substrate utilization from free fatty acids to glucose, a change that: (i) is oxygen-efficient; (ii) repletes glycogen stores; (iii) removes potentially toxic fatty acids; and (iv) restores intracellular potassium. Fatty Acids 67-78 insulin Homo sapiens 18-25 11453039-9 2001 While causal relationships are still to be clearly established, there are now quite plausible mechanistic links between muscle lipid accumulation and insulin resistance, which go beyond the classic Randle glucose-fatty acid cycle. Fatty Acids 213-223 insulin Homo sapiens 150-157 11206412-0 2001 Distinct long-term regulation of glycerol and non-esterified fatty acid release by insulin and TNF-alpha in 3T3-L1 adipocytes. Fatty Acids 61-71 insulin Homo sapiens 83-90 11206412-2 2001 Our study was to assess the long-term regulation of glycerol and non-esterified fatty acid (NEFA) release by insulin or TNF-alpha. Fatty Acids 80-90 insulin Homo sapiens 109-116 11172480-2 2001 The purpose of this study was to determine the relationship between intakes of specific dietary fatty acids (assessed by 3-day diet records and fatty acid composition of serum cholesterol esters [CEs] and phospholipids [PLs]) and glucose and insulin concentrations during an oral glucose tolerance test (OGTT). Fatty Acids 96-106 insulin Homo sapiens 242-249 11215514-3 2000 These insulin-like actions include stimulating glucose uptake and regulating metabolic processes such as glycolysis, gluconeogenesis, fatty acid synthesis and the pentose phosphate pathway. Fatty Acids 134-144 insulin Homo sapiens 6-13 11142411-3 2000 This evidence suggests the following mechanism: the consumption of excess dietary energy results in the development of insulin resistance with increased circulating levels of insulin, triglycerides, and non-esterified fatty acids. Fatty Acids 207-229 insulin Homo sapiens 119-126 11108733-1 2000 A polymorphism in FABP2 that results in an alanine-to-threonine substitution at amino acid 54 of the intestinal fatty acid-binding protein (IFABP) is associated with insulin resistance in Pima Indians. Fatty Acids 112-122 insulin Homo sapiens 166-173 11113614-6 2000 This abnormality along with a reduction in insulin concentration is assumed to induce a cascade-like process of disturbances including decreases in cellular glucose, acetylcholine, cholesterol, and ATP, associated with changes in the metabolism of amino acids and fatty acids. Fatty Acids 264-275 insulin Homo sapiens 43-50 11016898-1 2000 Recent studies suggest that insulin sensitivity is related to the fatty acid composition of phospholipids in skeletal muscle (SM) membranes. Fatty Acids 66-76 insulin Homo sapiens 28-35 11227245-0 2000 [Obesity and fatty acids in the etiology of insulin resistance]. Fatty Acids 13-24 insulin Homo sapiens 44-51 11227245-2 2000 In the last decades fatty acids (FA) have been implicated in the etiology of insulin resistance. Fatty Acids 20-31 insulin Homo sapiens 77-84 11001753-3 2000 PPAR-gamma is activated by fatty acids, and the membrane composition may have an impact on the activity of PPAR-gamma and thus on the sensitivity of adipocytes to insulin. Fatty Acids 27-38 insulin Homo sapiens 163-170 10954686-0 2000 The impairment in endothelial function induced by non-esterified fatty acids can be reversed by insulin. Fatty Acids 54-76 insulin Homo sapiens 96-103 10971546-12 2000 In conclusion, insulin treatment of patients with poorly controlled non-insulin-dependent diabetes mellitus increased the fast-twitch fibre area, reduced myoglobin levels and decreased muscle enzyme activity related to fatty acid oxidation. Fatty Acids 219-229 insulin Homo sapiens 15-22 11126404-0 2000 Stimulatory effect of increased non-esterified fatty acid concentrations on proinsulin processing in healthy humans. Fatty Acids 47-57 insulin Homo sapiens 76-86 11126404-1 2000 AIMS/HYPOTHESIS: To assess the effect of increased concentrations of non-esterified fatty acids (NEFA) on proinsulin processing in healthy humans. Fatty Acids 73-95 insulin Homo sapiens 106-116 11009601-10 2000 However, in its new position on the surface of the hexamer, the fatty acid chain affects the equilibria of the phenol-induced interconversions between the T(6), T(3)R(3), and R(6) allosteric states of the insulin hexamer. Fatty Acids 64-74 insulin Homo sapiens 205-212 10995598-8 2000 Plasma non-esterified (free) fatty acid and ketone body levels were significantly decreased in both groups by the infusion of exogenous insulin, but the sensitivity of lipolysis was impaired in patients with sepsis. Fatty Acids 29-39 insulin Homo sapiens 136-143 10866053-10 2000 The attachment of a fatty acid chain to LysB29 provided insulin detemir with reduced receptor affinities and metabolic and mitogenic potencies but did not change the balance between mitogenic and metabolic potencies. Fatty Acids 20-30 insulin Homo sapiens 56-63 10976521-7 2000 The peptide of hGH(8-13) dose-dependently enhanced the insulin-involved fatty acid synthesis in rat white adipocytes, and stabilized the C6-NBD-PC (1-acyl-2-[6-[(7-nitro-2,1,3benzoxadiazol-4-yl)amino]-caproyl]-sn- glycero-3-phosphatidylcholine) model membranes. Fatty Acids 72-82 insulin Homo sapiens 55-62 10909961-4 2000 During the low-dose insulin infusion, whole-body fatty acid oxidation, as determined by indirect calorimetry, decreased by 22% from a basal rate of 0.94 +/- 0.06 to 0.74 +/- 0.07 mg x kg(-1) x min(-1) (P = 0.005), but no increase in malonyl-CoA was observed. Fatty Acids 49-59 insulin Homo sapiens 20-27 10909961-5 2000 In contrast, during the high-dose insulin infusion, malonyl-CoA increased from 0.20 +/- 0.01 to 0.24 +/- 0.01 nmol/g (P < 0.001), and whole-body fatty acid oxidation decreased by an additional 41% to 0.44 +/- 0.06 mg x kg(-1) x min(-1) (P < 0.001). Fatty Acids 148-158 insulin Homo sapiens 34-41 10909961-9 2000 The results indicate that an infusion of insulin and glucose at a high rate leads to increases in the concentration of malonyl-CoA in skeletal muscle and to decreases in whole-body and, presumably, muscle fatty acid oxidation. Fatty Acids 205-215 insulin Homo sapiens 41-48 10856515-4 2000 Impaired insulin binding and/or glucose transporters has been related to changes in the fatty acid composition of the membrane induced by dietary fat modification. Fatty Acids 88-98 insulin Homo sapiens 9-16 10945143-2 2000 Fatty acids could play a role in the reduction of beta cell insulin secretion. Fatty Acids 0-11 insulin Homo sapiens 60-67 10945143-3 2000 On a short term basis (< 24 h), fatty acids stimulate glucose-dependent insulin secretion through an increase of ATP availability (due to acyl-CoA mitochondrial oxidation) and an extramitochondrial diacylglycerol and inositol tri phosphate (IP3) production (which stimulate insulin-containing granule exocytosis). Fatty Acids 35-46 insulin Homo sapiens 75-82 10945152-4 2000 Insulin 1) reduces glycosuria and its caloric expenditure; 2) stimulates the stockage of fatty acids into triglycerides in adipose tissue, thus favoring an increase in adipose mass; 3) yields a positive nitrogen balance through an inhibition of muscle proteolysis, thus favoring an increase in lean mass. Fatty Acids 89-100 insulin Homo sapiens 0-7 10787432-3 2000 Insulin stimulation of fatty acid incorporation into triglyceride (TG) was also less pronounced in hepatocytes from the FO-fed group than in those from the OO-fed group but there was no difference in the stimulatory effect of insulin on fatty acid incorporation into phospholipid (PL) in these two groups. Fatty Acids 23-33 insulin Homo sapiens 0-7 10830281-0 2000 Long-chain acyl CoA regulation of protein kinase C and fatty acid potentiation of glucose-stimulated insulin secretion in clonal beta-cells. Fatty Acids 55-65 insulin Homo sapiens 101-108 10882345-8 2000 ASP also influences the rate at which fatty acids are released by adipocytes, and it is clear that insulin and ASP interact in a variety of ways that involve energy storage and release. Fatty Acids 38-49 insulin Homo sapiens 99-106 11014617-3 2000 In addition, short term exposure of this cell type to dietary fatty acids potentiates glucose-induced insulin release. Fatty Acids 62-73 insulin Homo sapiens 102-109 10787432-3 2000 Insulin stimulation of fatty acid incorporation into triglyceride (TG) was also less pronounced in hepatocytes from the FO-fed group than in those from the OO-fed group but there was no difference in the stimulatory effect of insulin on fatty acid incorporation into phospholipid (PL) in these two groups. Fatty Acids 237-247 insulin Homo sapiens 0-7 10767564-2 2000 In a single administration study, rectal insulin absorption was enhanced markedly, and marked hypoglycemia was induced by the emulsion incorporating various fatty acids in an insulin dose-related fashion. Fatty Acids 157-168 insulin Homo sapiens 175-182 10753040-8 2000 Strong positive relations were found between the late increases in large triglyceride-rich lipoproteins and plasma non-esterified fatty acid concentrations after 6 h. CONCLUSION/INTERPRETATION: The degree of insulin sensitivity is a major determinant of postprandial lipaemia in healthy middle-aged men and could add to the regulation of the basal production of large triglyceride-rich lipoproteins. Fatty Acids 130-140 insulin Homo sapiens 208-215 10804328-1 2000 Elevated plasma non-esterified fatty acid (NEFA) levels in obese subjects may contribute to their higher insulin secretory rates by direct effects on the islet B-cells. Fatty Acids 31-41 insulin Homo sapiens 105-112 10889795-15 2000 Subcutaneous fat probably plays the major role in determining systemic plasma non-esterified fatty acid concentrations, which are relevant in determining insulin resistance. Fatty Acids 82-103 insulin Homo sapiens 154-161 10889798-4 2000 Cross-sectional studies show significant relationships between the serum lipid fatty acid composition, which at least partly mirrors the quality of the fatty acids in the diet, and insulin sensitivity. Fatty Acids 79-89 insulin Homo sapiens 181-188 10889798-5 2000 Insulin resistance, and disorders characterized by insulin resistance, are associated with a specific fatty acid pattern of the serum lipids with increased proportions of palmitic (16:0) and palmitoleic acids (16:1 n-7) and reduced levels of linoleic acid (18:2 n-6). Fatty Acids 102-112 insulin Homo sapiens 0-7 10889798-5 2000 Insulin resistance, and disorders characterized by insulin resistance, are associated with a specific fatty acid pattern of the serum lipids with increased proportions of palmitic (16:0) and palmitoleic acids (16:1 n-7) and reduced levels of linoleic acid (18:2 n-6). Fatty Acids 102-112 insulin Homo sapiens 51-58 10889798-8 2000 Several studies have shown that the fatty acid composition of the phosholipids of the skeletal muscle cell membranes is closely related to insulin sensitivity. Fatty Acids 36-46 insulin Homo sapiens 139-146 10889798-9 2000 An increased saturation of the membrane fatty acids and a reduced activity of delta 5 desaturase have been associated with insulin resistance. Fatty Acids 40-51 insulin Homo sapiens 123-130 10889798-12 2000 However, controlled dietary intervention studies in humans investigating the effects of different types of fatty acids on insulin sensitivity have so far been negative. Fatty Acids 107-118 insulin Homo sapiens 122-129 10819234-0 2000 Enhanced escape of non-esterified fatty acids from tissue uptake: its role in impaired insulin-induced lowering of total rate of appearance in obesity and Type II diabetes mellitus. Fatty Acids 34-45 insulin Homo sapiens 87-94 10819234-5 2000 RESULTS: Total arterial plasma non-esterified fatty acid rate of appearance was lower in non-obese healthy subjects than in the other groups at low insulin infusion (p < 0.05) and in obese Type II diabetic patients at high insulin infusion (p < 0.05). Fatty Acids 46-56 insulin Homo sapiens 148-155 10819234-5 2000 RESULTS: Total arterial plasma non-esterified fatty acid rate of appearance was lower in non-obese healthy subjects than in the other groups at low insulin infusion (p < 0.05) and in obese Type II diabetic patients at high insulin infusion (p < 0.05). Fatty Acids 46-56 insulin Homo sapiens 226-233 10889809-1 2000 Insulin sensitivity is potentially enhanced by a range of diet-related changes including reduction of visceral adiposity, a reduction in saturated fatty acids, and possibly a redistribution of the proportions of various unsaturated fatty acids. Fatty Acids 137-158 insulin Homo sapiens 0-7 10842663-5 1999 We demonstrate that fatty acids and amino acids inhibit early post-receptor steps in insulin action, including tyrosine phosphorylation of insulin receptor substrate (IRS) proteins and activation of phosphatidylinositol 3-kinase (PI3-kinase), both in vitro and in several in vivo models. Fatty Acids 20-31 insulin Homo sapiens 85-92 10816109-4 2000 This switch in insulin action was also shown to occur in vivo in experiments that involved the liver-specific targeting of both insulin (delivered within liposomes) and labelled fatty acids (delivered as cholesteryl esters within very-low-density lipoprotein remnants) in awake, unrestrained rats during a euglycaemic clamp. Fatty Acids 178-189 insulin Homo sapiens 15-22 10690951-3 2000 Efforts to alter the PL fatty acid composition in animal models have demonstrated induction of insulin resistance. Fatty Acids 24-34 insulin Homo sapiens 95-102 10690951-4 2000 However, it has been more difficult to determine if changes in insulin sensitivity are associated with changes in the skeletal muscle membrane fatty acid composition of PL in man. Fatty Acids 143-153 insulin Homo sapiens 63-70 10690951-11 2000 These studies suggest that the induction of insulin resistance with NA is associated with changes in the fatty acid composition of PC in man. Fatty Acids 105-115 insulin Homo sapiens 44-51 10639127-1 2000 The ability of unsaturated fatty acid methyl esters to modify amino acid residues in bovine serum albumin (BSA), glutamine synthetase, and insulin in the presence of a metal-catalyzed oxidation system [ascorbate/Fe(III)/O(2)] depends on the degree of unsaturation of the fatty acid. Fatty Acids 27-37 insulin Homo sapiens 139-146 10620001-10 2000 Non-esterified fatty acids at steady state were positively correlated with fasting markers of insulin resistance: fasting plasma glucose (P < 0.05), fasting plasma insulin (P < 0.005) and negatively correlated with the M-value (P < 0.0005). Fatty Acids 15-26 insulin Homo sapiens 94-101 10620001-10 2000 Non-esterified fatty acids at steady state were positively correlated with fasting markers of insulin resistance: fasting plasma glucose (P < 0.05), fasting plasma insulin (P < 0.005) and negatively correlated with the M-value (P < 0.0005). Fatty Acids 15-26 insulin Homo sapiens 167-174 10666005-12 2000 In adipose tissue, GIP has been reported to (1) stimulate fatty acid synthesis, (2) enhance insulin-stimulated incorporation of fatty acids into triglycerides, (3) increase insulin receptor affinity, and (4) increase sensitivity of insulin-stimulated glucose transport. Fatty Acids 128-139 insulin Homo sapiens 92-99 10842650-17 1999 The ASP pathway plays a critical role in fatty acid metabolism and storage, and it has been suggested that ineffective storage of fatty acids by adipocytes due to a defect in the ASP pathway may lead to insulin resistance and Type 2 diabetes. Fatty Acids 130-141 insulin Homo sapiens 203-210 10671999-0 2000 A switch in the direction of the effect of insulin on the partitioning of hepatic fatty acids for the formation of secreted triacylglycerol occurs in vivo, as predicted from studies with perfused livers. Fatty Acids 82-93 insulin Homo sapiens 43-50 10690948-0 2000 Insulin resistance directly correlates with increased saturated fatty acids in skeletal muscle triglycerides. Fatty Acids 54-75 insulin Homo sapiens 0-7 10600804-0 1999 Skeletal muscle fatty acid metabolism in association with insulin resistance, obesity, and weight loss. Fatty Acids 16-26 insulin Homo sapiens 58-65 10842663-5 1999 We demonstrate that fatty acids and amino acids inhibit early post-receptor steps in insulin action, including tyrosine phosphorylation of insulin receptor substrate (IRS) proteins and activation of phosphatidylinositol 3-kinase (PI3-kinase), both in vitro and in several in vivo models. Fatty Acids 20-31 insulin Homo sapiens 139-146 10418851-3 1999 Studies of the mechanisms by which free fatty acids (FFA) cause insulin resistance in humans indicate that increased FFA levels inhibit glucose transport, which may be a consequence of decreased insulin receptor substrate (IRS-1)-associated phosphatidylinositol 3-kinase activity. Fatty Acids 40-51 insulin Homo sapiens 64-71 10544188-0 1999 Markers of capacity to utilize fatty acids in human skeletal muscle: relation to insulin resistance and obesity and effects of weight loss. Fatty Acids 31-42 insulin Homo sapiens 81-88 10544188-2 1999 Less is known about the capacity of skeletal muscle for the metabolism of fatty acids in obesity-related insulin resistance and of the effects of weight loss, though it is evident that muscle contains increased triglyceride. Fatty Acids 74-85 insulin Homo sapiens 105-112 10610074-2 1999 The defects most likely to explain the insulin resistance of the insulin resistance syndrome include: 1) the glucose transport system of skeletal muscle (GLUT-4) and its different signalling proteins and enzymes; 2) glucose phosphorylation by hexokinase; 3) glycogen synthase activity and 4) competition between glucose and fatty acid oxidation (glucose-fatty acid cycle). Fatty Acids 324-334 insulin Homo sapiens 39-46 11122713-2 1999 The effect of dietary fat on insulin varies depending on the type of fatty acid consumed. Fatty Acids 69-79 insulin Homo sapiens 29-36 11122713-3 1999 Saturated fatty acids have been consistently associated with insulin resistance. Fatty Acids 0-21 insulin Homo sapiens 61-68 10525656-11 1999 Inadequate suppression of intramuscular lipolysis resulting in increased availability of non-esterified fatty acids, could represent a potential mechanism involved in the pathogenesis of impaired glucose disposal, i. e. insulin resistance, in muscle. Fatty Acids 104-115 insulin Homo sapiens 220-227 10761864-2 1999 Plasma leptin, tumour necrosis factor-alpha and non-esterified fatty acid levels are all elevated in obesity and play a role in causing insulin resistance. Fatty Acids 63-73 insulin Homo sapiens 136-143 10456206-4 1999 It is, however, possible that variations in non-esterified fatty acids (NEFA) could contribute to this variation because NEFA have been implicated in the pathogenesis of insulin resistance. Fatty Acids 59-70 insulin Homo sapiens 170-177 10471131-4 1999 However, we observed that obese hypertensive patients have elevated plasma concentrations of non-esterified fatty acids (NEFAs), including oleic acid, which are highly resistant to suppression by insulin. Fatty Acids 108-119 insulin Homo sapiens 196-203 10389846-15 1999 We conclude that 1) long-term exposure of human islets to elevated glucose leads to preferential secretion of proinsulin, and this effect persists also after glucose normalization; 2) the glucose effect appears secondary to depletion of mature insulin granules; and 3) elevated fatty acids influence PI/I ratios of secretion by mechanisms that are, in part, incongruous with an over-stimulation effect. Fatty Acids 278-289 insulin Homo sapiens 110-120 10389846-15 1999 We conclude that 1) long-term exposure of human islets to elevated glucose leads to preferential secretion of proinsulin, and this effect persists also after glucose normalization; 2) the glucose effect appears secondary to depletion of mature insulin granules; and 3) elevated fatty acids influence PI/I ratios of secretion by mechanisms that are, in part, incongruous with an over-stimulation effect. Fatty Acids 278-289 insulin Homo sapiens 113-120 10471131-12 1999 Collectively, these observations raise the possibility that fatty acids contribute to functional and structural vascular changes among insulin-resistant individuals. Fatty Acids 60-71 insulin Homo sapiens 135-142 10097910-6 1999 Another principle to prolong insulin action is the use of soluble fatty acid acylated insulins that are bound to albumin after absorption. Fatty Acids 66-76 insulin Homo sapiens 29-36 10360418-4 1999 Following insulin infusion, net splanchnic uptake of total fatty acids decreased from 3.0+/-0.3 to 1.0+/-0.1 micromol/kg min (p<0.01), whereas net renal balance remained neutral (-0.04+/-0.04 vs. -0.06+/-0.03 micromol/kg min, p=N.S.). Fatty Acids 59-70 insulin Homo sapiens 10-17 10220208-0 1999 Time-action profile of the soluble, fatty acid acylated, long-acting insulin analogue NN304. Fatty Acids 36-46 insulin Homo sapiens 69-76 10074631-2 1999 The aim of the study was to investigate whether changes in dietary fatty acids could modify plasma concentration of glucose, insulin and mean blood pressure (MBP). Fatty Acids 67-78 insulin Homo sapiens 125-156 10099938-2 1999 Evidence is reviewed that the growth of breast cancer is favoured by specific dietary fatty acids, visceral fat accumulation and inadequate physical exercise, all of which are thought to interact in favouring the development of the insulin resistance syndrome. Fatty Acids 86-97 insulin Homo sapiens 232-239 9950782-7 1999 These results suggest that insulin is not essential for HSL suppression or increased triacylglycerol clearance but is important in reesterification of fatty acids in adipose tissue but not uptake by skeletal muscle, thus affecting fatty acid partitioning between adipose tissue and the circulation, postprandial nonesterified fatty acid concentrations, and hepatic very low density lipoprotein secretion. Fatty Acids 151-162 insulin Homo sapiens 27-34 9950782-7 1999 These results suggest that insulin is not essential for HSL suppression or increased triacylglycerol clearance but is important in reesterification of fatty acids in adipose tissue but not uptake by skeletal muscle, thus affecting fatty acid partitioning between adipose tissue and the circulation, postprandial nonesterified fatty acid concentrations, and hepatic very low density lipoprotein secretion. Fatty Acids 151-161 insulin Homo sapiens 27-34 9950782-7 1999 These results suggest that insulin is not essential for HSL suppression or increased triacylglycerol clearance but is important in reesterification of fatty acids in adipose tissue but not uptake by skeletal muscle, thus affecting fatty acid partitioning between adipose tissue and the circulation, postprandial nonesterified fatty acid concentrations, and hepatic very low density lipoprotein secretion. Fatty Acids 231-241 insulin Homo sapiens 27-34 10396370-25 1999 Plasma oestrone-fatty acid ester levels are associated with insulin sensitivity in men, independently of body fat. Fatty Acids 16-32 insulin Homo sapiens 60-67 10229304-1 1999 AIM: To determine the relationship of the polymorphism at codon 54 of the intestinal fatty acid binding protein gene (FABP2) with insulin resistance and susceptibility to Type 2 diabetes mellitus (DM) in the Japanese population. Fatty Acids 85-95 insulin Homo sapiens 130-137 10576523-10 1999 Other effects involved in the blood glucose-lowering effect of metformin include an insulin-independent suppression of fatty acid oxidation and a reduction in hypertriglyceridaemia. Fatty Acids 119-129 insulin Homo sapiens 84-91 10513036-7 1999 The different factors that may impair insulin action and alter glucose uptake in skeletal muscle are: lower blood flow to muscle, produced by either decreased vasodilation or by increased sympathetic nerve activity; augmented diffusion distance from capillaries to muscle due to a decrease in capillary number or to enlarged muscle cells; decrease of insulin receptors; change in the fatty acid profile of major membrane structural phospholipids; decrease in glucose transporters (GLUT 4) and/or hexokinase; impairment in metabolic routes of glucose in muscle as reduction in glycogen synthase. Fatty Acids 384-394 insulin Homo sapiens 38-45 9892230-0 1999 Relationships between maternal risk of insulin resistance and the child"s muscle membrane fatty acid composition. Fatty Acids 90-100 insulin Homo sapiens 39-46 9892230-2 1999 The aim of the present study was to determine the relationship between young children"s muscle membrane fatty acid (FA) composition and indices of insulin resistance in their mothers. Fatty Acids 104-114 insulin Homo sapiens 147-154 10319913-4 1999 EFAs can suppress TNF-alpha production and secretion, a mechanism that may have relevance to the role of these fatty acids in the pathogenesis of insulin resistance, obesity and NIDDM. Fatty Acids 111-122 insulin Homo sapiens 146-153 9874192-7 1998 Insulin and glucose also stimulate glycolysis, but inhibit fatty acid oxidation. Fatty Acids 59-69 insulin Homo sapiens 0-7 9916795-0 1999 Identification of Cd36 (Fat) as an insulin-resistance gene causing defective fatty acid and glucose metabolism in hypertensive rats. Fatty Acids 77-87 insulin Homo sapiens 35-42 9787110-6 1998 Increased fatty acid (FA) oxidation has been traditionally viewed as the cause for increased PDK activity contributing to insulin resistance in obese subjects. Fatty Acids 10-20 insulin Homo sapiens 122-129 10095997-9 1998 A permissive role for fatty acids in the insulin secretory response of islet beta-cells has now been firmly established and can be visualised as a mechanism to protect continuing provision of respiratory substrate. Fatty Acids 22-33 insulin Homo sapiens 41-48 10095997-10 1998 Longer term exposure of islet beta-cells to fatty acids impairs the insulin secretory response to glucose and mechanisms are known. Fatty Acids 44-55 insulin Homo sapiens 68-75 9794097-0 1998 Lowering fatty acids potentiates acute insulin response in first degree relatives of people with type II diabetes. Fatty Acids 9-20 insulin Homo sapiens 39-46 9794097-2 1998 The effect of lowering the fatty acid concentration on the acute insulin response was investigated in first degree relatives of people with Type II diabetes in a double-blind, randomised, placebo-controlled trial. Fatty Acids 27-37 insulin Homo sapiens 65-72 9888641-8 1998 Factors stimulating tissue retention of fatty acids include insulin and acylation stimulating protein. Fatty Acids 40-51 insulin Homo sapiens 60-67 9833943-0 1998 Regional difference in insulin inhibition of non-esterified fatty acid release from human adipocytes: relation to insulin receptor phosphorylation and intracellular signalling through the insulin receptor substrate-1 pathway. Fatty Acids 49-70 insulin Homo sapiens 23-30 9755086-1 1998 The fatty acid composition of skeletal muscle membrane phospholipids (PL) is known to influence insulin responsiveness in humans. Fatty Acids 4-14 insulin Homo sapiens 96-103 9755086-3 1998 Fatty acid composition of PC and PE from biopsies of vastus lateralis from 27 normal men and women were correlated with insulin sensitivity determined by the hyperinsulinemic euglycemic clamp technique at insulin infusion rates of 0.4, 1.0, and 10.0 mU . Fatty Acids 0-10 insulin Homo sapiens 120-127 9755086-3 1998 Fatty acid composition of PC and PE from biopsies of vastus lateralis from 27 normal men and women were correlated with insulin sensitivity determined by the hyperinsulinemic euglycemic clamp technique at insulin infusion rates of 0.4, 1.0, and 10.0 mU . Fatty Acids 0-10 insulin Homo sapiens 163-170 9755086-10 1998 These studies suggest that the fatty acid composition of PC may be of particular importance in the relationship between fatty acids and insulin sensitivity in normal humans. Fatty Acids 31-41 insulin Homo sapiens 136-143 9755086-10 1998 These studies suggest that the fatty acid composition of PC may be of particular importance in the relationship between fatty acids and insulin sensitivity in normal humans. Fatty Acids 120-131 insulin Homo sapiens 136-143 9776502-6 1998 While menarche is likely to be triggered by a threshold level of fatness, manifestation of insulin resistance is genetically-determined and strongly influenced by the fatty acid profile of the diet. Fatty Acids 167-177 insulin Homo sapiens 91-98 9667226-1 1998 Hyperlipidemia is frequently associated with hyperinsulinemia, but because the effects of fatty acids on insulin secretion in in vitro studies using isolated perifused islets have mostly been described with supraphysiological concentrations of fatty acids, it has remained uncertain whether elevated lipid levels contribute to hyperinsulinemia by their direct stimulation of insulin secretion. Fatty Acids 90-101 insulin Homo sapiens 105-112 9808320-3 1998 YM268 facilitated the insulin-stimulated triglyceride accumulation in 3T3-L1 adipocytes and increased the mRNA expression of fatty acid-binding protein. Fatty Acids 125-135 insulin Homo sapiens 22-29 9566856-7 1998 We conclude that abdominal obesity is associated with a higher resistance to insulin mediated suppression of non-esterified fatty acids in obese subjects. Fatty Acids 124-135 insulin Homo sapiens 77-84 9497160-6 1998 Elevated circulating concentrations of fatty acids are also implicated in the etiology of type 2 diabetes by virtue of 1) their powerful acute insulinotropic effect, 2) their ability to exacerbate insulin resistance in muscle, and 3) their long-term detrimental action on pancreatic beta-cell function. Fatty Acids 39-50 insulin Homo sapiens 143-150 9519739-2 1998 The ability of fatty acids to mimic the effect of glucose and thereby augment insulin secretion in the absence of extracellular Ca2+ is the focus of the present study. Fatty Acids 15-26 insulin Homo sapiens 78-85 10923482-1 1998 OBJECTIVE: To study the effect of alteration of erythrocyte membrane fatty acid components and fluidity on insulin resistance (ISR) in NIDDM patients. Fatty Acids 69-79 insulin Homo sapiens 107-114 9530125-7 1998 We conclude that regular low-intensity exercise influences the fatty acid composition of the phospholipids in skeletal muscle, which hypothetically may contribute to changes of the skeletal muscle membrane fluidity and influence the peripheral insulin sensitivity. Fatty Acids 63-73 insulin Homo sapiens 244-251 9566856-0 1998 Body fat distribution, insulin mediated suppression of non-esterified fatty acids and plasma triglycerides in obese subjects. Fatty Acids 70-81 insulin Homo sapiens 23-30 9566856-2 1998 To test whether the pattern of fat distribution in obese subjects results in distinct insulin mediated suppression of non-esterified fatty acids which could account for differences in plasma triglycerides, we studied 59 obese subjects who were classified according to waist-to-hip ratio. Fatty Acids 133-144 insulin Homo sapiens 86-93 9505108-11 1997 The infusion of fatty acids and buffer did not alter gonadotrophin secretion, but depressed food intake and increased the plasma concentrations of glucose, insulin and cortisol. Fatty Acids 16-27 insulin Homo sapiens 156-163 9781321-2 1998 Insulin sensitivity relates to the fatty acid composition of the skeletal muscle phospholipids and the intramuscular triglyceride content. Fatty Acids 35-45 insulin Homo sapiens 0-7 9833175-7 1998 The results show that insulin can affect the expression rate of various genes, e.g. involved in cholesterol and fatty acid metabolism, by modulating the activity of transcription factors coupled to the MAP kinase cascade and that a genetic postreceptor defect in these intracellular signaling pathways might have a pleiotropic effect on cell metabolism and clinical phenotype. Fatty Acids 112-122 insulin Homo sapiens 22-29 9498640-1 1998 [Nepsilon-palmitoyl Lys (B29)] human insulin is a fatty acid-acylated derivative of insulin with extended action compared to unmodified insulin when infused intravenously (i.v.) Fatty Acids 50-60 insulin Homo sapiens 37-44 9498640-1 1998 [Nepsilon-palmitoyl Lys (B29)] human insulin is a fatty acid-acylated derivative of insulin with extended action compared to unmodified insulin when infused intravenously (i.v.) Fatty Acids 50-60 insulin Homo sapiens 84-91 9498640-1 1998 [Nepsilon-palmitoyl Lys (B29)] human insulin is a fatty acid-acylated derivative of insulin with extended action compared to unmodified insulin when infused intravenously (i.v.) Fatty Acids 50-60 insulin Homo sapiens 84-91 9773606-0 1998 [Role of fatty acids in hepatic and peripheral insulin resistance]. Fatty Acids 9-20 insulin Homo sapiens 47-54 9423147-0 1997 Effect of fatty acids and selected drugs on the albumin binding of a long-acting, acylated insulin analogue. Fatty Acids 10-21 insulin Homo sapiens 91-98 9439543-4 1997 This is the first report to display the influence of various fatty acids on the development of insulin resistance in OLETF rats. Fatty Acids 61-72 insulin Homo sapiens 95-102 9439543-9 1997 These findings suggest that dietary fatty acids may play a key role in the development of insulin resistance in patients with NIDDM. Fatty Acids 36-47 insulin Homo sapiens 90-97 9423147-9 1997 The unique ligand binding properties of serum albumin and its abundance in the extracellular fluids makes fatty acid acylation and albumin binding an attractive protraction principle for insulin and potentially also for other peptide drugs. Fatty Acids 106-116 insulin Homo sapiens 187-194 9329374-6 1997 Insulin sensitivity was assessed by the reduction in endogenous glucose concentration after exogenous insulin; the insulin, glucose, and fatty acid responses to oral glucose; and the fasting insulin concentration. Fatty Acids 137-147 insulin Homo sapiens 0-7 10889869-2 1997 Insulin is anabolic, increasing storage of glucose, fatty acids and amino acids, while glucagon namely stimulates hepatic glycogenolysis, gluconeogenesis, and ketogenesis. Fatty Acids 52-63 insulin Homo sapiens 0-7 9322948-0 1997 Fatty acid-induced insulin resistance in adipocytes. Fatty Acids 0-10 insulin Homo sapiens 19-26 9329374-12 1997 Although in PCOS, correlations were obtained between the free androgen index and cholesterol, triglyceride, and apoB levels and between the integrated glucose and insulin responses after oral glucose and fasting fatty acid and triglyceride levels, when age and adiposity were included as covariates only fatty acids and the integrated glucose response remained significantly correlated. Fatty Acids 212-222 insulin Homo sapiens 163-170 9329374-12 1997 Although in PCOS, correlations were obtained between the free androgen index and cholesterol, triglyceride, and apoB levels and between the integrated glucose and insulin responses after oral glucose and fasting fatty acid and triglyceride levels, when age and adiposity were included as covariates only fatty acids and the integrated glucose response remained significantly correlated. Fatty Acids 304-315 insulin Homo sapiens 163-170 9329754-0 1997 Impact of dietary fatty acid composition on insulin action at the nucleus. Fatty Acids 18-28 insulin Homo sapiens 44-51 9329760-0 1997 Relationships between fatty acid composition and insulin-induced oxidizability of low-density lipoproteins in healthy men. Fatty Acids 22-32 insulin Homo sapiens 49-56 9300248-1 1997 Although an increased plasma non-esterified fatty acid (NEFA) concentration has been shown to increase insulin resistance (Randle cycle), decrease insulin secretion and increase hepatic gluconeogenesis, the effect of NEFA on the deterioration of glucose tolerance has not been studied prospectively in Caucasian subjects. Fatty Acids 44-54 insulin Homo sapiens 103-110 9430382-2 1997 There is now a range of evidence in humans and experimental animals demonstrating strong relationships between the fatty acid composition of structural membrane lipids and insulin action. Fatty Acids 115-125 insulin Homo sapiens 172-179 9300238-0 1997 Chronic effect of fatty acids on insulin release is not through the alteration of glucose metabolism in a pancreatic beta-cell line (beta HC9). Fatty Acids 18-29 insulin Homo sapiens 33-40 9062110-1 1997 The fatty acid acylated insulin, Lys(B29)-tetradecanoyl, des-(B30) human insulin, has been crystallized and the structure determined by X-ray crystallography. Fatty Acids 4-14 insulin Homo sapiens 24-31 9267983-0 1997 Fatty acid induced insulin resistance in rat-1 fibroblasts overexpressing human insulin receptors: impaired insulin-stimulated mitogen-activated protein kinase activity. Fatty Acids 0-10 insulin Homo sapiens 19-26 9267983-0 1997 Fatty acid induced insulin resistance in rat-1 fibroblasts overexpressing human insulin receptors: impaired insulin-stimulated mitogen-activated protein kinase activity. Fatty Acids 0-10 insulin Homo sapiens 80-87 9267983-0 1997 Fatty acid induced insulin resistance in rat-1 fibroblasts overexpressing human insulin receptors: impaired insulin-stimulated mitogen-activated protein kinase activity. Fatty Acids 0-10 insulin Homo sapiens 80-87 9267983-1 1997 Saturated fatty acids cause insulin resistance but the underlying molecular mechanism is still unknown. Fatty Acids 0-21 insulin Homo sapiens 28-35 9200644-0 1997 Fatty acids mediate the acute extrahepatic effects of insulin on hepatic glucose production in humans. Fatty Acids 0-11 insulin Homo sapiens 54-61 9186264-0 1997 The adipocyte fatty acid-binding protein links obesity and insulin resistance. Fatty Acids 14-24 insulin Homo sapiens 59-66 9108790-0 1997 Defects of insulin action on fatty acid and carbohydrate metabolism in familial combined hyperlipidemia. Fatty Acids 29-39 insulin Homo sapiens 11-18 9108790-3 1997 We studied insulin action on carbohydrate and fatty acid metabolism in FCHL patients and healthy control subjects by a two-step euglycemic, hyperinsulinemic clamp. Fatty Acids 46-56 insulin Homo sapiens 11-18 9062110-1 1997 The fatty acid acylated insulin, Lys(B29)-tetradecanoyl, des-(B30) human insulin, has been crystallized and the structure determined by X-ray crystallography. Fatty Acids 4-14 insulin Homo sapiens 73-80 9062110-3 1997 Crystals of the fatty acid insulin grow in space group R3, with two dimers in the asymmetric unit, and diffract to 1.8 A spacing. Fatty Acids 16-26 insulin Homo sapiens 27-34 8971073-0 1997 Role of fatty acids in the pathogenesis of insulin resistance and NIDDM. Fatty Acids 8-19 insulin Homo sapiens 43-50 9491639-5 1997 Both nuclear proteins are phosphorylated through an insulin pathway, thereby inhibiting the expression of genes favoring obesity and stimulating that of genes accelerating fatty acid oxidation. Fatty Acids 172-182 insulin Homo sapiens 52-59 8911980-12 1996 Recently the role of elevated fatty acids in producing "hepatic" resistance to insulin in NIDDM has also been documented, but the site of insulin resistance may be the fat cell rather than the hepatocyte. Fatty Acids 30-41 insulin Homo sapiens 79-86 8914923-0 1996 Effect of insulin on fatty acid uptake and esterification in L-cell fibroblasts. Fatty Acids 21-31 insulin Homo sapiens 10-17 8914923-4 1996 Insulin also reduced [3H]oleic acid uptake up to 35%, depending on insulin concentration and decreased the amount of fatty acid esterified into the phospholipids and neutral lipids by 28 and 70%, respectively. Fatty Acids 117-127 insulin Homo sapiens 0-7 8914923-7 1996 Hence, insulin altered not only fatty acid uptake, as determined by cis-parinaric and oleic acid uptake, but also altered the intracellular oleic acid esterification. Fatty Acids 32-42 insulin Homo sapiens 7-14 8941640-10 1996 We conclude that glucose and/or insulin determine fatty acid oxidation by controlling the rate of long-chain fatty acid entrance into the mitochondria. Fatty Acids 50-60 insulin Homo sapiens 32-39 8927959-9 1996 Therefore, the increased insulin dose may be responsible for the relatively increased energy intake and, in addition, increased intake of saturated fatty acid which has been related to poor metabolic control and obesity. Fatty Acids 138-158 insulin Homo sapiens 25-32 8674884-6 1996 The overall effect of hyperinsulinemia on VLDL production is postulated to reflect both the effect of insulin on apolipoprotein B production and the hepatic synthesis of TG from either plasma FFAs or newly made fatty acids. Fatty Acids 211-222 insulin Homo sapiens 27-34 8675698-5 1996 Therefore in contrast to the originally postulated mechanism in which free fatty acids were thought to inhibit insulin-stimulated glucose uptake in muscle through initial inhibition of pyruvate dehydrogenase these results demonstrate that free fatty acids induce insulin resistance in humans by initial inhibition of glucose transport/phosphorylation which is then followed by an approximately 50% reduction in both the rate of muscle glycogen synthesis and glucose oxidation. Fatty Acids 75-86 insulin Homo sapiens 111-118 8669419-10 1996 Plasma fatty acid excursions were the lowest with insulin treatment. Fatty Acids 7-17 insulin Homo sapiens 50-57 8675698-5 1996 Therefore in contrast to the originally postulated mechanism in which free fatty acids were thought to inhibit insulin-stimulated glucose uptake in muscle through initial inhibition of pyruvate dehydrogenase these results demonstrate that free fatty acids induce insulin resistance in humans by initial inhibition of glucose transport/phosphorylation which is then followed by an approximately 50% reduction in both the rate of muscle glycogen synthesis and glucose oxidation. Fatty Acids 75-86 insulin Homo sapiens 263-270 8764301-2 1996 Futhermore, insulin resistance and obesity are associated with the fatty acid (FA) profile of structural membrane lipids. Fatty Acids 67-77 insulin Homo sapiens 12-19 8928782-0 1996 Glucose and insulin-induced inhibition of fatty acid oxidation: the glucose-fatty acid cycle reversed. Fatty Acids 42-52 insulin Homo sapiens 12-19 8928782-7 1996 We conclude that under the conditions of the present experiment, glucose and/or insulin directly inhibits fatty acid oxidation. Fatty Acids 106-116 insulin Homo sapiens 80-87 8732493-6 1996 A significant positive correlation was found between percentage decrease of MVA and non-esterified fatty acids following the insulin clamp in NIDDM (r = 0.83, P = 0.04). Fatty Acids 99-110 insulin Homo sapiens 125-132 8613231-0 1996 Obesity hypertension is related more to insulin"s fatty acid than glucose action. Fatty Acids 50-60 insulin Homo sapiens 40-47 8613231-5 1996 Fatty acid concentration and turnover were markedly more resistant to suppression by insulin in obese hypertensive than in lean or obese normotensive individuals. Fatty Acids 0-10 insulin Homo sapiens 85-92 8613231-10 1996 The data indicate that blood pressure is related to the effects of insulin on fatty acid metabolism. Fatty Acids 78-88 insulin Homo sapiens 67-74 8613231-11 1996 The findings raise the possibility that resistance of hormone-sensitive lipase to insulin participates in elevating the blood pressure of abdominally obese hypertensive subjects by increasing fatty acid concentration and turnover. Fatty Acids 192-202 insulin Homo sapiens 82-89 8729130-2 1996 This paper reviews the range of evidence in humans and experimental animals demonstrating close associations between insulin action and two major aspects of muscle morphology: fatty acid composition of the major structural lipid (phospholipid) in muscle cell membranes and relative proportions of major muscle fiber types. Fatty Acids 176-186 insulin Homo sapiens 117-124 8729131-4 1996 In some individuals, a single amino acid substitution in the intestinal fatty acid binding protein could result in increased rates of intestinal absorption of dietary NEFA and thereby contribute to increased lipid-oxidation rates and insulin resistance. Fatty Acids 72-82 insulin Homo sapiens 234-241 8720610-11 1996 In conclusion, our study found that in lean non-insulin-dependent diabetic subjects, an acute decrease in non-esterified fatty acid levels improves glucose tolerance, muscle glucose uptake, glucose oxidation and non-oxidative glycolysis, but is unable to normalize glucose storage. Fatty Acids 110-131 insulin Homo sapiens 48-55 8596494-1 1996 We determined whether plasma phospholipid fatty acid levels, an indicator of fatty acid composition in the diet, are associated with fasting serum insulin concentrations (a marker of insulin resistance). Fatty Acids 42-52 insulin Homo sapiens 147-154 8596494-1 1996 We determined whether plasma phospholipid fatty acid levels, an indicator of fatty acid composition in the diet, are associated with fasting serum insulin concentrations (a marker of insulin resistance). Fatty Acids 42-52 insulin Homo sapiens 183-190 8596494-4 1996 Fasting insulin was strongly and positively associated with the saturated fatty acid percentage in plasma phospholipids, moderately and inversely associated with the monounsaturated percentage, and not appreciably associated with the polyunsaturated percentage. Fatty Acids 64-84 insulin Homo sapiens 8-15 8596494-5 1996 Fasting insulin adjusted for age, smoking status, alcohol consumption, and sports participation, for example, was 29% higher in men and 33% higher in women per 1.9% greater level of saturated fatty acids (the interquartile range). Fatty Acids 182-203 insulin Homo sapiens 8-15 8596494-7 1996 A 1.9% greater increment in saturated fatty acid level was also associated with a 2.4-fold higher odds of hyperinsulinemia (fasting insulin > or = 143.5 pmol/L). Fatty Acids 28-48 insulin Homo sapiens 111-118 8596494-8 1996 These data are consistent with studies showing that fatty acid composition of cell membranes modulates insulin action, and support the hypothesis that increased habitual saturated fat intake or a related dietary pattern is a risk factor for hyperinsulinemia. Fatty Acids 52-62 insulin Homo sapiens 103-110 8596494-8 1996 These data are consistent with studies showing that fatty acid composition of cell membranes modulates insulin action, and support the hypothesis that increased habitual saturated fat intake or a related dietary pattern is a risk factor for hyperinsulinemia. Fatty Acids 170-183 insulin Homo sapiens 103-110 8582538-0 1995 Opposite effects of short- and long-term fatty acid infusion on insulin secretion in healthy subjects. Fatty Acids 41-51 insulin Homo sapiens 64-71 8554512-0 1995 Albumin binding of insulins acylated with fatty acids: characterization of the ligand-protein interaction and correlation between binding affinity and timing of the insulin effect in vivo. Fatty Acids 42-53 insulin Homo sapiens 19-26 8594950-6 1995 Importantly, these drugs, as well as insulin and glucagon, were demonstrated to increase plasma fatty acids as well as to decrease feeding. Fatty Acids 96-107 insulin Homo sapiens 37-44 8675650-1 1995 The cellular basis of insulin resistance is still unknown; however, relationships have been demonstrated between insulin action in muscle and the fatty acid profile of the major membrane structural lipid (phospholipid). Fatty Acids 146-156 insulin Homo sapiens 113-120 8675650-4 1995 Insulin action (high-dose clamp; MZ) correlated with composite measures of membrane unsaturation (% C20-22 polyunsaturated fatty acids [r= 0.463, P < 0.001], unsaturation index [r= -0.369, P < 0.01]), a number of individual fatty acids and with delta5 desaturase activity (r= 0.451, P < 0.001). Fatty Acids 123-134 insulin Homo sapiens 0-7 8851476-0 1995 Suppression of non-esterified fatty acid concentrations by insulin in patients with hypertension. Fatty Acids 30-40 insulin Homo sapiens 59-66 8582538-1 1995 Our study investigates short- and long-term effects of infusion of non-esterified fatty acids (NEFA) on insulin secretion in healthy subjects. Fatty Acids 82-93 insulin Homo sapiens 104-111 7562404-0 1995 Absorption characteristics of chemically modified-insulin derivatives with various fatty acids in the small and large intestine. Fatty Acids 83-94 insulin Homo sapiens 50-57 7562404-1 1995 Absorption characteristics of insulin derivatives chemically modified with various fatty acids in the intestine were determined by in situ loop and in vitro modified Ussing chamber methods. Fatty Acids 83-94 insulin Homo sapiens 30-37 7562404-2 1995 The pharmacological activities of these acyl derivatives, as assessed by their hypoglycemic effects after intravenous administration, were reduced upon increasing the carbon number of the fatty acid(s) chemically attached to native insulin. Fatty Acids 188-198 insulin Homo sapiens 232-239 7562404-7 1995 These in situ and in vitro results indicated that the chemical modification of insulin with fatty acids was a useful approach for improving insulin absorption from the large intestine. Fatty Acids 92-103 insulin Homo sapiens 79-86 7562404-7 1995 These in situ and in vitro results indicated that the chemical modification of insulin with fatty acids was a useful approach for improving insulin absorption from the large intestine. Fatty Acids 92-103 insulin Homo sapiens 140-147 7745004-2 1995 To further assess the clinical significance of these findings, we tested in human islets the effects of fatty acids on glucose-induced insulin release and biosynthesis and on pyruvate dehydrogenase (PDH) activity. Fatty Acids 104-115 insulin Homo sapiens 135-142 7745004-8 1995 The insulin content of islets exposed to fatty acids was significantly reduced, and glucose-induced proinsulin biosynthesis was inhibited by 59% after palmitate addition and by 51% after oleate exposure (P < 0.01). Fatty Acids 41-52 insulin Homo sapiens 4-11 7827358-0 1994 Effects of non-esterified fatty acids on insulin-stimulated glucose transport in isolated skeletal muscle from patients with type 2 (non-insulin-dependent) diabetes mellitus. Fatty Acids 26-37 insulin Homo sapiens 41-48 7587908-0 1995 Effects of insulin therapy upon plasma lipid fatty acids and platelet aggregation in NIDDM with secondary failure to oral antidiabetic agents. Fatty Acids 45-56 insulin Homo sapiens 11-18 7883976-0 1995 An amino acid substitution in the human intestinal fatty acid binding protein is associated with increased fatty acid binding, increased fat oxidation, and insulin resistance. Fatty Acids 51-61 insulin Homo sapiens 156-163 7883976-1 1995 The intestinal fatty acid binding protein locus (FABP2) was investigated as a possible genetic factor in determining insulin action in the Pima Indian population. Fatty Acids 15-25 insulin Homo sapiens 117-124 7725633-4 1995 Enhanced oxidation of non-esterified fatty acids leads to inhibition of glucose oxidation and this may participate in the development of insulin resistance. Fatty Acids 37-48 insulin Homo sapiens 137-144 7851683-0 1994 Insulin sensitivity is related to the fatty acid composition of serum lipids and skeletal muscle phospholipids in 70-year-old men. Fatty Acids 38-48 insulin Homo sapiens 0-7 7851683-6 1994 The fatty acid composition was also significantly related to insulin sensitivity in a stepwise multiple regression analysis in the presence of other clinical variables, which were associated with insulin action in univariate analysis. Fatty Acids 4-14 insulin Homo sapiens 61-68 7851683-6 1994 The fatty acid composition was also significantly related to insulin sensitivity in a stepwise multiple regression analysis in the presence of other clinical variables, which were associated with insulin action in univariate analysis. Fatty Acids 4-14 insulin Homo sapiens 196-203 7851683-8 1994 It is concluded that the fatty acid composition in serum and of the phospholipids of skeletal muscle may influence insulin action in elderly men. Fatty Acids 25-35 insulin Homo sapiens 115-122 8010722-9 1994 Plasma fatty acid concentrations were increased in all cancer patients and decreased appropriately after glucose administration, indicating that lipolysis remained sensitive to the action of insulin. Fatty Acids 7-17 insulin Homo sapiens 191-198 8063701-3 1994 In the pancreatic beta-cell, fatty acids have both acute and chronic effects on insulin secretion. Fatty Acids 29-40 insulin Homo sapiens 80-87 7971711-2 1994 When these compounds were incubated in small intestinal fluid at 37 degrees C, proteolysis of monoacyl insulins was reduced by increasing the carbon number of the fatty acid attached to Phe-B1 of the insulin molecule. Fatty Acids 163-173 insulin Homo sapiens 103-110 8022751-7 1994 When GIP concentrations of either 1 x 10(-9) or 1 x 10(-8) M were added to the fatty acid perifusate, insulin secretion stimulated by PUFA was significantly attenuated in a dose-dependent manner, but was completely restored after withdrawal of GIP. Fatty Acids 79-89 insulin Homo sapiens 102-109 8166251-6 1994 In the "clamped" experiments (with additional insulin), net fatty acid efflux in the venous blood was suppressed and positive transcapillary flux (storage) was more marked. Fatty Acids 60-70 insulin Homo sapiens 46-53 8166251-8 1994 Additional insulin caused no further suppression of HSL or activation of LPL but markedly stimulated fatty acid retention (presumed to represent esterification). Fatty Acids 101-111 insulin Homo sapiens 11-18 8059770-7 1994 In contrast, insulin levels increased with the increasing intake of saturated fatty acids and alcohol. Fatty Acids 68-89 insulin Homo sapiens 13-20 8059770-9 1994 Besides overweight, physical activity and dietary factors such as the intake of fatty acids, fiber, carbohydrates, and alcohol, were independently associated with hyperinsulinemia and insulin resistance. Fatty Acids 80-91 insulin Homo sapiens 168-175 7909102-6 1994 The glucose fatty-acid cycle may operate in patients with severe insulin resistance and hyperlipidaemia: high serum NEFA aggravates insulin resistance and hyperglycaemia by inhibiting glucose uptake and utilisation. Fatty Acids 12-22 insulin Homo sapiens 65-72 7909102-6 1994 The glucose fatty-acid cycle may operate in patients with severe insulin resistance and hyperlipidaemia: high serum NEFA aggravates insulin resistance and hyperglycaemia by inhibiting glucose uptake and utilisation. Fatty Acids 12-22 insulin Homo sapiens 132-139 8061346-8 1994 In conclusion, plasma fatty acids and ketone body concentrations rise less rapidly following withdrawal of insulin in patients with insulin-dependent diabetes and autonomic neuropathy suggesting that such patients may have a degree of protection against the development of diabetic ketoacidosis. Fatty Acids 22-33 insulin Homo sapiens 107-114 8405699-0 1993 Effects of insulin on fatty acid reesterification in healthy subjects. Fatty Acids 22-32 insulin Homo sapiens 11-18 8238081-8 1993 It is concluded that SHR express insulin resistance in terms of glucose and fatty acid metabolism, and therefore are a suitable model for insulin resistance and essential hypertension in non-obese humans. Fatty Acids 76-86 insulin Homo sapiens 33-40 8405699-7 1993 These data showed that insulin profoundly suppressed fatty acid release, oxidation as well as reesterification of those fatty acids that had entered the extracellular compartment. Fatty Acids 53-63 insulin Homo sapiens 23-30 8405699-7 1993 These data showed that insulin profoundly suppressed fatty acid release, oxidation as well as reesterification of those fatty acids that had entered the extracellular compartment. Fatty Acids 120-131 insulin Homo sapiens 23-30 8405699-8 1993 They suggested that physiological concentrations of insulin suppressed extracellular fatty acid reesterification primarily by inhibiting lipolysis. Fatty Acids 85-95 insulin Homo sapiens 52-59 8405699-4 1993 In response to insulin, fatty acid release declined by 71% (from 5.6 +/- 0.6 to 1.6 +/- 0.2 mumol.kg-1 x min-1). Fatty Acids 24-34 insulin Homo sapiens 15-22 8100834-10 1993 The clustering of risk factors associated with insulin resistance in FCH indicates a common metabolic basis for the FCH phenotype and the syndrome of insulin resistance probably mediated by an impaired fatty acid metabolism. Fatty Acids 202-212 insulin Homo sapiens 47-54 8243878-7 1993 The present results demonstrate that insulin-like growth factor I is capable of mimicking the acute effects of insulin on metabolic substrates (plasma glucose, non-esterified fatty acids, leucine). Fatty Acids 175-186 insulin Homo sapiens 37-44 8368288-8 1993 Fatty acid reesterification was not affected by insulin but tripled (from 0.6 to 1.9 mumol.kg-1 x min-1) in response to insulin plus ethanol. Fatty Acids 0-10 insulin Homo sapiens 120-127 24202501-9 1993 Binding of insulin to carp hepatocytes resulted in a significant reduction of glucose release and a significant increase of protein synthesis as of de novo fatty acid synthesis. Fatty Acids 156-166 insulin Homo sapiens 11-18 8338037-0 1993 Relationship of dietary saturated fatty acids and body habitus to serum insulin concentrations: the Normative Aging Study. Fatty Acids 24-45 insulin Homo sapiens 72-79 8338037-2 1993 Log-transformed fasting insulin was significantly associated with body mass index, abdomen-hip ratio, total fat energy, and saturated fatty acid energy, with correlation coefficients ranging from 0.14 for total fat to 0.45 for body mass index. Fatty Acids 124-144 insulin Homo sapiens 24-31 8338037-3 1993 When multivariate models were used, body mass index, abdomen-hip ratio, and saturated fatty acid intake were statistically significant independent predictors of both fasting and postprandial insulin concentrations, after age, cigarette smoking, and physical activity were adjusted for. Fatty Acids 76-96 insulin Homo sapiens 191-198 8338037-4 1993 If saturated fatty acids as a percentage of total energy were to decrease from 14% to 8%, there would be an 18% decrease in fasting insulin and a 25% decrease in postprandial insulin. Fatty Acids 3-24 insulin Homo sapiens 132-139 8338037-4 1993 If saturated fatty acids as a percentage of total energy were to decrease from 14% to 8%, there would be an 18% decrease in fasting insulin and a 25% decrease in postprandial insulin. Fatty Acids 3-24 insulin Homo sapiens 175-182 8338037-5 1993 These data suggest that overall adiposity, abdominal obesity, and a diet high in saturated fatty acids are independent predictors for both fasting and postprandial insulin concentrations. Fatty Acids 81-102 insulin Homo sapiens 164-171 8418404-0 1993 The relation between insulin sensitivity and the fatty-acid composition of skeletal-muscle phospholipids. Fatty Acids 49-59 insulin Homo sapiens 21-28 8334829-4 1993 Fatty acid levels decreased with insulin (area under curve, median (range) -23 (-41-10) mmol l-1) and with the low affinity analogue (-28 (-42-19) mmol l-1 h,), but the high affinity analogue had no significant effect compared with controls (high affinity analogue -8 (-28-35) mmol l-1 h; control +15 (11-53) mmol l-1). Fatty Acids 0-10 insulin Homo sapiens 33-40 8334829-6 1993 Thus at these low infusion rates insulin itself and the low affinity analogue suppressed lipolysis, as assessed by glycerol turnover and by circulating fatty acid concentrations. Fatty Acids 152-162 insulin Homo sapiens 33-40 11538517-3 1993 If it is so, the increased insulin should accelerate intake of neutral fat and to lower fatty acid in the fat tissues. Fatty Acids 88-98 insulin Homo sapiens 27-34 8249680-7 1993 We demonstrated that insulin can indirectly promote muscle glucose uptake during exercise by restraining the release and oxidation of fatty acids and decrease of hyperglycemia. Fatty Acids 134-145 insulin Homo sapiens 21-28 8472625-12 1993 However blood glycerol, 3-hydroxybutyrate and plasma-non-esterified fatty acids were suppressed significantly by proinsulin and insulin zinc compared to control injections. Fatty Acids 68-79 insulin Homo sapiens 113-123 8472625-12 1993 However blood glycerol, 3-hydroxybutyrate and plasma-non-esterified fatty acids were suppressed significantly by proinsulin and insulin zinc compared to control injections. Fatty Acids 68-79 insulin Homo sapiens 116-123 8418404-2 1993 Skeletal muscle is a major site of insulin action, and insulin sensitivity may be related to the fatty-acid composition of the phospholipids within the muscle membranes involved in the action of insulin. Fatty Acids 97-107 insulin Homo sapiens 55-62 8418404-2 1993 Skeletal muscle is a major site of insulin action, and insulin sensitivity may be related to the fatty-acid composition of the phospholipids within the muscle membranes involved in the action of insulin. Fatty Acids 97-107 insulin Homo sapiens 55-62 8418404-3 1993 METHODS: We determined the relation between the fatty-acid composition of skeletal-muscle phospholipids and insulin sensitivity in two groups of subjects. Fatty Acids 48-58 insulin Homo sapiens 108-115 8418404-8 1993 CONCLUSIONS: Decreased insulin sensitivity is associated with decreased concentrations of polyunsaturated fatty acids in skeletal-muscle phospholipids, raising the possibility that changes in the fatty-acid composition of muscles modulate the action of insulin. Fatty Acids 196-206 insulin Homo sapiens 23-30 1438102-5 1992 Glucocorticoids and fatty acids (which are produced in response to stress) antagonise the actions of insulin in promoting glucose uptake and protein synthesis, in decreasing gluconeogenesis and protein catabolism, and promoting the clearance of intermediate density lipoprotein and low density lipoprotein from the circulation by the liver. Fatty Acids 20-31 insulin Homo sapiens 101-108 8424122-0 1993 Fatty acids may regulate aldosterone secretion and mediate some of insulin"s effects on blood pressure. Fatty Acids 0-11 insulin Homo sapiens 67-74 1480147-5 1992 Insulin, needed for synthesis of lipoprotein lipase and esterification of fatty acids, is captured from the blood stream and delivered to myocytes by endothelial insulin receptors. Fatty Acids 74-85 insulin Homo sapiens 0-7 1480147-5 1992 Insulin, needed for synthesis of lipoprotein lipase and esterification of fatty acids, is captured from the blood stream and delivered to myocytes by endothelial insulin receptors. Fatty Acids 74-85 insulin Homo sapiens 162-169 1438102-7 1992 By contrast to this antagonism, cortisol can also facilitate the action of insulin in stimulating the storage of energy via glycogen and fatty acid synthesis and through lipoprotein lipase in adipose tissue. Fatty Acids 137-147 insulin Homo sapiens 75-82 1600836-1 1992 There are elevated fatty acid levels in non-insulin-dependent diabetes mellitus that are due to diminished insulin action in inhibiting fatty acid release from adipocytes. Fatty Acids 19-29 insulin Homo sapiens 44-51 1600836-2 1992 Insulin therapy and other inhibitors of fatty acid release from adipocytes (e.g., nicotinic acid) suppress these elevated fatty acid levels and bring about a reduction in hyperglycemia. Fatty Acids 40-50 insulin Homo sapiens 0-7 1600836-2 1992 Insulin therapy and other inhibitors of fatty acid release from adipocytes (e.g., nicotinic acid) suppress these elevated fatty acid levels and bring about a reduction in hyperglycemia. Fatty Acids 122-132 insulin Homo sapiens 0-7 1734231-6 1992 Case 3, a patient with severe hyperglycemia, illustrates that insulin will only promote the oxidation of glucose at a rapid rate once the levels of fatty acids and ketoacids decline to low levels. Fatty Acids 148-159 insulin Homo sapiens 62-69 1556096-13 1992 Furthermore, only when inhibition of fatty acid oxidation was associated with a rise in malonyl-CoA did the total (mitochondrial plus cytoplasmic) content of long chain acyl-CoA esters correlate inversely with insulin release promoted by various nutrients. Fatty Acids 37-47 insulin Homo sapiens 210-217 1290322-2 1992 Any change in insulin sensitivity is compensated in healthy subjects by a dynamic change in insulin secretion, which will decrease following a rise in insulin sensitivity and increase if insulin sensitivity is impaired (i.e. during insulin resistance induced by obesity, pregnancy, oral contraceptives, dehydration, saturated fatty acids, fever, drugs, etc.). Fatty Acids 316-337 insulin Homo sapiens 14-21 1290322-2 1992 Any change in insulin sensitivity is compensated in healthy subjects by a dynamic change in insulin secretion, which will decrease following a rise in insulin sensitivity and increase if insulin sensitivity is impaired (i.e. during insulin resistance induced by obesity, pregnancy, oral contraceptives, dehydration, saturated fatty acids, fever, drugs, etc.). Fatty Acids 316-337 insulin Homo sapiens 92-99 1290322-2 1992 Any change in insulin sensitivity is compensated in healthy subjects by a dynamic change in insulin secretion, which will decrease following a rise in insulin sensitivity and increase if insulin sensitivity is impaired (i.e. during insulin resistance induced by obesity, pregnancy, oral contraceptives, dehydration, saturated fatty acids, fever, drugs, etc.). Fatty Acids 316-337 insulin Homo sapiens 92-99 1290322-2 1992 Any change in insulin sensitivity is compensated in healthy subjects by a dynamic change in insulin secretion, which will decrease following a rise in insulin sensitivity and increase if insulin sensitivity is impaired (i.e. during insulin resistance induced by obesity, pregnancy, oral contraceptives, dehydration, saturated fatty acids, fever, drugs, etc.). Fatty Acids 316-337 insulin Homo sapiens 92-99 1372897-2 1992 Fatty acids are important metabolic substrates and may also be involved in pathological syndromes such as the insulin resistance of diabetes and obesity. Fatty Acids 0-11 insulin Homo sapiens 110-117 1311661-2 1992 Experimental elevation of plasma non-esterified fatty acid concentrations has been postulated to decrease insulin-stimulated glucose oxidation and storage rates. Fatty Acids 48-58 insulin Homo sapiens 106-113 1810020-1 1991 Ketone bodies and non-esterified fatty acids (NEFA) inhibit insulin stimulated glucose uptake in muscle in-vitro. Fatty Acids 33-44 insulin Homo sapiens 60-67 1934376-3 1991 METHODS AND RESULTS: After adjusting for age, the intake of saturated fatty acids and cholesterol were positively correlated (p less than 0.05) with body mass index (r = 0.18, r = 0.16), waist-to-hip circumference ratio (r = 0.21, r = 0.22), and fasting insulin (r = 0.26, r = 0.23). Fatty Acids 60-81 insulin Homo sapiens 254-261 1934376-7 1991 In multivariate analysis, intake of saturated fatty acids was significantly related to elevated fasting insulin concentration independently of body mass index. Fatty Acids 36-57 insulin Homo sapiens 104-111 1934376-8 1991 CONCLUSIONS: These cross-sectional findings in nondiabetic men with coronary artery disease suggest that increased consumption of saturated fatty acids is associated independently with higher fasting insulin concentrations. Fatty Acids 130-151 insulin Homo sapiens 200-207 1777992-0 1991 Effect of acute hyperinsulinemia on fatty acid composition of serum lipids in non-insulin-dependent diabetics and healthy men. Fatty Acids 36-46 insulin Homo sapiens 21-28 1843205-2 1991 In the current study, we have examined the effect of increased membrane fatty acid unsaturation on insulin action. Fatty Acids 72-82 insulin Homo sapiens 99-106 1713483-1 1991 The purpose of the present experiment was to investigate if the modulation by insulin of liver microsomal desaturase activities in the spontaneously diabetic adult male Bio-Breeding (BB) rat, with destructive insulitis resembling the lesions described in the human Type I (insulin-dependent) diabetes, corresponds to modifications in fatty acid composition, reflect of changes in fatty acid desaturation. Fatty Acids 334-344 insulin Homo sapiens 78-85 1713483-1 1991 The purpose of the present experiment was to investigate if the modulation by insulin of liver microsomal desaturase activities in the spontaneously diabetic adult male Bio-Breeding (BB) rat, with destructive insulitis resembling the lesions described in the human Type I (insulin-dependent) diabetes, corresponds to modifications in fatty acid composition, reflect of changes in fatty acid desaturation. Fatty Acids 380-390 insulin Homo sapiens 78-85 1884899-8 1991 In contrast, decreased non-esterified fatty acid availability enhances the suppression of hepatic glucose production by insulin. Fatty Acids 38-48 insulin Homo sapiens 120-127 1677322-0 1991 Regulation of non-esterified fatty acid and glycerol concentration by insulin in normal individuals and patients with type 2 diabetes. Fatty Acids 29-39 insulin Homo sapiens 70-77 1843205-9 1991 Internalization of insulin was identical in control cells and in cells with increased membrane fatty acid unsaturation. Fatty Acids 95-105 insulin Homo sapiens 19-26 1843205-10 1991 Thymidine incorporation, an insulin-dependent function in these cell, was measured in control and fatty acid treated cells. Fatty Acids 98-108 insulin Homo sapiens 28-35 2076525-4 1990 Under physiologic conditions (i.e., in the control group), the drop in linoleic acid content and the rise in saturated fatty acids were associated with increased insulin secretion, and decrease in maximal insulin action. Fatty Acids 109-130 insulin Homo sapiens 162-169 2076525-6 1990 Combined with the relationship between the fatty acid composition of lipids and insulin secretion and action, our findings suggest a common metabolic defect of atherosclerosis and Type 2 diabetes which is probably insulin resistance in glucose metabolism. Fatty Acids 43-53 insulin Homo sapiens 80-87 2265217-4 1990 The appearance of ketogenesis is also controlled by the changes of plasma insulin and glucagon that increase the capacity for liver fatty acid oxidation by decreasing lipogenesis and malonyl-CoA concentration, by reducing the sensitivity of carnitine palmitoyl-CoA I to the inhibitory influence of malonyl-CoA, and by activating hydroxymethylglutaryl-CoA synthase by desuccinylation. Fatty Acids 132-142 insulin Homo sapiens 74-81 2246969-6 1990 Both serum insulin and blood glucose concentrations probably have an effect on the elongation and desaturation of fatty acids, but the metabolism of linoleic acid to prostaglandin precursors seems to be different in different types of diabetes, NIDDM patients showing no abnormalities. Fatty Acids 114-125 insulin Homo sapiens 11-18 2246969-7 1990 The possibility that the fatty acid composition of plasma and membrane lipids has a role in insulin resistance and blood glucose regulation deserves further investigation. Fatty Acids 25-35 insulin Homo sapiens 92-99 2174434-2 1990 It was established previously that the 15-kDa protein phosphorylated in 3T3-L1 adipocytes treated with insulin and phenylarsine oxide is O-phospho-Tyr19 422(aP2) protein, a fatty acid-binding protein. Fatty Acids 173-183 insulin Homo sapiens 103-110 2174434-9 1990 These results indicate that upon binding fatty acid, 422(aP2) protein undergoes a conformational change whereby Tyr19, which lies within a consensus-type sequence for tyrosine kinase substrates, becomes accessible for phosphorylation by the insulin receptor tyrosine kinase and to iodination by lactoperoxidase. Fatty Acids 41-51 insulin Homo sapiens 241-248 2187112-7 1990 The mean integrated area under the curve/20 min showed an increase in both insulin and glucagon secretions with the addition of fatty acids. Fatty Acids 128-139 insulin Homo sapiens 75-82 2187112-9 1990 The fatty-acid-induced insulin but not glucagon secretion was blocked by the addition of 2 mM palmoxirate an inhibitor of fatty acid oxidation. Fatty Acids 4-14 insulin Homo sapiens 23-30 2187112-9 1990 The fatty-acid-induced insulin but not glucagon secretion was blocked by the addition of 2 mM palmoxirate an inhibitor of fatty acid oxidation. Fatty Acids 122-132 insulin Homo sapiens 23-30 1710741-4 1990 It has been suggested that raised fatty acid levels may be responsible in part for the increased hepatic glucose output and insulin insensitivity of NIDDM. Fatty Acids 34-44 insulin Homo sapiens 124-131 2086516-4 1990 Evidence is presented that changes in insulin level and the activity of carnitine palmitoyltransferase I modulate feeding by altering the partitioning of fatty acids. Fatty Acids 154-165 insulin Homo sapiens 38-45 34779480-0 2022 Insulin-stimulated adipocytes secrete lactate to promote endothelial fatty acid uptake and transport. Fatty Acids 69-79 insulin Homo sapiens 0-7 7011721-0 1981 Biosynthetic human insulin: effect in healthy men on plasma glucose and non-esterified fatty acids in comparison with highly purified pork insulin. Fatty Acids 87-98 insulin Homo sapiens 19-26 33765416-5 2021 We further provide our views regarding the timing, dominance, and physiological relevance of these effects and discuss novel concepts regarding insulin regulation of adipose tissue fatty acid metabolism and central nervous system (CNS) signaling to the liver, as regulators of insulin"s extrahepatic effects on glucose production. Fatty Acids 181-191 insulin Homo sapiens 144-151 7806018-8 1994 The most important determinant of the area under the non-esterified fatty acid suppression curve in men was the 30-min insulin increment, a measure of insulin secretion, (p < 0.001) whereas for women age (p < 0.001) and the body mass index (p < 0.01) were the most important. Fatty Acids 68-78 insulin Homo sapiens 119-126 7821731-6 1994 It seems likely that longer term effects of fatty acids on this and other aspects of glucose metabolism could be important in the development of insulin resistance in diabetes mellitus in man. Fatty Acids 44-55 insulin Homo sapiens 145-152 15925010-7 2005 This rise in blood glucose, now perhaps in concert with the excess fatty acids that are a typical feature of obesity and insulin resistance, cause additional deterioration in beta-cell function along with further insulin resistance, and the blood glucose levels rise to full-blown diabetes. Fatty Acids 67-78 insulin Homo sapiens 121-128 15925010-7 2005 This rise in blood glucose, now perhaps in concert with the excess fatty acids that are a typical feature of obesity and insulin resistance, cause additional deterioration in beta-cell function along with further insulin resistance, and the blood glucose levels rise to full-blown diabetes. Fatty Acids 67-78 insulin Homo sapiens 213-220 34779480-1 2022 Insulin stimulates adipose tissue to extract fatty acids from circulation and sequester them inside adipose cells. Fatty Acids 45-56 insulin Homo sapiens 0-7 34779480-3 2022 We modeled the relationship of adipocytes and endothelial cells in vitro to test the role of insulin in fatty acid transport. Fatty Acids 104-114 insulin Homo sapiens 93-100 34779480-4 2022 Treatment of endothelial cells with insulin did not affect endothelial fatty acid uptake, but endothelial cells took up more fatty acids when exposed to media conditioned by adipocytes treated with insulin. Fatty Acids 125-136 insulin Homo sapiens 36-43 34779480-4 2022 Treatment of endothelial cells with insulin did not affect endothelial fatty acid uptake, but endothelial cells took up more fatty acids when exposed to media conditioned by adipocytes treated with insulin. Fatty Acids 125-136 insulin Homo sapiens 198-205 34779480-8 2022 Together, these data suggest that insulin drives adipocytes to secrete lactate, which then acts in a paracrine fashion to promote fatty acid uptake and transport across the neighboring endothelial barrier. Fatty Acids 130-140 insulin Homo sapiens 34-41 34789923-2 2022 Insulin triggers the uptake of glucose and fatty acids into the liver, adipose tissue and muscle, and promotes the storage of these nutrients in the form of glycogen and lipids. Fatty Acids 43-54 insulin Homo sapiens 0-7 34321614-2 2021 We investigated if this also pertains to insulin-induced effects on fatty acid handling. Fatty Acids 68-78 insulin Homo sapiens 41-48 34643856-11 2022 High-dose intravenous infusion of insulin up to 10 units/kg per hour appears as an inotropic agent possibly through alterations in myocardial metabolism of fatty acids and augmentation of insulin secretion and uptake. Fatty Acids 156-167 insulin Homo sapiens 34-41 34972146-9 2021 We show the usefulness of the model by simulating new and more challenging experimental setups in silico, e.g. the extracellular concentration of fatty acids during an insulin clamp, and the difference in such simulations between individuals with and without type 2 diabetes. Fatty Acids 146-157 insulin Homo sapiens 168-175 34725844-0 2021 Fatty acids may influence insulin dynamics through modulation of albumin-Zn2+ interactions. Fatty Acids 0-11 insulin Homo sapiens 26-33 34321614-5 2021 Changes (delta) in circulating glycerol and fatty acid levels during hyperinsulinemic euglycemic clamp represented the insulin maximum antilipolytic effect. Fatty Acids 44-54 insulin Homo sapiens 119-126 34784930-9 2021 CONCLUSIONS: The associated SNPs of this study are known to be specifically related to insulin signaling, fatty acid metabolism and reproductive pathway genes and possibly suggesting the role of overlapping phenotypic features of insulin resistance, obesity and reproductive dysfunctions inherent in the development of diabetes. Fatty Acids 106-116 insulin Homo sapiens 230-237 34127848-4 2021 By contrast, PPARgamma promotes fatty acid uptake, triglyceride formation and storage in lipid droplets, thereby increasing insulin sensitivity and glucose metabolism. Fatty Acids 32-42 insulin Homo sapiens 124-131 34382222-1 2021 Previous studies have shown various metabolic stressors such as saturated fatty acids (SFA) and excess insulin promote insulin resistance in metabolically meaningful cell types (such as skeletal muscle). Fatty Acids 64-85 insulin Homo sapiens 119-126 34751700-2 2021 While insulin is secreted after food intake and is the primary hormone increasing glucose storage as glycogen and fatty acid storage as triglycerides, exercise is a condition where fuel stores need to be mobilized and oxidized. Fatty Acids 114-124 insulin Homo sapiens 6-13 34727748-0 2021 Docking protein 1 and free fatty acids are associated with insulin resistance in patients with type 2 diabetes mellitus. Fatty Acids 27-38 insulin Homo sapiens 59-66 34382222-1 2021 Previous studies have shown various metabolic stressors such as saturated fatty acids (SFA) and excess insulin promote insulin resistance in metabolically meaningful cell types (such as skeletal muscle). Fatty Acids 87-90 insulin Homo sapiens 119-126 34346724-2 2021 We have previously shown that acute insulin infusion induced a shift in fatty acid metabolism dependent on fasting duration. Fatty Acids 72-82 insulin Homo sapiens 36-43 34695228-5 2022 Insulin resistance, mainly in adipose tissue, is the main driver of NAFLD due to excess release of fatty acid. Fatty Acids 99-109 insulin Homo sapiens 0-7 34676601-2 2021 The focus of the current study was to characterize both the composition of fatty acids and their positional distribution in triglycerides of biopsied human subcutaneous adipose tissue, from subjects with wide ranges of body mass index (BMI) and insulin sensitivity, using 13 C nuclear magnetic resonance (NMR) spectroscopy. Fatty Acids 75-86 insulin Homo sapiens 245-252 34676601-6 2021 13 C NMR spectroscopy reveals for the first time a highly nonhomogenous distribution of fatty acids in the glycerol sites of human adipose tissue triglyceride, and that these distributions are correlated with different phenotypes, such as BMI and insulin sensitivity. Fatty Acids 88-99 insulin Homo sapiens 247-254 34679116-9 2021 The highest discriminant ratio was found for the non-esterified fatty acids-based insulin sensitivity index (NEFA-ISI, 2.70 (2.30-3.22)). Fatty Acids 64-75 insulin Homo sapiens 82-89 34647431-3 2022 OBJECTIVE: We evaluate the relationship between fetal adipose tissue accretion with insulin and fetal consumption of circulating fatty acid (FA). Fatty Acids 129-139 insulin Homo sapiens 84-91 34638763-0 2021 Maternal C-Peptide and Insulin Sensitivity, but Not BMI, Associate with Fatty Acids in the First Trimester of Pregnancy. Fatty Acids 72-83 insulin Homo sapiens 9-18 34266892-3 2021 Furthermore, insulin-stimulated muscle glucose uptake was not different between insulin-sensitive obese and lean participants even though adipocytes were larger, SAT perfusion and oxygenation were lower, and markers of SAT inflammation, fatty acid appearance in plasma in relation to fat-free mass, and plasma fatty acid concentration were higher in the insulin-sensitive obese than lean participants. Fatty Acids 237-247 insulin Homo sapiens 13-20 34266892-3 2021 Furthermore, insulin-stimulated muscle glucose uptake was not different between insulin-sensitive obese and lean participants even though adipocytes were larger, SAT perfusion and oxygenation were lower, and markers of SAT inflammation, fatty acid appearance in plasma in relation to fat-free mass, and plasma fatty acid concentration were higher in the insulin-sensitive obese than lean participants. Fatty Acids 237-247 insulin Homo sapiens 80-87 34266892-3 2021 Furthermore, insulin-stimulated muscle glucose uptake was not different between insulin-sensitive obese and lean participants even though adipocytes were larger, SAT perfusion and oxygenation were lower, and markers of SAT inflammation, fatty acid appearance in plasma in relation to fat-free mass, and plasma fatty acid concentration were higher in the insulin-sensitive obese than lean participants. Fatty Acids 237-247 insulin Homo sapiens 354-361 34266892-3 2021 Furthermore, insulin-stimulated muscle glucose uptake was not different between insulin-sensitive obese and lean participants even though adipocytes were larger, SAT perfusion and oxygenation were lower, and markers of SAT inflammation, fatty acid appearance in plasma in relation to fat-free mass, and plasma fatty acid concentration were higher in the insulin-sensitive obese than lean participants. Fatty Acids 310-320 insulin Homo sapiens 13-20 34266892-3 2021 Furthermore, insulin-stimulated muscle glucose uptake was not different between insulin-sensitive obese and lean participants even though adipocytes were larger, SAT perfusion and oxygenation were lower, and markers of SAT inflammation, fatty acid appearance in plasma in relation to fat-free mass, and plasma fatty acid concentration were higher in the insulin-sensitive obese than lean participants. Fatty Acids 310-320 insulin Homo sapiens 80-87 34266892-3 2021 Furthermore, insulin-stimulated muscle glucose uptake was not different between insulin-sensitive obese and lean participants even though adipocytes were larger, SAT perfusion and oxygenation were lower, and markers of SAT inflammation, fatty acid appearance in plasma in relation to fat-free mass, and plasma fatty acid concentration were higher in the insulin-sensitive obese than lean participants. Fatty Acids 310-320 insulin Homo sapiens 354-361 34086911-10 2021 At 104 weeks, basal and insulin-stimulated adipocyte glucose uptake increased by 3-fold vs baseline and expression of genes involved in glucose transport, fatty acid oxidation and adipogenesis was upregulated (p<0.01). Fatty Acids 155-165 insulin Homo sapiens 24-31 34638763-0 2021 Maternal C-Peptide and Insulin Sensitivity, but Not BMI, Associate with Fatty Acids in the First Trimester of Pregnancy. Fatty Acids 72-83 insulin Homo sapiens 23-30 34110637-5 2021 However, it is still unclear under what conditions neurons use fatty acids as energy substrates and the implications of their oxidative metabolism in modifying insulin-stimulated effects. Fatty Acids 63-74 insulin Homo sapiens 160-167 34563603-2 2022 Insulin resistance, due to enhanced free fatty acid substrate delivery, results in disrupted glucose homeostasis and altered mitochondrial oxidative capacity, which is a characteristic feature of an obese state. Fatty Acids 41-51 insulin Homo sapiens 0-7 34244155-1 2021 The inflammation-resolving and insulin-sensitizing properties of eicosapentaenoic (EPA) and docosahexaenoic (DHA) fatty acids have potential to augment effects of weight loss on breast cancer risk. Fatty Acids 114-125 insulin Homo sapiens 31-38 34180254-3 2022 Recent Advances: Mitochondrial redox signaling was implicated in several modes of insulin secretion (branched-chain ketoacid-, fatty acid-stimulated). Fatty Acids 127-137 insulin Homo sapiens 82-89 34180254-9 2022 Identifying the targets of cell signaling into mitochondria and of mitochondrial retrograde metabolic and redox signals to the cell will uncover further molecular mechanisms for insulin secretion stimulated by glucose, branched-chain keto acids, and fatty acids, and the amplification of secretion by GLP-1 and metabotropic receptors. Fatty Acids 250-261 insulin Homo sapiens 178-185 34471717-3 2021 Adiponectin is an adipocyte derived protein hormone that enhances insulin sensitivity and ameliorates diabetes by enhancing fatty acid oxidation and glucose uptake in skeletal muscle and reducing glucose production in the liver. Fatty Acids 124-134 insulin Homo sapiens 66-73 34564389-7 2021 Supra-therapeutic concentrations of simvastatin reduced glucose uptake in adipocytes and normalized fatty acid-induced insulin hypersecretion from beta-cells. Fatty Acids 100-110 insulin Homo sapiens 119-126 34426590-5 2021 Fasting glucose was associated with metabolites of intracellular insulin action and beta-cell dysfunction, namely cysteine-s-sulphate and n-acetylgarginine, whereas fasting insulin was predicted by myristoleoylcarnitine, propionylcarnitine and other metabolites of beta-oxidation of fatty acids. Fatty Acids 283-294 insulin Homo sapiens 65-72 34426590-5 2021 Fasting glucose was associated with metabolites of intracellular insulin action and beta-cell dysfunction, namely cysteine-s-sulphate and n-acetylgarginine, whereas fasting insulin was predicted by myristoleoylcarnitine, propionylcarnitine and other metabolites of beta-oxidation of fatty acids. Fatty Acids 283-294 insulin Homo sapiens 173-180 34426590-7 2021 Both insulin clamp and HOMA-IR were predicted by metabolites involved in beta-oxidation of fatty acids and biodegradation of triacylglycerol, namely tartrate and 3-phosphoglycerate, as well as pyruvate, xanthine and liver fat. Fatty Acids 91-102 insulin Homo sapiens 5-12 34405148-1 2021 Introduction: Collagen and omega-3 fatty acids (FAs) are suggested to have anti-inflammatory, anti-oxidant, and insulin-sensitizing properties. Fatty Acids 48-51 insulin Homo sapiens 112-119 34110637-7 2021 These findings reveal a novel mechanism by which saturated fatty acids produce Ca2+ entry and insulin resistance that may play a causal role in increasing neuronal vulnerability associated with metabolic diseases. Fatty Acids 49-70 insulin Homo sapiens 94-101 34136519-1 2021 The chain length of saturated fatty acids may dictate their impact on inflammation and mitochondrial dysfunction, two pivotal players in the pathogenesis of insulin resistance. Fatty Acids 20-41 insulin Homo sapiens 157-164 34258288-4 2021 This present study shows that there is a noteworthy crosstalk between NECA and insulin at various metabolic levels including glycolysis (HKII), fatty acid oxidation (ACCbeta), and insulin sensitivity (PDK4). Fatty Acids 144-154 insulin Homo sapiens 79-86 34115582-7 2021 After menopause, a decline in insulin sensitivity corresponds to an increase in fat mass, circulating fatty acids, low-density lipoproteins, and triglycerides. Fatty Acids 102-113 insulin Homo sapiens 30-37 35510803-0 2022 The Degree of Unsaturation of Fatty Acids in Phosphatidylserine Alters the Rate of Insulin Aggregation and the Structure and Toxicity of Amyloid Aggregates. Fatty Acids 30-41 insulin Homo sapiens 83-90 35367785-1 2022 Insulin detemir (IDt) is long-acting insulin whose protraction mechanism is based on a covalently attached fatty acid to an insulin molecule. Fatty Acids 107-117 insulin Homo sapiens 0-7 35367785-1 2022 Insulin detemir (IDt) is long-acting insulin whose protraction mechanism is based on a covalently attached fatty acid to an insulin molecule. Fatty Acids 107-117 insulin Homo sapiens 37-44 35367785-1 2022 Insulin detemir (IDt) is long-acting insulin whose protraction mechanism is based on a covalently attached fatty acid to an insulin molecule. Fatty Acids 107-117 insulin Homo sapiens 124-131 35367785-2 2022 Utilizing the high affinity of fatty acids towards human serum albumin (HA), the modified detemir molecule binds with good affinity to HA, which functions as a reservoir that leads to a slow and prolonged release of insulin. Fatty Acids 31-42 insulin Homo sapiens 216-223 35580189-0 2022 Unsaturation in the Fatty Acids of Phospholipids Drastically Alters the Structure and Toxicity of Insulin Aggregates Grown in Their Presence. Fatty Acids 20-31 insulin Homo sapiens 98-105 35621990-5 2022 However, maternal free fatty acid concentration, cord leptin, and intracellular triglyceride content were positively correlated with insulin action. Fatty Acids 23-33 insulin Homo sapiens 133-140 35534645-2 2022 Insulin stimulates glucose transport to cells and regulates other intracellular processes that are linked to cellular bioenergetics, such as autophagy, gluconeogenesis, fatty acid metabolism, and mitochondrial homeostasis. Fatty Acids 169-179 insulin Homo sapiens 0-7 35315332-1 2022 Fatty acid esters of hydroxy fatty acids (FAHFAs) are lipokines with extensive structural and regional isomeric diversity that impact multiple physiological functions, including insulin sensitivity and glucose homeostasis. Fatty Acids 0-17 insulin Homo sapiens 178-185 35525318-4 2022 Available data suggest that metformin inhibits complex I of the mitochondrial electron transport chain, crucial gluconeogenic enzymes, and fatty acid synthesis that leads to a significant improvement in glucose tolerance and maintenance of insulin sensitivity during glucocorticoid treatment. Fatty Acids 139-149 insulin Homo sapiens 240-247 35412022-9 2022 Second is insulin resistance that reduces the amount of glucose metabolized by cells that are not obligate glucose utilizers and increases the release of fatty acids and glycerol from adipose stores that are alternative fuels for tissues and cells. Fatty Acids 154-165 insulin Homo sapiens 10-17 34994805-4 2022 The hyperlipidaemic, hyperglycaemic and insulin resistant state of diabetes contributes to a perturbed energy metabolic milieu, whereby the heart increases its reliance on fatty acids and decreases glucose oxidative rates. Fatty Acids 172-183 insulin Homo sapiens 40-47 35134563-2 2022 In mechanisms of insulin resistance, the roles of glucose, fatty acids and amino acids have been extensively documented in literature. Fatty Acids 59-70 insulin Homo sapiens 17-24 35157107-2 2022 Non-esterified fatty acids (NEFA) enriched in saturated fatty acids (SFA) are thought to reduce vascular reactivity by attenuating insulin signalling via vasodilator pathways (phosphoinositide 3-kinase (PI3K)/Akt/endothelial nitric oxide synthase (eNOS)) and enhancing signalling via pro-inflammatory pathways. Fatty Acids 15-26 insulin Homo sapiens 131-138 35051813-1 2022 The free fatty acid receptor 1 (FFA1/GPR40) and peroxisome proliferator-activated receptor delta (PPARdelta) have been widely considered as promising targets for type 2 diabetes mellitus (T2DM) due to their respective roles in promoting insulin secretion and improving insulin sensitivity. Fatty Acids 9-19 insulin Homo sapiens 237-244 35051813-1 2022 The free fatty acid receptor 1 (FFA1/GPR40) and peroxisome proliferator-activated receptor delta (PPARdelta) have been widely considered as promising targets for type 2 diabetes mellitus (T2DM) due to their respective roles in promoting insulin secretion and improving insulin sensitivity. Fatty Acids 9-19 insulin Homo sapiens 269-276 2687637-7 1989 Thus, increasing fatty acid concentrations decreased rates of glycogen synthesis both basally and with insulin stimulation. Fatty Acids 17-27 insulin Homo sapiens 103-110 35079935-7 2022 Disturbance in bistability is linked with dysregulation of plasma macronutrient levels (glucose, fatty acids and amino acids) in abnormal conditions like insulin and glucagon resistance, which is associated with obesity, type 2 diabetes mellitus and non-alcoholic fatty liver disease. Fatty Acids 97-108 insulin Homo sapiens 154-161 2691176-6 1989 During the insulin infusion, the arterialized and abdominal venous levels of both non-esterified fatty acids and glycerol fell, and the arteriovenous differences for the release of these substances narrowed. Fatty Acids 97-108 insulin Homo sapiens 11-18 35157107-2 2022 Non-esterified fatty acids (NEFA) enriched in saturated fatty acids (SFA) are thought to reduce vascular reactivity by attenuating insulin signalling via vasodilator pathways (phosphoinositide 3-kinase (PI3K)/Akt/endothelial nitric oxide synthase (eNOS)) and enhancing signalling via pro-inflammatory pathways. Fatty Acids 46-67 insulin Homo sapiens 131-138 2676896-0 1989 Effect of fatty acid composition on insulin and IGF-I binding in retinoblastoma cells. Fatty Acids 10-20 insulin Homo sapiens 36-43 2676896-1 1989 Receptors for insulin and other hormones are often influenced by their environment, including fatty acid content and membrane fluidity. Fatty Acids 94-104 insulin Homo sapiens 14-21 2665779-4 1989 In adipose tissue it is involved in the activation and regulation of lipoprotein lipase (LPL); it also inhibits glucagon-induced lipolysis and potentiates the effect of insulin on incorporation of fatty acids into triglycerides. Fatty Acids 197-208 insulin Homo sapiens 169-176 2672773-1 1989 The effect of high- and low-fat diets with different levels of fatty acid unsaturation on insulin receptors of erythrocyte ghosts was studied during different phases of the menstrual cycle in 31 healthy premenopausal women. Fatty Acids 63-73 insulin Homo sapiens 90-97 2691123-0 1989 Use of combined oral contraceptive preparations alters the insulin sensitivity of fatty acid and ketone metabolism. Fatty Acids 82-92 insulin Homo sapiens 59-66 2643754-2 1989 The relationship was evaluated between the proportions of individual fatty acids (FA) in serum phospholipids and (1) insulin secretion, determined by fasting and postglucose plasma insulin levels, and (2) in vivo insulin action, assessed as metabolic clearance rates of glucose during euglycemic clamp studies at two insulin concentrations of approximately 70 microU/mL (MCRglu70) and 500 microU/mL (MCRglu500). Fatty Acids 69-80 insulin Homo sapiens 117-124 2646038-3 1989 On the other hand significant positive correlation between insulin binding and the content of nonessential fatty acids (r = +0.65, p less than 0.05) was seen. Fatty Acids 107-118 insulin Homo sapiens 59-66 2646038-4 1989 Data presented support the hypothesis that the fatty acid composition of membrane phospholipids may modify properties of insulin receptors. Fatty Acids 47-57 insulin Homo sapiens 121-128 2459120-0 1988 Insulin antagonism of catecholamine stimulation of fatty acid transport in the adipocyte. Fatty Acids 51-61 insulin Homo sapiens 0-7 2459120-13 1988 A 10-fold higher range of insulin concentrations was then required to produce inhibition of fatty acid transport. Fatty Acids 92-102 insulin Homo sapiens 26-33 2459120-16 1988 In conclusion, our studies support the involvement of cAMP lowering in insulin"s antagonism of fatty acid transport stimulation in the adipocyte. Fatty Acids 95-105 insulin Homo sapiens 71-78 2454111-9 1988 Dantrolene, in turn, may selectively probe such fatty acid-dependent insulin release; its inhibitory effect is predominantly, if not totally, independent of effects on Ca2+ fluxes, and may involve the inhibition of the effects of protein kinase C on exocytosis. Fatty Acids 48-58 insulin Homo sapiens 69-76 2900139-4 1988 Insulin also stimulated fatty acid synthesis from acetate 8.9 +/- 0.5-fold (three experiments), but TPA did not significantly increase fatty acid synthesis from this precursor. Fatty Acids 24-34 insulin Homo sapiens 0-7 3046601-0 1988 The response of adipocyte glucose metabolism and fatty acid release to adenosine deaminase, insulin and perifusion. Fatty Acids 49-59 insulin Homo sapiens 92-99 3287950-0 1988 Fatty acid-independent inhibition of hepatic ketone body production by insulin in humans. Fatty Acids 0-10 insulin Homo sapiens 71-78 3046601-3 1988 The decrease in fatty acid synthesis by perfusion was found to be dependent on the presence of insulin or fatty acids, and independent of the effects of ADA. Fatty Acids 16-26 insulin Homo sapiens 95-102 3286062-0 1988 Effect of insulin treatment on fatty acids of plasma and erythrocyte membrane lipids in type 2 diabetes. Fatty Acids 31-42 insulin Homo sapiens 10-17 3310656-2 1987 In small fat cells from 2-mo-old rats, donor"s food restriction led to decreased basal and insulin-stimulated glucose oxidation and fatty acid synthesis but led to increased lactate production, which increased from 4% of total glucose metabolized by cells from fed rats to 62% by cells from fasted rats. Fatty Acids 132-142 insulin Homo sapiens 91-98 3329089-0 1987 [Behavior of fatty acid patterns in serum lipids in type I diabetic patients in intensive conventional insulin therapy]. Fatty Acids 13-23 insulin Homo sapiens 103-110 3320694-4 1987 It is hypothesized that dietary enrichment with omega 3 fatty acids increases the incorporation of these fatty acids into the beta cell phospholipid membrane thus enhancing insulin secretion. Fatty Acids 56-67 insulin Homo sapiens 173-180 3550370-9 1987 In the presence of both norepinephrine and insulin (18 experiments), lipolysis was increased by 58% while 31 +/- 4% of the fatty acid released was reesterified. Fatty Acids 123-133 insulin Homo sapiens 43-50 3550370-12 1987 A substrate cycle exists, therefore, between triglyceride and fatty acid in human adipose tissue, and its activity is modified by norepinephrine and insulin. Fatty Acids 62-72 insulin Homo sapiens 149-156 3526480-3 1986 Significant lipogenic or lipolytic hormonal effects upon lactate metabolism were observed only in the presence of glucose, as insulin primarily increased lactate conversion to fatty acids while epinephrine promoted lactate oxidation. Fatty Acids 176-187 insulin Homo sapiens 126-133 3530857-1 1986 The metabolic actions of porcine insulin and biosynthetic human proinsulin on fatty acid and glucose metabolism were studied in rat hepatocytes cultured in monolayer for 24 h. Our aim was to establish whether proinsulin action in the liver is similar to insulin action and whether the relative potencies of the two hormones are the same for different metabolic processes. Fatty Acids 78-88 insulin Homo sapiens 64-74 3530857-1 1986 The metabolic actions of porcine insulin and biosynthetic human proinsulin on fatty acid and glucose metabolism were studied in rat hepatocytes cultured in monolayer for 24 h. Our aim was to establish whether proinsulin action in the liver is similar to insulin action and whether the relative potencies of the two hormones are the same for different metabolic processes. Fatty Acids 78-88 insulin Homo sapiens 67-74 3803743-0 1986 Improvement of diabetic control by continuous subcutaneous insulin infusion therapy changes fatty acid composition of serum lipids and erythrocytes in type 1 (insulin-dependent) diabetes. Fatty Acids 92-102 insulin Homo sapiens 59-66 3957707-4 1986 This confirms the concept of the third trimester as a catabolic phase within the maternal system, and provides support for the view that the insulin resistance of pregnancy may be a compensatory response to overcome the inhibitive effects of metabolites such as fatty acids on peripheral uptake of glucose. Fatty Acids 262-273 insulin Homo sapiens 141-148 3520336-2 1986 It is synthesized by the beta-cells of pancreatic islets, and circulating insulin levels are regulated by several small molecules, notably glucose, amino acids, fatty acids and certain pharmacological agents. Fatty Acids 161-172 insulin Homo sapiens 74-81 3890851-0 1985 Insulin-like stimulation of glucose transport in isolated adipocytes by fatty acids. Fatty Acids 72-83 insulin Homo sapiens 0-7 3908907-3 1985 To achieve half-maximal stimulation of fatty acid synthesis in rat hepatocytes about twenty one times higher concentrations of sulphated than neutral insulin were required (15.07 +/- 5.50 vs 0.71 +/- 0.34 nmol/l), this ratio being similar to the ratio of binding affinity in rat hepatocytes. Fatty Acids 39-49 insulin Homo sapiens 150-157 4066641-2 1985 Purification of this insulin-stimulating peptide (ISP) was monitored by an adipose-explant assay in which stimulation of fatty acid synthesis from glucose by insulin was measured. Fatty Acids 121-131 insulin Homo sapiens 21-28 4066641-2 1985 Purification of this insulin-stimulating peptide (ISP) was monitored by an adipose-explant assay in which stimulation of fatty acid synthesis from glucose by insulin was measured. Fatty Acids 121-131 insulin Homo sapiens 158-165 3516823-7 1986 Key intermediary metabolites were measured and blood glycerol, total ketone bodies, and plasma non-esterified fatty acids fell with the lowest insulin infusion rate. Fatty Acids 99-121 insulin Homo sapiens 143-150 3894356-4 1985 Treatment of other groups of ketotic diabetic animals with insulin produced substantial changes in the carnitine palmitoyltransferase apparent Ki value for malonyl-CoA within 4 h. These results suggest that insulin modulates the ketotic state, at least in part, by increasing the affinity of carnitine palmitoyltransferase for malonyl-CoA to bring about inhibition of fatty acid oxidation and ketogenesis. Fatty Acids 368-378 insulin Homo sapiens 59-66 3894356-4 1985 Treatment of other groups of ketotic diabetic animals with insulin produced substantial changes in the carnitine palmitoyltransferase apparent Ki value for malonyl-CoA within 4 h. These results suggest that insulin modulates the ketotic state, at least in part, by increasing the affinity of carnitine palmitoyltransferase for malonyl-CoA to bring about inhibition of fatty acid oxidation and ketogenesis. Fatty Acids 368-378 insulin Homo sapiens 207-214 3890851-4 1985 The results suggest that fatty acids may modulate the activity of the glucose transporter, providing an insulin-dependent supply of adipose tissue with glycerol-phosphate during lipolysis for reesterification of excess fatty acids. Fatty Acids 219-230 insulin Homo sapiens 104-111 3890851-4 1985 The results suggest that fatty acids may modulate the activity of the glucose transporter, providing an insulin-dependent supply of adipose tissue with glycerol-phosphate during lipolysis for reesterification of excess fatty acids. Fatty Acids 25-36 insulin Homo sapiens 104-111 6354230-5 1983 In comparison with a control group of patients, the insulin infusion caused a marked decrease in circulating glucose, non-esterified fatty acids and beta-hydroxybutyrate concentrations, and an increase in blood lactate values. Fatty Acids 133-144 insulin Homo sapiens 52-59 6529855-2 1984 Improvement of diabetic control, achieved by treatment with continuous subcutaneous insulin infusion coincided with an increase of arachidonic acid and a normalization of total polyunsaturated fatty acids, with a concomitant decrease of total saturated fatty acids and total monounsaturated fatty acids, especially 18:1c, omega 9. Fatty Acids 183-204 insulin Homo sapiens 84-91 6480801-0 1984 Mechanism of hyperglycemia and response to treatment with an inhibitor of fatty acid oxidation in a patient with insulin resistance due to antiinsulin receptor antibodies. Fatty Acids 74-84 insulin Homo sapiens 113-120 6480801-6 1984 The hypoglycemic action of the drug is consistent with the existence of an insulin-independent effect of fatty acid oxidation on glucose metabolism in man. Fatty Acids 105-115 insulin Homo sapiens 75-82 6696735-11 1984 Depletion of a mobile pool of fatty acids in plasma during fasting, as seen by n.m.r., paralleled that seen during insulin withdrawal. Fatty Acids 30-41 insulin Homo sapiens 115-122 6696735-12 1984 These fatty acids were thought to be largely in chylomicrons, acylglycerols and lipoproteins, and were grossly elevated in plasma samples from a non-insulin-dependent diabetic and in cases of known hyperlipidaemia. Fatty Acids 6-17 insulin Homo sapiens 149-156 6137007-0 1983 The role of phosphorylation in the regulation of fatty acid synthesis by insulin and other hormones. Fatty Acids 49-59 insulin Homo sapiens 73-80 6137007-1 1983 Insulin stimulates fatty acid synthesis in white and brown fat cells as well as in liver and mammary tissue. Fatty Acids 19-29 insulin Homo sapiens 0-7 7044833-6 1982 Insulin may promote lipid deposition by increasing adipocyte membrane permeability to glucose with subsequent metabolism to alpha-glycerolphosphoric acid and thereby stimulating fatty acid esterification. Fatty Acids 178-188 insulin Homo sapiens 0-7 6347779-4 1983 Considering the values at 23.00 h as reference, interruption of the insulin infusion resulted in (1) a rapid decrease in plasma free insulin significant after 1 h and reaching a nadir of 6 +/- 2 mU/l after 6 h; (2) a rise in blood glucose which was significant at hour 3 and reached 17.4 +/- 1.9 mmol/l at hour 6; (3) a moderate increase in plasma nonesterified fatty acids which remained in the range of 700-800 mumol/l; (4) an early and linear rise in plasma 3-hydroxybutyrate, significant after 1 h and averaging 1290 +/- 140 mumol/l after 6 h; (5) a late increase (hour 5) in plasma glucagon. Fatty Acids 362-373 insulin Homo sapiens 68-75 6337875-0 1983 The effect of N6-phenylisopropyladenosine on the regulation of fat cell hexose transport, glucose oxidation and fatty acid release by insulin and catecholamines. Fatty Acids 112-122 insulin Homo sapiens 134-141 6751811-3 1982 In its presence, insulin stimulates and glucagon inhibits incorporation of labelled acetate into fatty acids. Fatty Acids 97-108 insulin Homo sapiens 17-24 7044833-7 1982 Insulin also stimulates adipose lipoprotein lipase, which would increase the supply of fatty acids for esterification in adipose tissue. Fatty Acids 87-98 insulin Homo sapiens 0-7 7017343-5 1981 During the insulin infusion, plasma non-esterified fatty acids fell during rest and failed to rise with exercise, indicating a limited availability of this substrate to working muscle. Fatty Acids 40-62 insulin Homo sapiens 11-18 6128738-0 1982 The regulation of fatty acid synthesis in brown adipose tissue by insulin. Fatty Acids 18-28 insulin Homo sapiens 66-73 6818005-7 1982 The authors show that analysis of the relationships of triglycerides, insulin and serum fatty acids could be of value for identifying the factors involved in a faster progression of atherosclerosis. Fatty Acids 88-99 insulin Homo sapiens 70-77 6994726-0 1980 Stimulation of glucose transport and oxidation in adipocytes by fatty acids: evidence for a regulatory role in the cellular response to insulin. Fatty Acids 64-75 insulin Homo sapiens 136-143 7021276-0 1981 The effects of a low-dose intravenous insulin infusion upon plasma glucose and non-esterified fatty acid levels in very obese and non-obese human subjects. Fatty Acids 94-104 insulin Homo sapiens 38-45 7021276-4 1981 In the controls the fall in plasma glucose and non-esterified fatty acids was significantly and inversely correlated with the basal plasma insulin level. Fatty Acids 62-73 insulin Homo sapiens 139-146 7021276-6 1981 Weight lost in the obese subjects led to increased insulin sensitivity; in particular, the degree of change in insulin-induced non-esterified fatty acids was significantly related to the percentage change in weight. Fatty Acids 131-153 insulin Homo sapiens 51-58 7021276-6 1981 Weight lost in the obese subjects led to increased insulin sensitivity; in particular, the degree of change in insulin-induced non-esterified fatty acids was significantly related to the percentage change in weight. Fatty Acids 131-153 insulin Homo sapiens 111-118 7021278-11 1981 Insulin levels, similar to those found after a meal, rapidly reversed the effects of glucagon on non-esterified fatty acid, glucose and potassium. Fatty Acids 112-122 insulin Homo sapiens 0-7 7006515-0 1980 Hormones and liver mitochondria: influence of growth hormone, thyroxine, testosterone, and insulin on thermotropic effects of respiration and fatty acid composition of membranes. Fatty Acids 142-152 insulin Homo sapiens 91-98 385136-6 1979 However, during clinical ketosis, the hormonal status (low insulin, high glucagon/insulin ratio) in combination with hypoglycemia promotes excessive lipid mobilization and a greater hepatic removal of fatty acids and switches the liver to a higher rate of ketogenesis. Fatty Acids 201-212 insulin Homo sapiens 59-66 118029-2 1979 Fatty acid synthesis in subcutaneous adipose tissue expressed on a cell basis was greater in obese than control subjects and was stimulated by a high concentration of insulin (1000 micro U/ml), but not by a lower amount (100 micro U/ml). Fatty Acids 0-10 insulin Homo sapiens 167-174 6986299-5 1980 It is suggested that an insulin-mediated increase of glucose utilization in the GIP cell interferes only with increased GIP secretion stimulated by the utilization of fatty acids but not of glucose. Fatty Acids 167-178 insulin Homo sapiens 24-31 582421-0 1978 Insulin effect on the biosynthesis of lung phospholipids and their fatty acid composition. Fatty Acids 67-77 insulin Homo sapiens 0-7 749914-19 1978 In the presence of insulin there is a small increase in fatty acid mobilization from adipose tissue, secondary to impaired glucose entry, and perhaps a small effect on lipolysis itself. Fatty Acids 56-66 insulin Homo sapiens 19-26 101402-5 1978 In the individual patient the changes in blood glycerol and plasma non-esterified fatty acids were related to changes in circulating insulin concentration and did not appear to be a true extra-pancreatic effect of glibenclamide. Fatty Acids 82-93 insulin Homo sapiens 133-140 19873627-8 1968 The effect of work or insulin is strongly inhibited by metabolism, of fatty acids. Fatty Acids 70-81 insulin Homo sapiens 22-29 908274-0 1977 Insulin stimulation of fatty acid synthesis in human breast cancer in long term tissue culture. Fatty Acids 23-33 insulin Homo sapiens 0-7 1170119-0 1975 Diurnal variation in the effects of insulin on blood glucose, plasma non-esterified fatty acids and growth hormone. Fatty Acids 84-95 insulin Homo sapiens 36-43 4817159-7 1974 Fasting non-esterified fatty acid levels were significantly higher before the afternoon test.The relatively impaired glucose tolerance in the afternoon is associated with a delayed insulin response to the glucose load. Fatty Acids 23-33 insulin Homo sapiens 181-188 4454393-0 1974 [Effect of insulin on fatty acid metabolism in the liver in endogenous hypertriglyceridemia. Fatty Acids 22-32 insulin Homo sapiens 11-18 4404963-11 1972 The rate of glucose metabolism via the pentose phosphate cycle as well as the rate of fatty acid synthesis, however, was not affected by 6-aminonicotinamide treatment and could still be stimulated by addition of insulin. Fatty Acids 86-96 insulin Homo sapiens 212-219 5158898-2 1971 In epididymal adipose tissue synthesizing fatty acids from fructose in vitro, addition of insulin led to a moderate increase in fructose uptake, to a considerable increase in the flow of fructose carbon atoms to fatty acid, to a decrease in the steady-state concentration of lactate and pyruvate in the medium, and to net uptake of lactate and pyruvate from the medium. Fatty Acids 42-53 insulin Homo sapiens 90-97 5158898-2 1971 In epididymal adipose tissue synthesizing fatty acids from fructose in vitro, addition of insulin led to a moderate increase in fructose uptake, to a considerable increase in the flow of fructose carbon atoms to fatty acid, to a decrease in the steady-state concentration of lactate and pyruvate in the medium, and to net uptake of lactate and pyruvate from the medium. Fatty Acids 42-52 insulin Homo sapiens 90-97 5158898-3 1971 It is concluded that insulin accelerates a step in the span pyruvate-->fatty acid. Fatty Acids 74-84 insulin Homo sapiens 21-28 4321574-0 1971 Mechanism of insulin action on control of fatty acid synthesis independent of glucose transport. Fatty Acids 42-52 insulin Homo sapiens 13-20 559098-0 1977 Insulin stimulation of fatty acid synthesis in human breast cancer cells. Fatty Acids 23-33 insulin Homo sapiens 0-7 559098-2 1977 Physiologic concentrations of insulin enhanced the incorporation of [14C]acetate into fatty acids in two of four cell lines tested. Fatty Acids 86-97 insulin Homo sapiens 30-37 4526203-0 1974 Effect of insulin on sterol and fatty acid synthesis and hydroxymethylglutaryl CoA reductase activity in mammalian cells grown in culture. Fatty Acids 32-42 insulin Homo sapiens 10-17 4526203-1 1974 The effects of insulin on the synthesis of sterols and fatty acids and on the activity of 3-hydroxy-3-methylglutaryl coenzyme A reductase (EC 1.1.1.34), a rate-limiting enzyme for sterol synthesis, were studied in mammalian cells grown in culture. Fatty Acids 55-66 insulin Homo sapiens 15-22 4752490-0 1973 Growth effects on the insulin alteration of Chang liver fatty acid metabolism. Fatty Acids 56-66 insulin Homo sapiens 22-29 5051799-0 1972 In vitro and in vivo effects of insulin on the quality of fatty acids synthesized by adipose tissue. Fatty Acids 58-69 insulin Homo sapiens 32-39 4143971-0 1972 [Mechanism of action of insulin and fasting on fatty acid synthesis in the liver and adipose tissue]. Fatty Acids 47-57 insulin Homo sapiens 24-31 4319952-0 1970 An additional role for insulin in the control of fatty acid synthesis independent of glucose transport. Fatty Acids 49-59 insulin Homo sapiens 23-30 5445770-0 1970 Effect of insulin on fatty acid ynthesis from pyruvate, lactage, or endogenous sources in adipose tissue: evidence for the hormonal regulation of pyruvate dehydrogenase. Fatty Acids 21-31 insulin Homo sapiens 10-17 16695927-8 1967 The responsiveness of human adipose tissue to exogenous insulin in concentrations comparable to those detected in blood reemphasizes the importance of adipose tissue as a major site for fatty acid synthesis. Fatty Acids 186-196 insulin Homo sapiens 56-63 5714494-0 1968 [Action of fasting and insulin on the synthesis of fatty acids beginning with glucose specifically marked with carbon and hydrogen]. Fatty Acids 51-62 insulin Homo sapiens 23-30 13295301-0 1956 The effect of insulin on the pathways of conversion of glucose to fatty acids in the liver. Fatty Acids 66-77 insulin Homo sapiens 14-21 24173299-6 1966 The difference in changes in concentration of non-esterified fatty acids and glyoerol in response to a variety of test situations may well be the result of both the glucose-dependent lipogenetic and the glucose-independent antilipolytic effect of insulin. Fatty Acids 50-72 insulin Homo sapiens 247-254 13902277-0 1962 The effect of insulin on brain cholesterol and fatty acid biosynthesis. Fatty Acids 47-57 insulin Homo sapiens 14-21 13697718-0 1961 [The behavior of esterified and non-esterified fatty acids in the serum under the influence of glucagon and insulin in man]. Fatty Acids 47-58 insulin Homo sapiens 108-115 13478743-0 1957 Action of insulin on release of fatty acids from tissue stores. Fatty Acids 32-43 insulin Homo sapiens 10-17 13988641-0 1962 Effect of insulin on fatty acid transport and regional metabolism. Fatty Acids 21-31 insulin Homo sapiens 10-17 13474672-0 1957 [Decrease in esterified fatty acids after insulin administration]. Fatty Acids 13-35 insulin Homo sapiens 42-49 13331942-0 1956 The action of insulin in sparing fatty acid oxidation: a study with palmitic acid-1-C14 and octanoate-1-C14. Fatty Acids 33-43 insulin Homo sapiens 14-21 13097937-0 1953 [Preliminary report on decline of fatty acid esters in blood after insulin administration]. Fatty Acids 34-51 insulin Homo sapiens 67-74 13221262-0 1954 [The decrease of esterified fatty acids and amino acids in the blood after insulin administration]. Fatty Acids 17-39 insulin Homo sapiens 75-82 33924347-5 2021 Peripheral insulin resistance was related to fatty acid metabolism and glycerolphosphorylcholine. Fatty Acids 45-55 insulin Homo sapiens 11-18 33631318-5 2021 A large number of studies reported an association between elevated circulating fatty acids and the development of insulin resistance. Fatty Acids 79-90 insulin Homo sapiens 114-121 33919366-1 2021 Macrophages in pathologically expanded dysfunctional white adipose tissue are exposed to a mix of potential modulators of inflammatory response, including fatty acids released from insulin-resistant adipocytes, increased levels of insulin produced to compensate insulin resistance, and prostaglandin E2 (PGE2) released from activated macrophages. Fatty Acids 155-166 insulin Homo sapiens 181-188 33858855-9 2021 Insulin-induced suppression of EGP (-1.71 [-2.75, -0.63] mumol/kg/min, P = 0.0036) and plasma free fatty acids (-21.93% [-39.31, -4.54], P = 0.016) was greater with dapagliflozin. Fatty Acids 99-110 insulin Homo sapiens 0-7 33841514-7 2021 KEGG analysis indicated that the significant pathways were the calcium signaling pathway, fatty acid biosynthesis, and pathways in cancer and insulin resistance. Fatty Acids 90-100 insulin Homo sapiens 142-149 33561215-0 2021 Associations of Serum Fatty Acid Proportions with Obesity, Insulin Resistance, Blood Pressure, and Fatty Liver: The Cardiovascular Risk in Young Finns Study. Fatty Acids 22-32 insulin Homo sapiens 59-66 33522398-0 2021 100th Anniversary of the discovery of insulin Perspective: Insulin and Adipose Tissue Fatty Acid Metabolism. Fatty Acids 86-96 insulin Homo sapiens 38-45 33522398-3 2021 Insulin also regulates adipose tissue fatty acid esterification, glycerol and TG synthesis, lipogenesis and possibly oxidation, contributing to the trapping of dietary fatty acids in the postprandial state. Fatty Acids 38-48 insulin Homo sapiens 0-7 33522398-3 2021 Insulin also regulates adipose tissue fatty acid esterification, glycerol and TG synthesis, lipogenesis and possibly oxidation, contributing to the trapping of dietary fatty acids in the postprandial state. Fatty Acids 168-179 insulin Homo sapiens 0-7 33522398-6 2021 This review focusses on the in vivo regulation of adipose tissue fatty acid metabolism by insulin and the mechanistic significance of the current definition of adipose tissue insulin resistance. Fatty Acids 65-75 insulin Homo sapiens 90-97 33825246-1 2021 Free fatty acids (FFAs) and fatty acid synthesis (FAS) activity have significantly contributed to disease states such as insulin resistance, obesity, type 2 diabetes, myocardial infarction, blood pressure, and several types of cancer. Fatty Acids 5-15 insulin Homo sapiens 121-128 33549440-1 2021 BACKGROUND AND AIMS: Omentin, as an adipokine, has been reported to improve insulin resistance and inflammation may be related to fatty acids (FAs). Fatty Acids 130-141 insulin Homo sapiens 76-83 33687877-9 2021 Interestingly, the metabolites (short chain fatty acids and other bioactive components) have been shown to improve gut health, control glycemia, lower lipids, reduce insulin resistance, and alleviate inflammation. Fatty Acids 44-55 insulin Homo sapiens 166-173 33686181-1 2021 Saturated fatty acids such as palmitic acid promote inflammation and insulin resistance in peripheral tissues, contrasting with the protective action of polyunsaturated fatty acids such docosahexaenoic acid. Fatty Acids 0-21 insulin Homo sapiens 69-76 33549440-1 2021 BACKGROUND AND AIMS: Omentin, as an adipokine, has been reported to improve insulin resistance and inflammation may be related to fatty acids (FAs). Fatty Acids 143-146 insulin Homo sapiens 76-83 33572903-8 2021 ATP plus H2O2 are also required for branched-chain ketoacids (BCKAs); and partly for fatty acids (FAs) to secrete insulin, while BCKA or FA beta-oxidation provide redox signaling from mitochondria, which proceeds by H2O2 diffusion or hypothetical SH relay via peroxiredoxin "redox kiss" to target proteins. Fatty Acids 85-96 insulin Homo sapiens 114-121 33572903-8 2021 ATP plus H2O2 are also required for branched-chain ketoacids (BCKAs); and partly for fatty acids (FAs) to secrete insulin, while BCKA or FA beta-oxidation provide redox signaling from mitochondria, which proceeds by H2O2 diffusion or hypothetical SH relay via peroxiredoxin "redox kiss" to target proteins. Fatty Acids 98-101 insulin Homo sapiens 114-121 33053159-0 2021 Metabolomics of lean/overweight insulin resistant females reveals alterations in steroids and fatty acids. Fatty Acids 94-105 insulin Homo sapiens 32-39 33446880-5 2021 Higher levels of TG saturated fatty acids were associated with greater body mass index (BMI, r = 0.230), waist circumference (r = 0.203), triceps skinfold (r = 0.197), fat tissue index (r = 0.150), serum insulin (r = 0.280), and homeostatic model assessment of insulin resistance (r = 0.276), but lower malnutrition inflammation score (MIS, r = - 0.160). Fatty Acids 20-41 insulin Homo sapiens 204-211 32891999-6 2021 The key lipid remodeling in response to exposure was found to involve the cardiolipins, phosphatidylglycerols and fatty acids metabolic pathways, providing novel clues of potential mechanism in which both BPA and BPS exposure could be associated with increased risk of insulin resistance. Fatty Acids 114-125 insulin Homo sapiens 269-276 33613155-1 2021 Background: Saturated fatty acids (SFAs) generally have been thought to worsen insulin-resistance and increase the risk of developing type 2 diabetes mellitus (T2DM). Fatty Acids 12-33 insulin Homo sapiens 79-86 33446880-5 2021 Higher levels of TG saturated fatty acids were associated with greater body mass index (BMI, r = 0.230), waist circumference (r = 0.203), triceps skinfold (r = 0.197), fat tissue index (r = 0.150), serum insulin (r = 0.280), and homeostatic model assessment of insulin resistance (r = 0.276), but lower malnutrition inflammation score (MIS, r = - 0.160). Fatty Acids 20-41 insulin Homo sapiens 261-268 32338219-1 2021 BACKGROUND: Elevation of plasma free fatty acids as a principal aspect of type 2 diabetes maintains etiologically insulin insensitivity in target cells. Fatty Acids 37-48 insulin Homo sapiens 114-121 33435282-8 2021 Lipogenesis and fatty acid oxidation, which are also associated with insulin resistance, are regulated by AMP-activated protein kinase (AMPK) activation. Fatty Acids 16-26 insulin Homo sapiens 69-76 33159991-5 2021 High fatty acid stimulation decreased insulin secretion along with CASK, APBA1, and STXBP1 expression; Cask overexpression enhanced CASK/APBA1/STXBP1 tripartite complex function, and may thereby rescue lipotoxicity-induced insulin-release defects. Fatty Acids 5-15 insulin Homo sapiens 38-45 32844500-2 2021 In addition to the fat concentration, also the fatty acid chemical composition (FAC) of the triglyceride molecules may play an important part in diseases such as obesity, insulin resistance, hepatic steatosis, osteoporosis, and cancer. Fatty Acids 47-57 insulin Homo sapiens 171-178 32995848-11 2021 CONCLUSIONS: Ethnic differences in fatty acid-derived desaturation indices were observed, with insulin resistant black SA women paradoxically showing a fatty acid pattern typical for higher insulin sensitivity in European populations. Fatty Acids 152-162 insulin Homo sapiens 95-102 33320449-1 2021 Deleterious effects of free fatty acids, FFAs, on insulin sensitivity are observed in vivo studies in humans. Fatty Acids 28-39 insulin Homo sapiens 50-57 32954825-1 2020 Saturated fatty acid (SFA) induces pro-inflammatory response through a toll-like receptor (TLR)-mediated mechanism, which is associated with cardiometabolic diseases such as obesity, insulin resistance, and endothelial dysfunction. Fatty Acids 0-20 insulin Homo sapiens 183-190 33365210-6 2020 Hyperinsulinemic hypoglycemia (HH), caused by dysregulation of insulin secretion from pancreatic beta-cells, leads to insulin driven glucose entry into the tissues and inhibits glycolysis, gluconeogenesis, fatty acid release, and ketone body synthesis. Fatty Acids 206-216 insulin Homo sapiens 5-12 33365210-6 2020 Hyperinsulinemic hypoglycemia (HH), caused by dysregulation of insulin secretion from pancreatic beta-cells, leads to insulin driven glucose entry into the tissues and inhibits glycolysis, gluconeogenesis, fatty acid release, and ketone body synthesis. Fatty Acids 206-216 insulin Homo sapiens 63-70 32954825-1 2020 Saturated fatty acid (SFA) induces pro-inflammatory response through a toll-like receptor (TLR)-mediated mechanism, which is associated with cardiometabolic diseases such as obesity, insulin resistance, and endothelial dysfunction. Fatty Acids 22-25 insulin Homo sapiens 183-190 33051490-8 2020 Changes in amino acid, carbohydrate and fatty acid metabolism in response to insulin were impaired in subjects with low IS. Fatty Acids 40-50 insulin Homo sapiens 77-84 32683035-2 2020 As a key criterion in MetS, the onset of insulin resistance is related to abnormal levels of circulating free fatty acids and adipokines. Fatty Acids 110-121 insulin Homo sapiens 41-48 33116712-2 2020 In individuals who are obese, higher amounts of non-esterified fatty acids, glycerol, hormones, and pro-inflammatory cytokines that could participate in the development of insulin resistance are released by adipose tissue. Fatty Acids 63-74 insulin Homo sapiens 172-179 32822725-7 2020 When cells were exposed to these fatty acids, elaidate suppressed insulin-induced fusion, but not translocation, of GLUT4 storage vesicles in the PM, whereas stearate did not suppress the fusion and translocation of GLUT4 storage, indicating that elaidate has suppressive effects on the accumulation of Akt and fusion of GLUT4 storage vesicles and that both elaidate and stearate vary in the mechanisms by which they impair insulin-dependent glucose uptake. Fatty Acids 33-44 insulin Homo sapiens 66-73 33036203-6 2020 This work shows that HFD induces insulin resistance, which is accompanied by an increase in the concentration of plasma fatty acids and the level of bioactive lipids in muscle. Fatty Acids 120-131 insulin Homo sapiens 33-40 33013697-5 2020 This review provides a comprehensive summary of the mechanisms through which BCAAs and fatty acids modulate energy metabolism, insulin sensitivity, and inflammation synergistically. Fatty Acids 87-98 insulin Homo sapiens 127-134 33101053-1 2020 Saturated fatty acids such as palmitate contribute to the development of Type 2 Diabetes by reducing insulin sensitivity, increasing inflammation and potentially contributing to anabolic resistance. Fatty Acids 0-21 insulin Homo sapiens 101-108 32962087-9 2020 All of the examined fatty acids attenuated the insulin-signaling pathway and radically reduced glucose uptake following insulin stimulation. Fatty Acids 20-31 insulin Homo sapiens 47-54 32962087-9 2020 All of the examined fatty acids attenuated the insulin-signaling pathway and radically reduced glucose uptake following insulin stimulation. Fatty Acids 20-31 insulin Homo sapiens 120-127 32962087-13 2020 Furthermore, all of the examined fatty acids attenuated insulin signaling and secretion of cytokines and adipokines. Fatty Acids 33-44 insulin Homo sapiens 56-63 32663099-1 2020 Insulin resistance in obesity and type 2 diabetes has been shown to be associated with decreased de novo fatty acid (FA) synthesis in adipose tissue. Fatty Acids 105-115 insulin Homo sapiens 0-7 32963827-3 2020 In light of recent evidence, it has been shown that lipids, especially fatty acids (FAs), are important signaling molecules that regulate the signaling pathways of insulin and inflammatory mediators. Fatty Acids 71-82 insulin Homo sapiens 164-171 32535333-2 2020 Lipopolysaccharide (LPS) and the saturated fatty acid (FA) palmitate polarise macrophages towards a pro-inflammatory phenotype in vitro and indirectly cause insulin resistance (IR) in myotubes. Fatty Acids 33-53 insulin Homo sapiens 157-164 32556615-5 2020 RESULTS: Per-metabolite and network analyses across the four ancestries identified numerous metabolites associated with maternal insulin sensitivity before and 1 h after a glucose load, ranging from amino acids and carbohydrates to fatty acids and lipids. Fatty Acids 232-243 insulin Homo sapiens 129-136 32963827-3 2020 In light of recent evidence, it has been shown that lipids, especially fatty acids (FAs), are important signaling molecules that regulate the signaling pathways of insulin and inflammatory mediators. Fatty Acids 84-87 insulin Homo sapiens 164-171 32963827-7 2020 The purpose of this review is to highlight recent advances in the study of the effect of fatty acids as modulators of insulin response and inflammatory process in the pathogenesis and treatment for MetS. Fatty Acids 89-100 insulin Homo sapiens 118-125 32891058-4 2020 Insulin stimulated glycolysis by promoting Glut4 activity by enhancing phosphorylation of AS160 at S595, stimulated fatty acid synthesis by promoting Acly activity through allosteric activation by glucose 6-phosphate or fructose 6-phosphate, and stimulated glutamate synthesis by alleviating allosteric inhibition of Gls by glutamate. Fatty Acids 116-126 insulin Homo sapiens 0-7 33520860-12 2020 Insulin promotes the Pi transport from the blood to tissues, activates the mitochondrial respiratory activity, and glutamine metabolism, which activates the synthesis of cholesterol and the de novo fatty acids for reorganising and stabilising the lipid membranes for nutrient transport and signal transduction in response to fluctuations in the microenvironmental cues. Fatty Acids 198-209 insulin Homo sapiens 0-7 32806641-13 2020 Fatty acid-induced regulation of genes related to the IRS1/PI3K pathway may be a novel mechanism by which fatty acids regulate insulin sensitivity in visceral adipocytes. Fatty Acids 0-10 insulin Homo sapiens 127-134 32806641-13 2020 Fatty acid-induced regulation of genes related to the IRS1/PI3K pathway may be a novel mechanism by which fatty acids regulate insulin sensitivity in visceral adipocytes. Fatty Acids 106-117 insulin Homo sapiens 127-134 33786271-0 2021 Basal insulin ameliorates post-breakfast hyperglycemia via suppression of post-breakfast proinsulin/C-peptide ratio and fasting serum free fatty acid levels in patients with type 2 diabetes. Fatty Acids 139-149 insulin Homo sapiens 6-13 32480033-5 2020 In muscle, ghrelin has been shown to acutely stimulate fat oxidation, which may protect the muscle from the insulin-desensitizing effects of high fatty acid concentrations. Fatty Acids 146-156 insulin Homo sapiens 108-115 32543943-5 2020 The ablation of insulin resulted in reductions in absolute mitochondrial oxidative capacity and ADP-supported respiration and reduced the ability for malonyl-CoA to inhibit carnitine palmitoyltransferase I (CPT-I) and suppress fatty acid-supported respiration. Fatty Acids 227-237 insulin Homo sapiens 16-23 32543943-7 2020 Together, these data suggest that attenuated/ablated insulin signaling does not affect mitochondrial ADP sensitivity, whereas the increased reliance on fatty acid oxidation in situations where insulin action is reduced may occur as a result of altered regulation of mitochondrial fatty acid transport through CPT-I. Fatty Acids 152-162 insulin Homo sapiens 193-200 32543943-7 2020 Together, these data suggest that attenuated/ablated insulin signaling does not affect mitochondrial ADP sensitivity, whereas the increased reliance on fatty acid oxidation in situations where insulin action is reduced may occur as a result of altered regulation of mitochondrial fatty acid transport through CPT-I. Fatty Acids 280-290 insulin Homo sapiens 193-200 33643468-11 2021 We also confirmed defects of disrupted insulin signaling through reduction of lipid accumulation from fatty acid uptake and elevation of glycerol secretion. Fatty Acids 102-112 insulin Homo sapiens 39-46 32579369-1 2020 B29Nepsilon-lithocholyl-L-Glu-desB30 human insulin [NN344] belongs to a group of insulins with fatty acid or sterol modications. Fatty Acids 95-105 insulin Homo sapiens 43-50 32520824-4 2020 Excessive fatty acids play a determinant role in the pathogenesis of insulin resistance in obese children, inducing an increased production of acetyl-CoA in the liver and enhancing inflammation in adipose tissue. Fatty Acids 10-21 insulin Homo sapiens 69-76 32760285-0 2020 PPARdelta Attenuates Alcohol-Mediated Insulin Resistance by Enhancing Fatty Acid-Induced Mitochondrial Uncoupling and Antioxidant Defense in Skeletal Muscle. Fatty Acids 70-80 insulin Homo sapiens 38-45 31649307-0 2020 A dominant insulin-specific and islet-destructive T-cell response is sufficient to activate CD8 T cells directed against the fatty-acid receptor GPR40. Fatty Acids 125-135 insulin Homo sapiens 11-18 32494174-3 2020 Insulin plays an important role in regulating normal fatty acid levels by inhibiting lipolysis. Fatty Acids 53-63 insulin Homo sapiens 0-7 31828866-2 2020 In particular, saturated fatty acids such as palmitic acid (PA) have been implicated in the development of insulin resistance (IR). Fatty Acids 15-36 insulin Homo sapiens 107-114 32483543-9 2020 Furthermore, a major contributor to the development of insulin resistance is an overabundance of circulating fatty acids. Fatty Acids 109-120 insulin Homo sapiens 55-62 31988048-7 2020 In addition, we show that ELOVL fatty acid elongase 6 (Elovl6) is a direct target of miR-125a, and participates in miR-125a mediated regulation of insulin sensitivity and lipid metabolism. Fatty Acids 32-42 insulin Homo sapiens 147-154 31340878-6 2020 In the present paper, we review the influence of a person"s sex on key aspects of metabolism involved in the cardiometabolic disease process, including insulin action on endogenous glucose production, tissue glucose disposal, and adipose tissue lipolysis, insulin secretion and insulin plasma clearance, postprandial glucose, fatty acid, and triglyceride kinetics, hepatic lipid metabolism and myocardial substrate use. Fatty Acids 326-336 insulin Homo sapiens 152-159 32326226-2 2020 KATP channel activation is mechanistically involved in the regulation of appetite in the arcuate nucleus; the regulation of hyperinsulinemia, glycemic control, appetite and satiety in the dorsal motor nucleus of vagus; insulin secretion by beta-cells; and the synthesis and beta-oxidation of fatty acids in adipocytes. Fatty Acids 292-303 insulin Homo sapiens 129-136 32704559-1 2020 Aims: Recent clinical studies have shown enhanced brain glucose uptake during clamp and brain fatty acid uptake in insulin-resistant individuals. Fatty Acids 94-104 insulin Homo sapiens 115-122 31925734-3 2020 The degree of adipose tissue insulin resistance was assessed using the index of adipose tissue insulin resistance (Adipo-IRI), calculated as the product of fasting insulin and free fatty acids. Fatty Acids 181-192 insulin Homo sapiens 95-102 32312974-2 2020 Hepatic saturated fatty acids (SFA) may be a marker of DNL and are suggested to be most detrimental in contributing to insulin resistance. Fatty Acids 8-29 insulin Homo sapiens 119-126 32290181-4 2020 In consequence, fatty acids are stored into epicardial fat and its accumulation provokes inflammation, insulin resistance, and oxidative stress, which enhance the myocardium dysfunction. Fatty Acids 16-27 insulin Homo sapiens 103-110 31925734-3 2020 The degree of adipose tissue insulin resistance was assessed using the index of adipose tissue insulin resistance (Adipo-IRI), calculated as the product of fasting insulin and free fatty acids. Fatty Acids 181-192 insulin Homo sapiens 95-102 32034158-1 2020 Fatty acid and triglyceride synthesis increases greatly in response to feeding and insulin. Fatty Acids 0-10 insulin Homo sapiens 83-90 32105829-2 2020 Diet-induced obesity and fatty acids surplus promote mitochondrial dysfunction in liver, triggering oxidative stress and activation of c-Jun N-terminal kinase (JNK) which has been related to the development of insulin resistance and steatosis, the main hallmarks of NAFLD. Fatty Acids 25-36 insulin Homo sapiens 210-217 32105829-3 2020 Considering that estrogen, in particular 17beta-estradiol (E2), have been reported to improve mitochondrial biogenesis and function in liver, our aim was to elucidate the role of E2 in preventing fatty acid-induced insulin resistance in hepatocytes through modulation of mitochondrial function, oxidative stress and JNK activation. Fatty Acids 196-206 insulin Homo sapiens 215-222 32105829-7 2020 Altogether, our data highlights the importance of E2 as a mitigating factor of fatty acid-insulin resistance in hepatocytes through downregulation of JNK activation, by means of mitochondrial function improvement. Fatty Acids 79-89 insulin Homo sapiens 90-97 31910030-0 2020 Trafficking of non-esterified fatty acids in insulin resistance and relationship to dys-glycemia. Fatty Acids 30-41 insulin Homo sapiens 45-52 31910030-1 2020 In adipose, insulin functions to suppress intracellular lipolysis and secretion of non-esterified fatty acid (NEFA) into plasma. Fatty Acids 98-108 insulin Homo sapiens 12-19 32048247-1 2020 BACKGROUND: Currently, there is overwhelming evidence linking elevated plasma free fatty acids with insulin resistance and inflammation. Fatty Acids 83-94 insulin Homo sapiens 100-107 32069846-9 2020 Analysis of the interactions of these microRNAs with gene expression pathways suggests their potential contribution to the regulation of the activity of genes associated with insulin resistance, fatty acids metabolism, and adipocytokines signaling. Fatty Acids 195-206 insulin Homo sapiens 175-182 31850803-6 2020 These mutant cells show enhanced baseline phosphorylation of insulin signaling protein as indicated by increased Akt, AMPK and ACC phosphorylation that may negatively influence fatty acid oxidation and enhance lipid uptake, and are insulin insensitive. Fatty Acids 177-187 insulin Homo sapiens 61-68 31891539-1 2020 BACKGROUND: Increased myocardial partitioning of dietary fatty acids (DFA) and decreased left-ventricular (LV) function is associated with insulin resistance in prediabetes. Fatty Acids 57-68 insulin Homo sapiens 139-146 30396212-0 2020 Impact of Brain Fatty Acid Signaling on Peripheral Insulin Action in Mice. Fatty Acids 16-26 insulin Homo sapiens 51-58 31646540-1 2020 Insulin secretion in humans is usually induced by mixed meals, which upon ingestion, increase the plasma concentration of glucose, fatty acids, amino acids, and incretins like glucagon-like peptide 1. Fatty Acids 131-142 insulin Homo sapiens 0-7 30396212-2 2020 Especially insulin signaling in the brain seems to impact whole body glucose homeostasis and interacts with fatty acid signaling. Fatty Acids 108-118 insulin Homo sapiens 11-18 31571412-1 2019 OBJECTIVE: Insulin resistance is associated with increased lipolysis and elevated concentrations of free fatty acids (FFA), which in turn contribute to impaired vascular function. Fatty Acids 105-116 insulin Homo sapiens 11-18 31888144-6 2019 Alterations in peripheral glucose metabolism due to insulin resistance (IR) were assesed by HOMA-IR (Glucose x Insulin/22.5), while adipose tissue IR was estimated as (Adipo-IR = Free Fatty Acids x Insulin). Fatty Acids 184-195 insulin Homo sapiens 52-59 30844447-2 2019 Muscles of patients with T2D are affected with insulin resistance and mitochondrial dysfunction, which result in impaired glucose and fatty acid metabolism. Fatty Acids 134-144 insulin Homo sapiens 47-54 31703434-2 2019 Both fatty acids and amino acids stimulate insulin secretion by distinct mechanisms; fatty acids enhance glucose-stimulated insulin secretion, while amino acids may have a direct effect on pancreatic beta cells. Fatty Acids 5-16 insulin Homo sapiens 43-50 31703434-2 2019 Both fatty acids and amino acids stimulate insulin secretion by distinct mechanisms; fatty acids enhance glucose-stimulated insulin secretion, while amino acids may have a direct effect on pancreatic beta cells. Fatty Acids 5-16 insulin Homo sapiens 124-131 31703434-2 2019 Both fatty acids and amino acids stimulate insulin secretion by distinct mechanisms; fatty acids enhance glucose-stimulated insulin secretion, while amino acids may have a direct effect on pancreatic beta cells. Fatty Acids 85-96 insulin Homo sapiens 124-131 31445205-2 2019 Given that insulin resistance-related endothelial dysfunction in obesity attributes to fatty-acid-induced reactive oxygen species (ROS) overproduction, in this study, we addressed the possible role of TRPM2 in obesity-related endothelial insulin resistance and the underlying mechanisms. Fatty Acids 87-97 insulin Homo sapiens 11-18 31870728-0 2020 A global perspective on the crosstalk between saturated fatty acids and Toll-like receptor 4 in the etiology of inflammation and insulin resistance. Fatty Acids 46-67 insulin Homo sapiens 129-136 31519735-9 2019 In conclusion, our results reveal mechanisms of control by insulin and beta-adrenergic stimulation - in human adipocytes - that define a network of checks and balances ensuring robust control to secure uninterrupted supply of fatty acids without reaching concentrations that put cellular integrity at risk. Fatty Acids 226-237 insulin Homo sapiens 59-66 31432628-5 2019 RESULTS: SFA interacted with rs12143966, wherein each 1% increase in SFA intake increased insulin by 0.0063 IU mL-1 (SE +- 0.002, p = 0.001) per each major (G) allele copy. Fatty Acids 9-12 insulin Homo sapiens 90-97 31432628-6 2019 rs4925663, interacted with SFA (beta +- SE = -0.0058 +- 0.002, p = 0.004) to increase insulin by 0.0058 IU mL-1 , per additional copy of the major (C) allele. Fatty Acids 27-30 insulin Homo sapiens 86-93 31649547-3 2019 Current research has shown that hepatic fatty acid accumulation can cause hepatic insulin resistance through increased gluconeogenesis, lipogenesis, chronic inflammation, oxidative stress and endoplasmic reticulum stress, and impaired insulin signal pathway. Fatty Acids 40-50 insulin Homo sapiens 82-89 31649547-5 2019 Mitochondrial dysfunction has been shown to be involved in the development of hepatic fatty acid-induced hepatic insulin resistance. Fatty Acids 86-96 insulin Homo sapiens 113-120 31649547-7 2019 Therefore, mitophagy can promote mitochondrial fatty acid oxidation to inhibit hepatic fatty acid accumulation and improve hepatic insulin resistance. Fatty Acids 47-57 insulin Homo sapiens 131-138 31543975-0 2019 Risk of diabetes associated with fatty acids in the de novo lipogenesis pathway is independent of insulin sensitivity and response: the Insulin Resistance Atherosclerosis Study (IRAS). Fatty Acids 33-44 insulin Homo sapiens 136-143 31581129-6 2019 Here we discuss the direct and indirect effects of insulin on intrahepatic processes such as the synthesis of fatty acids and peripherally regulating the flux of fatty acids to the liver; processes that may play a role in the development of insulin resistance and/or IHTAG accumulation in humans. Fatty Acids 110-121 insulin Homo sapiens 51-58 31581129-6 2019 Here we discuss the direct and indirect effects of insulin on intrahepatic processes such as the synthesis of fatty acids and peripherally regulating the flux of fatty acids to the liver; processes that may play a role in the development of insulin resistance and/or IHTAG accumulation in humans. Fatty Acids 162-173 insulin Homo sapiens 51-58 31332276-1 2019 BACKGROUND/OBJECTIVES: Acylcarnitines, intermediates of fatty acid oxidation, are known to be involved in obesity and insulin resistance. Fatty Acids 56-66 insulin Homo sapiens 118-125 30039435-6 2019 RESULTS: Individuals with the highest consumption of saturated fatty acids (SFA) presented the highest rate of progression in PWV, AI and aortic diastolic BP (p < 0.05 for all) after adjustment for age, gender, smoking, body mass index, hyperlipidemia, insulin resistance, changes in systolic BP and treatment with antihypertensive and hypolipidemic drugs. Fatty Acids 53-74 insulin Homo sapiens 253-260 31467335-9 2019 Finally, the unique combination of experimental data and modelling predictions suggested that HFHS feeding was associated with changes in tryptophan metabolism and fatty acid beta-oxidation, which may play an important role in lipid hepatic accumulation and insulin sensitivity. Fatty Acids 164-174 insulin Homo sapiens 258-265 31112997-10 2019 In addition, measures of respiration in response to fatty acids were significantly and positively correlated with both insulin resistance and plasma insulin concentrations. Fatty Acids 52-63 insulin Homo sapiens 119-126 31112997-10 2019 In addition, measures of respiration in response to fatty acids were significantly and positively correlated with both insulin resistance and plasma insulin concentrations. Fatty Acids 52-63 insulin Homo sapiens 149-156 31474943-5 2019 The impact of lipid deposition within insulin responsive tissues such as the liver and skeletal muscle relates to the ability of fatty acid derivates to inhibit elements of the insulin signal transduction pathway. Fatty Acids 129-139 insulin Homo sapiens 38-45 31474943-5 2019 The impact of lipid deposition within insulin responsive tissues such as the liver and skeletal muscle relates to the ability of fatty acid derivates to inhibit elements of the insulin signal transduction pathway. Fatty Acids 129-139 insulin Homo sapiens 177-184 31130874-7 2019 We then review current evidence on nutritional tools, including fatty acids, amino acids, caloric restriction and food bioactive derivatives, which may enhance insulin sensitivity by therapeutically targeting mitochondrial function and biogenesis. Fatty Acids 64-75 insulin Homo sapiens 160-167 31412623-0 2019 Fatty Acid and Lipopolysaccharide Effect on Beta Cells Proteostasis and its Impact on Insulin Secretion. Fatty Acids 0-10 insulin Homo sapiens 86-93 31109791-2 2019 When activated by fatty acids, GPR40 elicits increased insulin secretion from islet beta-cells only in the presence of elevated glucose levels. Fatty Acids 18-29 insulin Homo sapiens 55-62 31073968-1 2019 Increased levels of circulating fatty acids, such as palmitic acid (PA), are associated with the development of obesity, insulin resistance, type-2 diabetes and metabolic syndrome. Fatty Acids 32-43 insulin Homo sapiens 121-128 31214041-5 2019 Moreover in the case of type-2 diabetes, underlying insulin resistance is likely to prevent the canonical substrate switch of the failing heart away from fatty acid oxidation toward increased use of glycolysis. Fatty Acids 154-164 insulin Homo sapiens 52-59 31294084-6 2019 Consuming protein-rich food, avoiding saturated fatty acids and making small changes in eating habits such as eating slowly with longer mastication time can have a positive impact on the GLP-1 secretion and insulin levels. Fatty Acids 38-59 insulin Homo sapiens 207-214 31050161-1 2019 Elevated levels of non-esterified fatty acids (NEFA) play a role in insulin resistance, impaired beta-cell function and they are a denominator of the abnormal atherogenic lipid profile that characterizes obese patients with type 2 diabetes (T2DM). Fatty Acids 34-45 insulin Homo sapiens 68-75 30921636-5 2019 Here, we show that saturated fatty acids are more lipotoxic in SELENON-devoid cells, and blunt the insulin-mediated glucose uptake of SELENON-devoid myotubes by increasing ER stress and mounting a maladaptive ER stress response. Fatty Acids 19-40 insulin Homo sapiens 99-106 31245005-0 2019 Individual free fatty acids have unique associations with inflammatory biomarkers, insulin resistance and insulin secretion in healthy and gestational diabetic pregnant women. Fatty Acids 16-27 insulin Homo sapiens 83-90 31245005-0 2019 Individual free fatty acids have unique associations with inflammatory biomarkers, insulin resistance and insulin secretion in healthy and gestational diabetic pregnant women. Fatty Acids 16-27 insulin Homo sapiens 106-113 30993115-3 2019 Pathologic conditions associated with type 2 diabetes (such as high blood glucose, inflammation, hypoxia, and fatty acids) can alter the quantity and components of ELVs secreted from the pancreas or peripheral insulin-targeting tissues. Fatty Acids 110-121 insulin Homo sapiens 210-217 30970006-0 2019 A lipid-free and insulin-supplemented medium supports De Novo fatty acid synthesis gene activation in melanoma cells. Fatty Acids 62-72 insulin Homo sapiens 17-24 30513311-11 2019 Microarray studies have identified several molecular and cellular candidate processes altered by insulin in obese pregnancies, including cell cycle regulation and fatty acid and cholesterol metabolism. Fatty Acids 163-173 insulin Homo sapiens 97-104 30730834-2 2019 Thus, it seems intuitive that the brain senses elevated amounts of fatty acids (FAs) and affects adaptive metabolic response, which is connected to mitochondrial function and insulin signaling. Fatty Acids 67-78 insulin Homo sapiens 175-182 29594475-9 2019 Total amount of saturated FA (SFA) and specifically palmitic acid, correlated positively with waist circumference (rS = 0.354), triglycerides (rS = 0.400) and fasting insulin (rS = 0.287). Fatty Acids 30-33 insulin Homo sapiens 167-174 30287050-1 2019 BACKGROUND: Serum concentrations of fatty acid binding protein 4, an adipose tissue fatty acid chaperone, have been correlated with insulin resistance and cardiovascular risk factors. Fatty Acids 36-46 insulin Homo sapiens 132-139 30452912-6 2019 Increased fatty acid level by adipose tissue in circulation would translocate into the liver and dysregulates AHR, PXR, PPARgamma, ATGL and Apo B,which further develop insulin resistance and hepatic steatosis condition. Fatty Acids 10-20 insulin Homo sapiens 168-175 30899527-9 2019 Evidence from randomized controlled trials indicated that plant-derived PUFA as an isocaloric replacement for SFA or carbohydrates probably reduces fasting insulin and HOMA-IR in populations without diabetes. Fatty Acids 110-113 insulin Homo sapiens 156-163 29907844-0 2019 Insulin suppression of fatty acid skeletal muscle enzyme activity in postmenopausal women, and improvements in metabolic flexibility and lipoprotein lipase with aerobic exercise and weight loss. Fatty Acids 23-33 insulin Homo sapiens 0-7 30678043-3 2019 It is now clear that circulating fatty acids (FA), which are highly increased in T2D, play a major role in the development of muscle insulin-resistance. Fatty Acids 33-44 insulin Homo sapiens 133-140 30666198-1 2018 Recently, the endogenous fatty acid palmitic acid-5-hydroxystearic acid (5-PAHSA) was found to increase insulin sensitivity and have anti-inflammatory effects in mice with high-fat diet (HFD)-induced diabetes. Fatty Acids 25-35 insulin Homo sapiens 104-111 30666212-1 2018 Fatty acid infiltration of the myocardium, acquired in metabolic disorders (obesity, type-2 diabetes, insulin resistance, and hyperglycemia) is critically associated with the development of lipotoxic cardiomyopathy. Fatty Acids 0-10 insulin Homo sapiens 102-109 30655940-1 2019 GPR40 is a G-protein-coupled receptor which mediates fatty acid-induced glucose-stimulated insulin secretion from pancreatic beta cells and incretion release from enteroendocrine cells of the small intestine. Fatty Acids 53-63 insulin Homo sapiens 91-98 32694809-2 2019 Here we identify a pathway linking the lipolytic enzyme hormone-sensitive lipase (HSL) to insulin action via the glucose-responsive transcription factor ChREBP and its target, the fatty acid elongase ELOVL6. Fatty Acids 180-190 insulin Homo sapiens 90-97 30343320-3 2019 While hepatic simple steatosis seems to be a rather benign manifestation of hepatic triglyceride accumulation, the buildup of highly toxic free fatty acids associated with insulin resistance-induced massive free fatty acid mobilization from adipose tissue and the increased de novo hepatic fatty acid synthesis from glucose acts as the "first hit" for NAFLD development. Fatty Acids 144-154 insulin Homo sapiens 172-179 31984379-2 2019 We hypothesized that saturated fatty acid (SFA) intake, monounsaturated fatty acid (MUFA) and low intake of polyunsaturated fatty acids (PUFA) would be associated with markers of insulin resistance, hyperlipidemia, and hypertriglyceridemia. Fatty Acids 31-41 insulin Homo sapiens 179-186 31666474-2 2019 In skeletal muscle, 3-hydroxy-isobutyrate produced by valine promotes skeletal muscle fatty acid uptake, resulting in the accumulation of incompletely oxidized lipids in skeletal muscle, causing skeletal muscle insulin resistance. Fatty Acids 86-96 insulin Homo sapiens 211-218 31200402-0 2019 [Insulin resistance is an alimentary deficiency of energy substrates (glucose) in the biological reaction of exotrophy and aphysiology compensation by fatty acids via the biological reaction of endothrophy.] Fatty Acids 151-162 insulin Homo sapiens 1-8 29637572-1 2018 Insulin is critical for the regulation of de novo fatty acid synthesis, which converts glucose to lipid in the liver. Fatty Acids 50-60 insulin Homo sapiens 0-7 30262144-0 2018 Cellular fatty acid level regulates the effect of tolylfluanid on mitochondrial dysfunction and insulin sensitivity in C2C12 skeletal myotubes. Fatty Acids 9-19 insulin Homo sapiens 96-103 30262144-12 2018 Our results demonstrate that the effect of 1 ppm TF on mitochondrial function and insulin-dependent protein synthesis in skeletal myotubes was largely dependent upon cellular fatty acid levels. Fatty Acids 175-185 insulin Homo sapiens 82-89 30290216-7 2018 Activation of AMPK inhibits synthesis and induces oxidation of fatty acids, which may reduce ectopic lipid accumulation and improve insulin action. Fatty Acids 63-74 insulin Homo sapiens 132-139 30183308-1 2018 In obese children with high circulating concentrations of free fatty acid palmitate, we have observed that insulin levels at fasting and in response to a glucose challenge were several times higher than in obese children with low concentrations of the fatty acid as well as in lean controls. Fatty Acids 63-73 insulin Homo sapiens 107-114 30178895-6 2018 ABSTRACT: High rates of fatty acid (FA) mobilization from adipose tissue are associated with insulin resistance (IR) in obesity. Fatty Acids 24-34 insulin Homo sapiens 93-100 30344301-1 2018 Cardiac insulin signaling can be impaired due to the altered fatty acid metabolism to induce insulin resistance. Fatty Acids 61-71 insulin Homo sapiens 8-15 29588286-5 2018 Among the 2,086 participants without diabetes, higher levels of plasma ceramides carrying the fatty acids 16:0 (16 carbons, 0 double bond), 18:0, 20:0, or 22:0 were associated with higher plasma insulin and higher HOMA-IR at baseline and at follow-up an average of 5.4 years later. Fatty Acids 94-105 insulin Homo sapiens 195-202 29667734-1 2018 Elevated plasma statured fatty acids (FFAs) cause TLR4/MD2 activation-dependent inflammation and insulin tolerance, which account for the occurrence and development of obesity. Fatty Acids 25-36 insulin Homo sapiens 97-104 30012333-3 2018 Increased lipogenesis with decreased fatty acid beta-oxidation leads to the accumulation of triglycerides in hepatocytes, which, combined with increased levels of reactive oxygen species, contributes to insulin resistance in patients with steatohepatitis. Fatty Acids 37-47 insulin Homo sapiens 203-210 30830367-10 2018 These metabolites, mainly involved in fatty acid metabolism, glycerophospholipid metabolism, alanine, aspartate and glutamate metabolism, are implicated in insulin resistance, vascular remodeling, macrophage activation and oxidised LDL formation. Fatty Acids 38-48 insulin Homo sapiens 156-163 30033101-0 2018 Saturated fatty acids-induced miR-424-5p aggravates insulin resistance via targeting insulin receptor in hepatocytes. Fatty Acids 0-21 insulin Homo sapiens 52-59 30033101-0 2018 Saturated fatty acids-induced miR-424-5p aggravates insulin resistance via targeting insulin receptor in hepatocytes. Fatty Acids 0-21 insulin Homo sapiens 85-92 30033101-1 2018 The excessive intake of saturated fatty acids (SFA) causes obesity and liver steatosis, which are major risk factors for insulin resistance and type 2 diabetes. Fatty Acids 24-45 insulin Homo sapiens 121-128 30033101-1 2018 The excessive intake of saturated fatty acids (SFA) causes obesity and liver steatosis, which are major risk factors for insulin resistance and type 2 diabetes. Fatty Acids 47-50 insulin Homo sapiens 121-128 30033101-2 2018 Although the expression of certain microRNAs (miRNAs) targeting the insulin signaling molecules are regulated aberrantly in SFA-induced obesity, their implications on hepatic insulin resistance are largely unknown. Fatty Acids 124-127 insulin Homo sapiens 68-75 29956790-11 2018 Thus, isomaltulose may have a beneficial effect on insulin resistance through alterations of bile acid and fatty acid metabolisms in NAFLD patients. Fatty Acids 107-117 insulin Homo sapiens 51-58 29277329-2 2018 Evidence indicates that this increased risk is linked to an altered cardiac substrate preference of the insulin resistant heart, which shifts from a balanced utilization of glucose and long-chain fatty acids (FAs) towards an almost complete reliance on FAs as main fuel source. Fatty Acids 209-212 insulin Homo sapiens 104-111 29921789-0 2018 Fatty Acid-Stimulated Insulin Secretion vs. Lipotoxicity. Fatty Acids 0-10 insulin Homo sapiens 22-29 29921789-1 2018 Fatty acid (FA)-stimulated insulin secretion (FASIS) is reviewed here in contrast to type 2 diabetes etiology, resulting from FA overload, oxidative stress, intermediate hyperinsulinemia, and inflammation, all converging into insulin resistance. Fatty Acids 0-10 insulin Homo sapiens 27-34 29607651-9 2018 In HIV-positive persons, lower levels of plasma acylcarnitines, including the C2 product of complete fatty acid oxidation, are a more prominent feature of insulin resistance than changes in BCAA, suggesting impaired fatty acid uptake and/or mitochondrial oxidation is a central aspect of glucose intolerance in this population. Fatty Acids 101-111 insulin Homo sapiens 155-162 29768196-1 2018 Elevated circulating fatty acids (FAs) contribute to obesity-associated metabolic complications, but the mechanisms by which insulin suppresses lipolysis are poorly understood. Fatty Acids 21-32 insulin Homo sapiens 125-132 29768196-1 2018 Elevated circulating fatty acids (FAs) contribute to obesity-associated metabolic complications, but the mechanisms by which insulin suppresses lipolysis are poorly understood. Fatty Acids 34-37 insulin Homo sapiens 125-132 30011790-4 2018 The release of fatty acids from dysfunctional and insulin-resistant adipocytes results in lipotoxicity, which is caused by the ectopic accumulation of triglyceride-derived toxic metabolites and the subsequent activation of inflammatory pathways, cellular dysfunction, and lipoapoptosis. Fatty Acids 15-26 insulin Homo sapiens 50-57 29762376-3 2018 Recent data in humans and in animal models have demonstrated the extensive effects of short-chain fatty acids on whole body energy metabolism, appetite, insulin resistance, fatty acid oxidation, fat accretion, obesity, and diabetes. Fatty Acids 98-108 insulin Homo sapiens 153-160 29277329-2 2018 Evidence indicates that this increased risk is linked to an altered cardiac substrate preference of the insulin resistant heart, which shifts from a balanced utilization of glucose and long-chain fatty acids (FAs) towards an almost complete reliance on FAs as main fuel source. Fatty Acids 253-256 insulin Homo sapiens 104-111 28960312-0 2018 Effects of immediate-release niacin and dietary fatty acids on acute insulin and lipid status in individuals with metabolic syndrome. Fatty Acids 48-59 insulin Homo sapiens 69-76 29735021-12 2018 The observed unfavorable effects on fatty acid metabolism were related to the induction of glucocorticoid-induced insulin resistance. Fatty Acids 36-46 insulin Homo sapiens 114-121 29398050-9 2018 The increase in triglycerides and plasma nonesterified fatty acids stabilized after insulin was started, independent of HbA1c. Fatty Acids 55-66 insulin Homo sapiens 84-91 28541810-11 2018 CONCLUSION: Rectal cancer surgery induced profound insulin resistance, affecting glucose and fatty acid metabolism. Fatty Acids 93-103 insulin Homo sapiens 51-58 29368094-0 2018 Correction to: Tryptophan depletion under conditions that imitate insulin resistance enhances fatty acid oxidation and induces endothelial dysfunction through reactive oxygen species-dependent and independent pathways. Fatty Acids 94-104 insulin Homo sapiens 66-73 29155999-0 2018 High Incomplete Skeletal Muscle Fatty Acid Oxidation Explains Low Muscle Insulin Sensitivity in Poorly Controlled T2D. Fatty Acids 32-42 insulin Homo sapiens 73-80 29439143-3 2018 Fatty acid oversupply to hepatocytes can establish a vicious cycle involving diminished protein folding, endoplasmic reticulum (ER) stress, insulin resistance and further lipogenesis. Fatty Acids 0-10 insulin Homo sapiens 140-147 29290500-1 2018 Increased plasma non-esterified fatty acids (NEFAs) link obesity with insulin resistance and type 2 diabetes mellitus (T2DM). Fatty Acids 32-43 insulin Homo sapiens 70-77 29466985-0 2018 Association between plasma fatty acids and inflammatory markers in patients with and without insulin resistance and in secondary prevention of cardiovascular disease, a cross-sectional study. Fatty Acids 27-38 insulin Homo sapiens 93-100 29466985-11 2018 CONCLUSIONS: Subjects in secondary prevention for cardiovascular disease with insulin resistance have a higher concentration of hs-CRP and IL-6 than individuals without insulin resistance, and these inflammatory biomarkers are positively associated with saturated fatty acids and negatively associated with unsaturated fatty acids. Fatty Acids 254-275 insulin Homo sapiens 78-85 29288757-3 2018 Excessive circulating saturated fatty acids ectopically accumulate in insulin-sensitive tissues and impair insulin action. Fatty Acids 22-43 insulin Homo sapiens 107-114 28986361-3 2018 The development of insulin resistance in cardiac tissue decreases cellular glucose import and enhances mitochondrial fatty acid uptake. Fatty Acids 117-127 insulin Homo sapiens 19-26 27632019-0 2018 The amount and types of fatty acids acutely affect insulin, glycemic and gastrointestinal peptide responses but not satiety in metabolic syndrome subjects. Fatty Acids 24-35 insulin Homo sapiens 51-58 29288757-3 2018 Excessive circulating saturated fatty acids ectopically accumulate in insulin-sensitive tissues and impair insulin action. Fatty Acids 22-43 insulin Homo sapiens 70-77 28867301-3 2018 Peripheral insulin resistance indirectly influences hepatic glucose and lipid metabolism by increasing flux of substrates that promote lipogenesis (glucose and fatty acids) and gluconeogenesis (glycerol and fatty acid-derived acetyl-CoA, an allosteric activator of pyruvate carboxylase). Fatty Acids 160-171 insulin Homo sapiens 11-18 29298881-4 2018 Pathway analysis on the up-regulated gene list untraveled enrichment in multiple signaling pathways including insulin receptor signaling, focal Adhesion, metapathway biotransformation, a number of metabolic pathways e.g. selenium metabolism, Benzo(a)pyrene metabolism, fatty acid, triacylglycerol, ketone body metabolism, tryptophan metabolism, and catalytic cycle of mammalian flavin-containing monooxygenase (FMOs). Fatty Acids 269-279 insulin Homo sapiens 110-117 28867301-3 2018 Peripheral insulin resistance indirectly influences hepatic glucose and lipid metabolism by increasing flux of substrates that promote lipogenesis (glucose and fatty acids) and gluconeogenesis (glycerol and fatty acid-derived acetyl-CoA, an allosteric activator of pyruvate carboxylase). Fatty Acids 160-170 insulin Homo sapiens 11-18 28605158-9 2018 CONCLUSIONS: Liraglutide blunted the SFA-enriched diet-induced peripheral insulin resistance. Fatty Acids 37-40 insulin Homo sapiens 74-81 29381796-0 2018 Substitution of dietary omega-6 polyunsaturated fatty acids for saturated fatty acids decreases LDL apolipoprotein B-100 production rate in men with dyslipidemia associated with insulin resistance: a randomized controlled trial. Fatty Acids 38-59 insulin Homo sapiens 178-185 30550084-26 2018 In the frst place, insulin regulates in vivo metabolism of fatty acids and only in second place metabolism of glucose. Fatty Acids 59-70 insulin Homo sapiens 19-26 29043930-0 2018 Associations Among Fatty Acids, Desaturase and Elongase, and Insulin Resistance in Children. Fatty Acids 19-30 insulin Homo sapiens 61-68 30673191-4 2018 Phylogenetically, in vivo insulin is primarily involved in the metabolism of fatty acids (FA) and only in the second turn in glucose metabolism; regulation of FA metabolism in cells started millions of years earlier than that of glucose metabolism. Fatty Acids 77-88 insulin Homo sapiens 26-33 30702221-9 2018 Hyperlipoproteinemia coincides with insulin resistance yndrome, hyperglycemia and hyperinsulinemia, which is based on blood increase of fatty acids in the form of polar unesterified fatty acids (UFA). Fatty Acids 136-147 insulin Homo sapiens 36-43 30702221-9 2018 Hyperlipoproteinemia coincides with insulin resistance yndrome, hyperglycemia and hyperinsulinemia, which is based on blood increase of fatty acids in the form of polar unesterified fatty acids (UFA). Fatty Acids 182-193 insulin Homo sapiens 36-43 28980402-2 2018 Since this monounsaturated fatty acid is described as a lipokine, studies with cell culture and rodent models have suggested it enhances whole body insulin sensitivity, stimulates insulin secretion by beta cells, increases hepatic fatty acid oxidation, improves the blood lipid profile, and alters macrophage differentiation. Fatty Acids 27-37 insulin Homo sapiens 148-155 30550084-4 2018 The fatty acids are transferred by chylomicrons + lipoproteins of very low density + lipoproteins of low density and non-polar triglycerides are hydrolyzed by hepatic glycerolhydrogenase and co-enzyme apoC-III; according WHO classifcation, hyperlipoproteinemia corresponds to type V. On land, in herbivorous who are not yet synthesized insulin, apoB-48 and chylomicrons left process of non-polar triglycerides transferring. Fatty Acids 4-15 insulin Homo sapiens 336-343 30550084-13 2018 At later stages of phylogenesis insulin formed fatty acids transferring in form of oleic triglycerides in lipoproteins of very low density of the same name without forming of oleic lipoproteins of low density; the electrophoregram of lipoproteins reflects absence of hepatic glycerol hydrogenase. Fatty Acids 47-58 insulin Homo sapiens 32-39 30550084-17 2018 Insulin initiated: a) transferring of oleic fatty acids to lipoproteins of very low density without forming oleic lipoproteins of low density; b) highly effective oleic metabolism of fatty acids in vivo: c) becoming of biological function of locomotion. Fatty Acids 44-55 insulin Homo sapiens 0-7 30785686-8 2018 The formation of an oleic variant of the metabolism of fatty acids under the action of insulin led to the improvement of the energy supply of cells and the high kinetic parameters of many species of herbivorous mammals, including Homo sapiens. Fatty Acids 55-66 insulin Homo sapiens 87-94 28980402-2 2018 Since this monounsaturated fatty acid is described as a lipokine, studies with cell culture and rodent models have suggested it enhances whole body insulin sensitivity, stimulates insulin secretion by beta cells, increases hepatic fatty acid oxidation, improves the blood lipid profile, and alters macrophage differentiation. Fatty Acids 27-37 insulin Homo sapiens 180-187 28724742-0 2017 The Myokine Irisin Is Released in Response to Saturated Fatty Acids and Promotes Pancreatic beta-Cell Survival and Insulin Secretion. Fatty Acids 46-67 insulin Homo sapiens 115-122 29325335-0 2017 [Association between serum adipocyte fatty acid binding protein level and insulin resistance in patients with OSAS]. Fatty Acids 37-47 insulin Homo sapiens 74-81 29159212-1 2017 Dietary fats rich in saturated fatty acid (SFA) increase the risk of metabolic diseases, and certain microRNAs (miRNAs) dysregulated by SFA are associated with the pathogenesis of insulin resistance and type 2 diabetes. Fatty Acids 21-41 insulin Homo sapiens 180-187 28919254-2 2017 In particular, saturated fatty acids such as palmitic acid (PA) have been implicated in the development of insulin resistance in peripheral tissues. Fatty Acids 15-36 insulin Homo sapiens 107-114 28919254-7 2017 This work provides novel evidence of the mechanisms behind saturated fatty acid-induced insulin resistance and its metabolic consequences on neuronal cells. Fatty Acids 59-79 insulin Homo sapiens 88-95 29159212-1 2017 Dietary fats rich in saturated fatty acid (SFA) increase the risk of metabolic diseases, and certain microRNAs (miRNAs) dysregulated by SFA are associated with the pathogenesis of insulin resistance and type 2 diabetes. Fatty Acids 136-139 insulin Homo sapiens 180-187 29023424-2 2017 The loss of insulin sensitivity is generally associated with persistent hyperglycemia (diabetes), hyperinsulinemia, fatty acids and/or lipid dysregulation which are often prevalent under obesity conditions. Fatty Acids 116-127 insulin Homo sapiens 12-19 29124099-1 2017 Diets containing a high saturated fatty acid (SFA) increase the risk of metabolic diseases, and microRNAs (miRNAs) induced by SFA have been implicated in the pathogenesis of insulin resistance and type 2 diabetes. Fatty Acids 24-44 insulin Homo sapiens 174-181 29124099-6 2017 More detailed analysis and understanding of the roles of miR-96 in diet-induced insulin resistance can be found in "Induction of miR-96 by dietary saturated fatty acids exacerbates hepatic insulin resistance through the suppression of INSR and IRS-1" (Yang et al., 2016) [1]. Fatty Acids 147-168 insulin Homo sapiens 80-87 28827061-3 2017 Here, we reveal the importance of reduced MAM formation in the induction of fatty acid-evoked insulin resistance in hepatocytes. Fatty Acids 76-86 insulin Homo sapiens 94-101 28679624-1 2017 Although the rate of fatty acid release from adipose tissue into the systemic circulation is very high in most obese adults, some obese adults maintain relatively low rates of fatty acid release, which helps protect them against the development of systemic insulin resistance. Fatty Acids 176-186 insulin Homo sapiens 257-264 28914811-5 2017 To this end, we tested the hypothesis that leptolide should protect against fatty acid-induced insulin resistance in hepatocytes. Fatty Acids 76-86 insulin Homo sapiens 95-102 28958691-1 2017 BACKGROUND & AIMS: 3-Hydroxyisobutyrate (3-HIB), a catabolic intermediate of the BCAA valine, which stimulates muscle fatty acid uptake, has been implicated in the pathogenesis of insulin resistance. Fatty Acids 122-132 insulin Homo sapiens 184-191 29088862-4 2017 In mitochondria, malonyl-CoA-acyl carrier protein transacylase (MCAT) is the key enzyme of mitochondrial fatty acid synthesis and is estimated to contribute to insulin resistance. Fatty Acids 105-115 insulin Homo sapiens 160-167 28731188-2 2017 Excessive saturated fatty acids are considered to be a major contributing factor to insulin resistance in skeletal muscle cells. Fatty Acids 10-31 insulin Homo sapiens 84-91 32908425-8 2017 KEGG enrichment analysis showed that DEGs were enriched in pyruvate metabolism, glycolysis/gluconeogenesis, fatty acid metabolism, insulin signaling pathway and others. Fatty Acids 108-118 insulin Homo sapiens 131-138 27358332-2 2017 This can be an adaptation to relative abundancy of fatty acid over glucose caused by insulin resistance. Fatty Acids 51-61 insulin Homo sapiens 85-92 31662726-3 2019 Insulin resistance is one of the primary factors contributing to metabolic syndrome (MetS), causing elevated glucose and fatty acid concentrations in the blood. Fatty Acids 121-131 insulin Homo sapiens 0-7 28461124-6 2017 The results showed, that the modulation of PPARgamma, counteracted the insulin-induced altered lipogenesis, evident through a decrease in gene expression of key enzymes responsible for the synthesis of fatty acids, and through a reduction of lipid species synthesis analyzed by Oil/Nile Red staining and GC-MS. PPARgamma modulation also regulated the insulin-induced proliferation, inhibiting the cell cycle progression and p21WAF1/CIP1 (p21) protein reduction. Fatty Acids 202-213 insulin Homo sapiens 71-78 28584168-1 2017 Saturated fatty acids are implicated in the development of insulin resistance, whereas unsaturated fatty acids may have a protective effect on metabolism. Fatty Acids 0-21 insulin Homo sapiens 59-66 28680093-9 2017 We conclude that fatty acids enhance both glucagon and insulin secretion at fasting glucose concentrations and that FFAR1 and enhanced mitochondrial metabolism but not lowered somatostatin secretion are crucial in this effect. Fatty Acids 17-28 insulin Homo sapiens 55-62 28584168-9 2017 Exposure of human myotubes to excess fatty acids increases ROS production and induces insulin resistance. Fatty Acids 37-48 insulin Homo sapiens 86-93 28400405-5 2017 In addition, inflammatory mediators, e.g., proinflammatory cytokines, and excessive nutrients, e.g., glucose and fatty acids, act together to aggravate local insulin resistance and form a vicious cycle to further disturb the local metabolic pathways and exacerbate systemic metabolic dysregulation. Fatty Acids 113-124 insulin Homo sapiens 158-165 28468951-6 2017 Loxl2 up-regulation was not a cell autonomous property of insulin resistant HSCs, but was dependent on microparticles (MPs) released specifically by insulin resistant hepatocytes (HEPs) exposed to fatty acids. Fatty Acids 197-208 insulin Homo sapiens 149-156 28587267-0 2017 Insulin Treatment May Alter Fatty Acid Carriers in Placentas from Gestational Diabetes Subjects. Fatty Acids 28-38 insulin Homo sapiens 0-7 28587267-10 2017 We conclude that insulin promotes the phosphorylation of placental insulin mediators contributing to higher levels of some specific fatty acid carriers in the placenta and fetal adiposity in GDM. Fatty Acids 132-142 insulin Homo sapiens 17-24 28587267-10 2017 We conclude that insulin promotes the phosphorylation of placental insulin mediators contributing to higher levels of some specific fatty acid carriers in the placenta and fetal adiposity in GDM. Fatty Acids 132-142 insulin Homo sapiens 67-74 28045398-5 2017 Increased influx of fatty acids and inflammatory molecules from other tissues, particularly visceral adipose tissue, can also induce muscle inflammation and negatively regulate myocyte metabolism, leading to insulin resistance. Fatty Acids 20-31 insulin Homo sapiens 208-215 28369884-0 2017 The blood-brain barrier and protein-mediated fatty acid uptake: role of the blood-brain barrier as a metabolic barrier: An Editorial Comment for "The blood-brain barrier fatty acid transport protein 1 (FATP1/SLC27A1) supplies docosahexaenoic acid to the brain, and insulin facilitates transport". Fatty Acids 45-55 insulin Homo sapiens 265-272 28115493-5 2017 d-Amino acid substitutions at positions 7(Arg), 15(Lys) and 23(Lys) and fatty acid (l-octanoate) attachment to Lys at position 15 of esculentin-2CHa(1-30) conveyed resistance to plasma enzyme degradation whilst preserving insulin-releasing activity. Fatty Acids 72-82 insulin Homo sapiens 222-229 27530911-1 2017 BACKGROUND: The purpose of this study was to compare acute changes of non-esterified fatty acids (NEFA) in relation to beta cell function (BCF) and insulin resistance in obese patients with type 2 diabetes (T2D) who underwent laparoscopic gastric bypass (GBP), laparoscopic sleeve gastrectomy (SG) or very low calorie diet (VLCD). Fatty Acids 85-96 insulin Homo sapiens 148-155 30615382-7 2017 To synthesize endogenous oleic mono unsaturated fatty acid the late in phylogenesis insulin expresses two enzymes of coupled biochemical reactions: palmitoyl-KoA-elongase andstearyl-KoA-desaturase, activating synthesis of fatty acids following the path glucose-endogenous palmitic unsaturated fatty acid-stearic unsaturated fatty acid-oleic mono unsaturated fatty acid. Fatty Acids 222-233 insulin Homo sapiens 84-91 28100287-0 2017 Characterisation of fatty acid metabolism in different insulin-resistant phenotypes by means of stable isotopes. Fatty Acids 20-30 insulin Homo sapiens 55-62 28955759-1 2017 Adipocyte fatty acid-binding protein (AFABP: FABP4) is a member of the intracellular lipid-binding protein family that is thought to target long-chain fatty acids to nuclear receptors such as peroxisome proliferator-activated receptor gamma (PPARgamma), which in turn plays roles in insulin resistance and obesity. Fatty Acids 10-20 insulin Homo sapiens 283-290 27966196-5 2017 Both human and animal studies have reported a significant increase in circulating free fatty acids and triacylglycerol, increased cardiac reliance on fatty acid oxidation, and subsequent decrease in glucose oxidation which all contributes to insulin resistance and lipotoxicity seen in obesity and diabetes. Fatty Acids 87-97 insulin Homo sapiens 242-249 28340361-1 2017 BACKGROUND AND AIMS: Peripheral insulin resistance is associated with several metabolic abnormalities, including elevated serum fatty acids that contribute to vascular injury and atherogenesis. Fatty Acids 128-139 insulin Homo sapiens 32-39 28161804-0 2017 Tryptophan depletion under conditions that imitate insulin resistance enhances fatty acid oxidation and induces endothelial dysfunction through reactive oxygen species-dependent and independent pathways. Fatty Acids 79-89 insulin Homo sapiens 51-58 28161804-2 2017 Insulin resistance is an independent cardiovascular risk factor and induces endothelial dysfunction by increasing fatty acid oxidation. Fatty Acids 114-124 insulin Homo sapiens 0-7 28161804-11 2017 Thus, TRP depletion, an amino acid whose low levels have been related to worse cardiovascular outcome and to inflammatory atherosclerosis-associated pathologic entities, under conditions that imitate insulin resistance enhances fatty acid oxidation and induces endothelial dysfunction through ROS-dependent and independent pathways. Fatty Acids 228-238 insulin Homo sapiens 200-207 28067391-4 2017 The effects of HF diets on gene expression are mediated by insulin, leptin and nutrients such as fatty acids (FA) and glucose that alter insulin signalling. Fatty Acids 97-108 insulin Homo sapiens 137-144 28933059-1 2017 Adipose tissue is an endocrine organ which is responsible for postprandial uptake of glucose and fatty acids, consequently producing a broad range of adipokines controlling several physiological functions like appetite, insulin sensitivity and secretion, immunity, coagulation, and vascular tone, among others. Fatty Acids 97-108 insulin Homo sapiens 220-227 27627982-0 2016 Altered skeletal muscle fatty acid handling is associated with the degree of insulin resistance in overweight and obese humans. Fatty Acids 24-34 insulin Homo sapiens 77-84 28110332-8 2017 Since treatment with insulin at the end of pregnancy may activate placental nutrient transport to the fetus and promote placental fatty acid transfer, it would be interesting to improve maternal hyperlipidemia control in GDM subjects treated with this hormone. Fatty Acids 130-140 insulin Homo sapiens 21-28 29414963-2 2017 It has now been shown that high levels of free fatty acids, particularly saturated fatty acids, may be associated with insulin resistance in obese patients with type 2 diabetes mellitus. Fatty Acids 73-94 insulin Homo sapiens 119-126 28540308-0 2017 Relationships between Composition of Major Fatty Acids and Fat Distribution and Insulin Resistance in Japanese. Fatty Acids 43-54 insulin Homo sapiens 80-87 30615357-2 2017 The visceral fatty cells of omentum and insulin-depended subcutaneous adipocytes implement simultaneously three reactions: a) biological reaction of exotrophy - absorption of fatty acids in the form of non-polar triglycerides; b) active depositing of fatty acids in non-polar triglycerides and c) releasing of fatty acids in blood plasma only in the form of unesterified fatty acids. Fatty Acids 175-186 insulin Homo sapiens 40-47 30615357-2 2017 The visceral fatty cells of omentum and insulin-depended subcutaneous adipocytes implement simultaneously three reactions: a) biological reaction of exotrophy - absorption of fatty acids in the form of non-polar triglycerides; b) active depositing of fatty acids in non-polar triglycerides and c) releasing of fatty acids in blood plasma only in the form of unesterified fatty acids. Fatty Acids 251-262 insulin Homo sapiens 40-47 30615357-2 2017 The visceral fatty cells of omentum and insulin-depended subcutaneous adipocytes implement simultaneously three reactions: a) biological reaction of exotrophy - absorption of fatty acids in the form of non-polar triglycerides; b) active depositing of fatty acids in non-polar triglycerides and c) releasing of fatty acids in blood plasma only in the form of unesterified fatty acids. Fatty Acids 251-262 insulin Homo sapiens 40-47 30615357-2 2017 The visceral fatty cells of omentum and insulin-depended subcutaneous adipocytes implement simultaneously three reactions: a) biological reaction of exotrophy - absorption of fatty acids in the form of non-polar triglycerides; b) active depositing of fatty acids in non-polar triglycerides and c) releasing of fatty acids in blood plasma only in the form of unesterified fatty acids. Fatty Acids 251-262 insulin Homo sapiens 40-47 30802390-5 2017 The synthesis of fatty acids in phylogenesis millions of years before of glucose, preference of cells to absorb fatty acids instead of glucose; previously in phylogenesis effect of hyperglycemia, glucagon and late function of insulin formed priority of metabolism of fatty acids in energetics of organisms and glucose only in the second instance. Fatty Acids 17-28 insulin Homo sapiens 226-233 30840368-2 2017 The uniformity of biologic effect of exogenous nicotinic acid and endogenous insulin permits to become aware that a) the hypo-lipidemic activity of insulin, inhibition of lipolysis in phylogenetically late insulin-dependent adipocytes and decreasing of content of unesterified fatty acids in blood plasma are considered as a basis of hypoglycemic effect of insulin; b) nicotinic acid similar to insulin blocks lipolysis too but in hormoneindependent visceral fatty cells. Fatty Acids 277-288 insulin Homo sapiens 148-155 30840368-2 2017 The uniformity of biologic effect of exogenous nicotinic acid and endogenous insulin permits to become aware that a) the hypo-lipidemic activity of insulin, inhibition of lipolysis in phylogenetically late insulin-dependent adipocytes and decreasing of content of unesterified fatty acids in blood plasma are considered as a basis of hypoglycemic effect of insulin; b) nicotinic acid similar to insulin blocks lipolysis too but in hormoneindependent visceral fatty cells. Fatty Acids 277-288 insulin Homo sapiens 148-155 30840368-2 2017 The uniformity of biologic effect of exogenous nicotinic acid and endogenous insulin permits to become aware that a) the hypo-lipidemic activity of insulin, inhibition of lipolysis in phylogenetically late insulin-dependent adipocytes and decreasing of content of unesterified fatty acids in blood plasma are considered as a basis of hypoglycemic effect of insulin; b) nicotinic acid similar to insulin blocks lipolysis too but in hormoneindependent visceral fatty cells. Fatty Acids 277-288 insulin Homo sapiens 148-155 30840368-2 2017 The uniformity of biologic effect of exogenous nicotinic acid and endogenous insulin permits to become aware that a) the hypo-lipidemic activity of insulin, inhibition of lipolysis in phylogenetically late insulin-dependent adipocytes and decreasing of content of unesterified fatty acids in blood plasma are considered as a basis of hypoglycemic effect of insulin; b) nicotinic acid similar to insulin blocks lipolysis too but in hormoneindependent visceral fatty cells. Fatty Acids 277-288 insulin Homo sapiens 148-155 27479696-2 2016 High rates of fatty acid beta-oxidation with cardiac insulin resistance represent a cardiac metabolic hallmark of diabetes and obesity, while a marginal decrease in fatty acid oxidation and a prominent decrease in insulin-stimulated glucose oxidation are commonly seen in the early stages of heart failure. Fatty Acids 14-24 insulin Homo sapiens 53-60 27796854-8 2016 One possible explanation involves enhanced metabolism of fatty acid stores in the skeletal muscle by moderate-intensity exercise, which may directly improve insulin sensitivity. Fatty Acids 57-67 insulin Homo sapiens 157-164 28585201-2 2017 However, excessive fatty acid release may worsen adipose tissue inflammation and contributes to insulin resistance. Fatty Acids 19-29 insulin Homo sapiens 96-103 28585204-3 2017 Increased circulating levels of lipids and the metabolic alterations in fatty acid utilization and intracellular signaling, have been related to insulin resistance in muscle and liver. Fatty Acids 72-82 insulin Homo sapiens 145-152 26648072-4 2017 It has been proposed that insulin resistance is, in part, a consequence of impaired signal transduction of insulin caused by several molecules released from adipose tissue that include (adipo)cytokines and fatty acids. Fatty Acids 206-217 insulin Homo sapiens 26-33 26648072-4 2017 It has been proposed that insulin resistance is, in part, a consequence of impaired signal transduction of insulin caused by several molecules released from adipose tissue that include (adipo)cytokines and fatty acids. Fatty Acids 206-217 insulin Homo sapiens 107-114 26648072-5 2017 However, not all fatty acids exert a negative impact on insulin sensitivity. Fatty Acids 17-28 insulin Homo sapiens 56-63 27809652-12 2017 Within all 64 MZ twin pairs, lower insulin sensitivity associated with higher levels of VLDLs, triglycerides, FAs, and isoleucine. Fatty Acids 110-113 insulin Homo sapiens 35-42 30840368-4 2017 The biological role of insulin consists in regulation of metabolism of fatty acids mainly unesterified fatty acids and in absorption of glucose by all insulin-dependent cells. Fatty Acids 71-82 insulin Homo sapiens 23-30 30840368-4 2017 The biological role of insulin consists in regulation of metabolism of fatty acids mainly unesterified fatty acids and in absorption of glucose by all insulin-dependent cells. Fatty Acids 103-114 insulin Homo sapiens 23-30 30856301-9 2017 The main role in development of herbivorous animals belongs to insulin; the hormone regulating in the first-place metabolism of fatty acids, expresses transmutation of all endogenously synthesized from glucose palmitic saturated fatty acid in oleic monosaturated fatty acid. Fatty Acids 128-139 insulin Homo sapiens 63-70 30856301-11 2017 Under effect of insulin in vivo an active oleic type of metabolism of fatty acids is developed; and outside if effect of insulin palmitic type of metabolism of fatty acids is developed. Fatty Acids 70-81 insulin Homo sapiens 16-23 27749056-1 2016 The G protein-coupled receptor 40 (GPR40) also known as free fatty acid receptor 1 (FFAR1) is highly expressed in pancreatic, islet beta-cells and responds to endogenous fatty acids, resulting in amplification of insulin secretion only in the presence of elevated glucose levels. Fatty Acids 170-181 insulin Homo sapiens 213-220 27627982-1 2016 INTRODUCTION/HYPOTHESIS: Disturbances in skeletal muscle fatty acid (FA) handling may contribute to the development and progression of whole-body insulin resistance (IR). Fatty Acids 57-67 insulin Homo sapiens 146-153 27591854-5 2016 At a cellular level, there is evidence that increasing the turnover of cellular substrates such as fatty acids is associated with preventive effects against lipid-induced insulin resistance. Fatty Acids 99-110 insulin Homo sapiens 171-178 27900351-1 2016 Certain microRNAs (miRNAs) targeting the molecules in the insulin signaling cascades are dysregulated by saturated fatty acids (SFA), which can lead to insulin resistance and type 2 diabetes. Fatty Acids 105-126 insulin Homo sapiens 58-65 27900351-1 2016 Certain microRNAs (miRNAs) targeting the molecules in the insulin signaling cascades are dysregulated by saturated fatty acids (SFA), which can lead to insulin resistance and type 2 diabetes. Fatty Acids 105-126 insulin Homo sapiens 152-159 27900351-1 2016 Certain microRNAs (miRNAs) targeting the molecules in the insulin signaling cascades are dysregulated by saturated fatty acids (SFA), which can lead to insulin resistance and type 2 diabetes. Fatty Acids 128-131 insulin Homo sapiens 58-65 27900351-1 2016 Certain microRNAs (miRNAs) targeting the molecules in the insulin signaling cascades are dysregulated by saturated fatty acids (SFA), which can lead to insulin resistance and type 2 diabetes. Fatty Acids 128-131 insulin Homo sapiens 152-159 27892898-0 2016 The role of adipose tissue and excess of fatty acids in the induction of insulin resistance in skeletal muscle. Fatty Acids 41-52 insulin Homo sapiens 73-80 27892898-8 2016 The aim of the present work is to present the current knowledge of the role of adipose tissue and excess of fatty acids in the induction of insulin resistance. Fatty Acids 108-119 insulin Homo sapiens 140-147 27582778-0 2016 Fatty acids stimulate insulin secretion from human pancreatic islets at fasting glucose concentrations via mitochondria-dependent and -independent mechanisms. Fatty Acids 0-11 insulin Homo sapiens 22-29 27733250-0 2016 A human model of dietary saturated fatty acid induced insulin resistance. Fatty Acids 25-45 insulin Homo sapiens 54-61 27733250-3 2016 In the present study we developed and characterized an acute dietary model of saturated fatty acid-enriched diet induced insulin resistance. Fatty Acids 78-98 insulin Homo sapiens 121-128 27733250-11 2016 CONCLUSIONS: A short-term SFA-enriched diet induced whole body insulin resistance in both NGT and IGT subjects. Fatty Acids 26-29 insulin Homo sapiens 63-70 27733250-13 2016 This model offers opportunities for identifying early mechanisms and potential treatments of dietary saturated fat induced insulin resistance. Fatty Acids 101-114 insulin Homo sapiens 123-130 27694528-1 2016 We hypothesized that an increased, incomplete fatty acid beta-oxidation in mitochondria could be part of the metabolic events leading to insulin resistance and thereby an increased type 2 diabetes risk in low birth weight (LBW) compared with normal birth weight (NBW) individuals. Fatty Acids 46-56 insulin Homo sapiens 137-144 27692243-4 2016 In view of current controversies regarding their adequate intakes and effects, this review aims to summarize research regarding this heterogenic group of fatty acids and the mechanisms relating them to (chronic) systemic low-grade inflammation, insulin resistance, metabolic syndrome and notably CVD. Fatty Acids 154-165 insulin Homo sapiens 245-252 27694528-7 2016 This indicates that an increased fatty acid omega-oxidation could be a compensatory mechanism to prevent an accumulation of lipid species that impair insulin signaling. Fatty Acids 33-43 insulin Homo sapiens 150-157 27613089-2 2016 Although microRNAs (miRNAs) participate widely in the pathogenesis of a range of diseases through the suppression of target gene expression at the post-transcriptional level, the implications of SFA-induced miRNAs in the dysregulation of metabolism, particularly in the development of insulin resistance, are largely unclear. Fatty Acids 195-198 insulin Homo sapiens 285-292 27444119-1 2016 Acylcarnitines, fatty acid oxidation (FAO) intermediates, have been implicated in diet-induced insulin resistance and type 2 diabetes mellitus, as increased levels are found in obese insulin resistant humans. Fatty Acids 16-26 insulin Homo sapiens 95-102 27582778-5 2016 The contribution of mitochondrial metabolism to the effects of fatty acid-stimulated insulin secretion was explored. Fatty Acids 63-73 insulin Homo sapiens 85-92 27689005-5 2016 RESULTS: Our data demonstrate perturbed BCAA metabolism and fatty acid oxidation in muscle from insulin resistant humans. Fatty Acids 60-70 insulin Homo sapiens 96-103 27064244-11 2016 CONCLUSION: The rapid accentuated and delayed insulin secretory responses observed in obese children and adolescents, respectively, with high palmitate levels may reflect changes in islet secretory activity and integrity induced by extended exposure to the fatty acid. Fatty Acids 257-267 insulin Homo sapiens 46-53 27112275-1 2016 AIM: Acylcarnitines are fatty acid oxidation (FAO) intermediates, which have been implicated in diet-induced insulin resistance. Fatty Acids 24-34 insulin Homo sapiens 109-116 27311759-1 2016 Fatty acid transport proteins rapidly translocate to the plasma membrane in response to various stimuli, including insulin, influencing lipid uptake into muscle. Fatty Acids 0-10 insulin Homo sapiens 115-122 27382199-1 2016 Elevated plasma triglyceride and non-esterified fatty acid concentrations may cause insulin resistance and type 2 diabetes mellitus. Fatty Acids 48-58 insulin Homo sapiens 84-91 27255710-4 2016 Here, we show that insulin inhibits triglyceride secretion and intestinal microsomal triglyceride transfer protein expression in vivo in healthy mice force-fed monounsaturated fatty acid-rich olive oil but not in mice force-fed saturated fatty acid-rich palm oil. Fatty Acids 166-186 insulin Homo sapiens 19-26 27255710-5 2016 Moreover, when mouse intestine and human Caco-2/TC7 enterocytes were treated with the saturated fatty acid, palmitic acid, the insulin-signaling pathway was impaired. Fatty Acids 86-106 insulin Homo sapiens 127-134 27207513-0 2016 Fasting Plasma Insulin Concentrations Are Associated With Changes in Hepatic Fatty Acid Synthesis and Partitioning Prior to Changes in Liver Fat Content in Healthy Adults. Fatty Acids 77-87 insulin Homo sapiens 15-22 27207513-1 2016 Resistance to the action of insulin affects fatty acid delivery to the liver, fatty acid synthesis and oxidation within the liver, and triglyceride export from the liver. Fatty Acids 44-54 insulin Homo sapiens 28-35 27207513-1 2016 Resistance to the action of insulin affects fatty acid delivery to the liver, fatty acid synthesis and oxidation within the liver, and triglyceride export from the liver. Fatty Acids 78-88 insulin Homo sapiens 28-35 26542285-6 2016 Excessive circulating fatty acids may ectopically accumulate in insulin-sensitive tissues and impair insulin action. Fatty Acids 22-33 insulin Homo sapiens 64-71 26542285-6 2016 Excessive circulating fatty acids may ectopically accumulate in insulin-sensitive tissues and impair insulin action. Fatty Acids 22-33 insulin Homo sapiens 101-108 26542285-8 2016 Finally, excessive fatty acid release may also worsen adipose tissue inflammation, a well-known parameter contributing to insulin resistance. Fatty Acids 19-29 insulin Homo sapiens 122-129 26542285-10 2016 Modulation of fatty acid fluxes and, putatively, of fat cell secretory pattern may explain the amelioration of insulin sensitivity whereas changes in adipose tissue immune response do not seem involved. Fatty Acids 14-24 insulin Homo sapiens 111-118 27100497-5 2016 It is also associated with decreased oxidative phosphorylation and fatty acid oxidation in insulin sensitive tissues. Fatty Acids 67-77 insulin Homo sapiens 91-98 26983645-1 2016 Lots of experimental and clinical evidences indicate that chronic exposure to saturated fatty acids and high level of glucose is implicated in insulin resistance, beta cell failure and ultimately type 2 diabetes. Fatty Acids 78-99 insulin Homo sapiens 143-150 27197730-10 2016 Based on the intermediates observed, insulin resistance in T1D is characterized by an insulin-desensitizing intramyocellular fatty acid metabolite profile that is ameliorated with exercise training. Fatty Acids 125-135 insulin Homo sapiens 37-44 27197730-10 2016 Based on the intermediates observed, insulin resistance in T1D is characterized by an insulin-desensitizing intramyocellular fatty acid metabolite profile that is ameliorated with exercise training. Fatty Acids 125-135 insulin Homo sapiens 86-93 26886198-0 2016 ANT1-mediated fatty acid-induced uncoupling as a target for improving myocellular insulin sensitivity. Fatty Acids 14-24 insulin Homo sapiens 82-89 27128935-5 2016 Inflammatory mediators, such as TNF-alpha and IL-1beta, are induced by saturated fatty acids and disrupt insulin signaling. Fatty Acids 71-92 insulin Homo sapiens 105-112 30586235-1 2016 The insulin regulation of metabolism of fatty acids, number of double binds and cell absorption of glucose]. Fatty Acids 40-51 insulin Homo sapiens 4-11 26912497-3 2016 OBJECTIVE: We determined the association between adipose tissue n-3 FAs (total n-3 FAs, ALA, and EPA plus DHA) and insulin resistance in healthy adults. Fatty Acids 68-71 insulin Homo sapiens 115-122 27104558-4 2016 We therefore hypothesized that insulin augments the sensitivity of hepatocyte to SFA-induced lipotoxicity. Fatty Acids 81-84 insulin Homo sapiens 31-38 27104558-6 2016 Unexpectedly, our results indicated that insulin protected hepatocytes against SFA-induced lipotoxicity, based on the LDH, MTT, and nuclear morphological measurements, and the detection from cleaved-Parp-1 and -caspase-3 expressions. Fatty Acids 79-82 insulin Homo sapiens 41-48 27104558-7 2016 We subsequently clarified that insulin led to a rapid and short-period inhibition of autophagy, which was gradually recovered after 1 h incubation in hepatocytes, and such extent of inhibition was insufficient to aggravate SFA-induced lipotoxicity. Fatty Acids 223-226 insulin Homo sapiens 31-38 27104558-9 2016 Pre-treating hepatocytes with insulin significantly stimulated phosphorylated-Akt and reversed SFA-induced up-regulation of p53. Fatty Acids 95-98 insulin Homo sapiens 30-37 27104558-14 2016 Our study demonstrated that insulin strongly protected against SFA-induced lipotoxicity in hepatocytes mechanistically through alleviating ER stress via a PI3K/Akt/p53 involved pathway but independently from autophagy. Fatty Acids 63-66 insulin Homo sapiens 28-35 30586235-8 2016 The insulin substitutes in vivo ineffective palmitic alternative of metabolism of fatty acids for potentially more effective oleic metabolism of fatty acids. Fatty Acids 82-93 insulin Homo sapiens 4-11 30586235-8 2016 The insulin substitutes in vivo ineffective palmitic alternative of metabolism of fatty acids for potentially more effective oleic metabolism of fatty acids. Fatty Acids 145-156 insulin Homo sapiens 4-11 30586235-9 2016 The insulin increases unsaturation of fatty acids and number of double binds in them. Fatty Acids 38-49 insulin Homo sapiens 4-11 27023786-1 2016 Obesity, in particular abdominal obesity, alters the composition of plasma and tissue fatty acids (FAs), which contributes to inflammation and insulin resistance. Fatty Acids 86-97 insulin Homo sapiens 143-150 27027977-0 2016 Erratum: Adipose tissue fatty acid chain length and mono-unsaturation increases with obesity and insulin resistance. Fatty Acids 24-34 insulin Homo sapiens 97-104 27023786-1 2016 Obesity, in particular abdominal obesity, alters the composition of plasma and tissue fatty acids (FAs), which contributes to inflammation and insulin resistance. Fatty Acids 99-102 insulin Homo sapiens 143-150 26985905-1 2016 Altered skeletal muscle fatty acid (FA) metabolism contributes to insulin resistance. Fatty Acids 24-34 insulin Homo sapiens 66-73 26732686-6 2016 Insulin suppressed available nonesterified fatty acids (P < 0.0001), but fatty acid concentrations were higher in T2DM under both conditions (P < 0.001). Fatty Acids 43-53 insulin Homo sapiens 0-7 26732686-7 2016 Insulin-induced suppression of fatty acid oxidation was seen in both groups (P < 0.0001). Fatty Acids 31-41 insulin Homo sapiens 0-7 26732686-10 2016 Augmented fatty acid oxidation is present under baseline and insulin-treated conditions in T2DM, with impaired insulin-induced shifts away from fatty acid oxidation. Fatty Acids 10-20 insulin Homo sapiens 61-68 26732686-10 2016 Augmented fatty acid oxidation is present under baseline and insulin-treated conditions in T2DM, with impaired insulin-induced shifts away from fatty acid oxidation. Fatty Acids 144-154 insulin Homo sapiens 111-118 27069870-0 2016 Granulocyte colony-stimulating factor (G-CSF): A saturated fatty acid-induced myokine with insulin-desensitizing properties in humans. Fatty Acids 49-69 insulin Homo sapiens 91-98 26706043-5 2016 Significant treatment x time effects were found for postprandial insulin (P = 0.009) and non-esterified fatty acids (P = 0.046) with a significantly lower insulin response for l-rhamnose (P = 0.023) than control. Fatty Acids 104-115 insulin Homo sapiens 155-162 26698173-1 2016 In vivo, ectopic accumulation of fatty acids in muscles leads to alterations in insulin signaling at both the IRS1 and Akt steps. Fatty Acids 33-44 insulin Homo sapiens 80-87 26883301-1 2016 Development of type 2 diabetes mellitus and insulin resistance is associated with a quality of dietary fatty acids such as saturated and unsaturated fatty acids. Fatty Acids 103-114 insulin Homo sapiens 44-51 26394161-9 2016 Liraglutide increased adipose tissue insulin sensitivity enhancing the ability of insulin to suppress lipolysis both globally (-24.9 vs. +54.8pmol/L insulin required to 1/2 maximally suppress serum non-esterified fatty acids; p<0.05), and specifically within subcutaneous adipose tissue (p<0.05). Fatty Acids 213-224 insulin Homo sapiens 82-89 26394161-9 2016 Liraglutide increased adipose tissue insulin sensitivity enhancing the ability of insulin to suppress lipolysis both globally (-24.9 vs. +54.8pmol/L insulin required to 1/2 maximally suppress serum non-esterified fatty acids; p<0.05), and specifically within subcutaneous adipose tissue (p<0.05). Fatty Acids 213-224 insulin Homo sapiens 82-89 26819531-6 2016 Regarding the pathophysiology of NAFLD, this work focuses on the close correlation between insulin resistance and hepatic triglyceride accumulation, highlighting the potential harmful effects of systemic insulin resistance on hepatic metabolism of fatty acids on the one side and the role of lipid intermediates on insulin signalling on the other side. Fatty Acids 248-259 insulin Homo sapiens 91-98 26819531-6 2016 Regarding the pathophysiology of NAFLD, this work focuses on the close correlation between insulin resistance and hepatic triglyceride accumulation, highlighting the potential harmful effects of systemic insulin resistance on hepatic metabolism of fatty acids on the one side and the role of lipid intermediates on insulin signalling on the other side. Fatty Acids 248-259 insulin Homo sapiens 204-211 26819531-6 2016 Regarding the pathophysiology of NAFLD, this work focuses on the close correlation between insulin resistance and hepatic triglyceride accumulation, highlighting the potential harmful effects of systemic insulin resistance on hepatic metabolism of fatty acids on the one side and the role of lipid intermediates on insulin signalling on the other side. Fatty Acids 248-259 insulin Homo sapiens 204-211 27455563-7 2016 Increasing of content of unesterifed fatty acids in blood plasma, as it always occurs in vivo, stops absorption of glucose by cells initiating hyperglycemia, hyperinsulinemia, and syndrome of resistance to insulin. Fatty Acids 37-48 insulin Homo sapiens 163-170 26472664-7 2016 Glucose controls also basal and compensatory beta-cell proliferation and, along with fatty acids, regulates insulin biosynthesis. Fatty Acids 85-96 insulin Homo sapiens 108-115 26755581-1 2016 Obesity, and the associated disturbed glycerolipid/fatty acid (GL/FA) cycle, contribute to insulin resistance, islet beta-cell failure, and type 2 diabetes. Fatty Acids 51-61 insulin Homo sapiens 91-98 26475209-6 2016 The mechanism by which palmitic acid impairs insulin signaling may involve endoplasmic reticulum stress, because this fatty acid induced activation of both PERK, an ER stress marker, and JNK, a kinase associated with insulin resistance. Fatty Acids 118-128 insulin Homo sapiens 45-52 26475209-6 2016 The mechanism by which palmitic acid impairs insulin signaling may involve endoplasmic reticulum stress, because this fatty acid induced activation of both PERK, an ER stress marker, and JNK, a kinase associated with insulin resistance. Fatty Acids 118-128 insulin Homo sapiens 217-224 26447084-5 2016 It has become evident that nutrients such as glucose, fatty acids, and amino acids act upon the hypothalamus together with insulin, affecting HGP. Fatty Acids 54-65 insulin Homo sapiens 123-130 31529902-12 2016 All "metabolic pandemics" such as syndrome of resistance to insulin, atherosclerosis, metabolic arterial hypertension, metabolic syndrome and obesity are primarily pathologies of fatty acids. Fatty Acids 179-190 insulin Homo sapiens 60-67 27919361-2 2016 OBJECTIVE: To assess the chronic effects of the substitution of refined carbohydrate or MUFA for SAFA on insulin secretion and insulin sensitivity in centrally obese subjects. Fatty Acids 97-101 insulin Homo sapiens 105-112 31529916-13 2016 The syndrome of resistance to insulin is, at the first place, pathology of metabolism of fatty acids and only in the second place metabolism of glucose. Fatty Acids 89-100 insulin Homo sapiens 30-37 31529916-2 2016 Inconsistency of Randle cycle, regulation metabolism of fatty acids and glucose by insulin.] Fatty Acids 56-67 insulin Homo sapiens 83-90 31529916-6 2016 The insulin is late activator of absorption by glucose cells in phylogenesis; using induction by substrate, insulin inhibits absorption of fatty acids by cells and specifically activates absorption of glucose by them. Fatty Acids 139-150 insulin Homo sapiens 4-11 31529916-6 2016 The insulin is late activator of absorption by glucose cells in phylogenesis; using induction by substrate, insulin inhibits absorption of fatty acids by cells and specifically activates absorption of glucose by them. Fatty Acids 139-150 insulin Homo sapiens 108-115 31529916-7 2016 The insulin activates absorption of glucose only by insulin-dependent cells by force of decreasing of "bioavailability" of fatty acids. Fatty Acids 123-134 insulin Homo sapiens 4-11 31529916-7 2016 The insulin activates absorption of glucose only by insulin-dependent cells by force of decreasing of "bioavailability" of fatty acids. Fatty Acids 123-134 insulin Homo sapiens 52-59 31529916-9 2016 The insulin, blocking lipolysis in insulin-dependent adipocytes "forces" mitochondria, instead of formation of acetyl-KoA from fatty acids, to produce it from pyruvate at activation of glycolysis and pyruvate-dehydrogenased complex. Fatty Acids 127-138 insulin Homo sapiens 4-11 31529916-9 2016 The insulin, blocking lipolysis in insulin-dependent adipocytes "forces" mitochondria, instead of formation of acetyl-KoA from fatty acids, to produce it from pyruvate at activation of glycolysis and pyruvate-dehydrogenased complex. Fatty Acids 127-138 insulin Homo sapiens 35-42 26545916-0 2016 Involvement of dietary saturated fats, from all sources or of dairy origin only, in insulin resistance and type 2 diabetes. Fatty Acids 23-37 insulin Homo sapiens 84-91 26545916-3 2016 A literature search was performed to identify prospective studies and clinical trials in humans that explored the association between dietary intake of saturated fatty acids and risk of insulin resistance and T2DM. Fatty Acids 152-173 insulin Homo sapiens 186-193 26356502-3 2015 Of particular interest is the intertwined regulation of glucose and non-esterified fatty acids (NEFA), due to the association between disturbed NEFA metabolism and insulin resistance. Fatty Acids 83-94 insulin Homo sapiens 164-171 27397605-3 2016 Insulin exerts diverse effects on cells by targeting distinct functions such as gene expression, fatty acid synthesis, glucose transport and receptor translocation. Fatty Acids 97-107 insulin Homo sapiens 0-7 26546820-2 2015 Insulin secretion is controlled by metabolic stimuli (glucose, fatty acids), but also by monoamine neurotransmitters, like dopamine, serotonin, and norepinephrine. Fatty Acids 63-74 insulin Homo sapiens 0-7 26561628-1 2015 BACKGROUND: Previous data support the benefits of reducing dietary saturated fatty acids (SFAs) on insulin resistance (IR) and other metabolic risk factors. Fatty Acids 67-88 insulin Homo sapiens 99-106 26629522-0 2015 Relationship of Circulating Fatty Acid Profile to Metabolic Disorders Associated with Insulin Resistance. Fatty Acids 28-38 insulin Homo sapiens 86-93 26415887-0 2015 The role of fatty acids in insulin resistance. Fatty Acids 12-23 insulin Homo sapiens 27-34 26415887-2 2015 The underlying cause of insulin appears to be inflammation that can either be increased or decreased by the fatty acid composition of the diet. Fatty Acids 108-118 insulin Homo sapiens 24-31 26415887-4 2015 This review deals with various types of inflammatory inputs mediated by fatty acids, which affect the extent of insulin resistance in various organs. Fatty Acids 72-83 insulin Homo sapiens 112-119 26679101-0 2015 Adipose tissue fatty acid chain length and mono-unsaturation increases with obesity and insulin resistance. Fatty Acids 15-25 insulin Homo sapiens 88-95 26580662-6 2015 The seemingly inevitable progression to overt insulin resistance that characterizes MetS may in part be the consequence of the body"s attempt to cope with NAFLD by driving systemic insulin sensitivity and, thus, fatty acid breakdown. Fatty Acids 212-222 insulin Homo sapiens 46-53 26545114-10 2015 Moreover, saturated fatty acids specifically promote insulin resistance by disturbing the cytoarchitecture of podocytes. Fatty Acids 10-31 insulin Homo sapiens 53-60 26041603-2 2015 A fundamental aim of such therapy is to mimic the pattern of "normal" physiological insulin secretion, thereby controlling basal and meal-time plasma glucose and fatty acid turnover. Fatty Acids 162-172 insulin Homo sapiens 84-91 26179344-1 2015 Disturbances in fatty acid metabolism in adipose tissue, liver, skeletal muscle, gut and pancreas play an important role in the development of insulin resistance, impaired glucose metabolism and type 2 diabetes mellitus. Fatty Acids 16-26 insulin Homo sapiens 143-150 26345110-0 2015 Simvastatin may induce insulin resistance through a novel fatty acid mediated cholesterol independent mechanism. Fatty Acids 58-68 insulin Homo sapiens 23-30 26345110-5 2015 Our data show that simvastatin induces insulin resistance in a cholesterol biosynthesis inhibition independent fashion but does so by a fatty acid mediated effect on insulin signaling pathway. Fatty Acids 136-146 insulin Homo sapiens 166-173 25972572-5 2015 Pathway analysis indicated downshifting of fatty acid oxidation, ketone body production and breakdown, and the tricarboxylic acid cycle, which inversely correlated with adiposity, insulin resistance, and inflammatory cytokines. Fatty Acids 43-53 insulin Homo sapiens 180-187 26108617-10 2015 Nevertheless, recent data indicate that individual lipid species and their degree of fatty acid saturation, particularly membrane and cytosolic C18:2 DAG, specifically activate PKCtheta and induce both acute lipid-induced and chronic insulin resistance in humans. Fatty Acids 85-95 insulin Homo sapiens 234-241 26596041-13 2015 The metabolic syndrome is a pathology of phylogenetically earlier insulin-independent visceral fatty acids. Fatty Acids 95-106 insulin Homo sapiens 66-73 26319827-11 2015 CONCLUSIONS: in patients with DM2 a greater intake of fat and saturated fatty acids it associated with greater fasting glycemia and insulin resistance. Fatty Acids 62-83 insulin Homo sapiens 132-139 30367750-7 2015 The rapid decrease in insulin at the onset of FT1DM likely freed fatty acids derived from triglycerides in peripheral adipocytes into the bloodstream. Fatty Acids 65-76 insulin Homo sapiens 22-29 30367750-12 2015 Learning Points: FT1DM is rare but should be considered in patients with pancreatitis and a decreased level of consciousness.Fatty liver should be considered in patients with FT1DM when liver dysfunction is observed.Insulin is involved in mechanisms that promote fatty liver formation.Pathophysiological changes in fatty acid metabolism may provide clues on lipid metabolism in the early phases of FT1DM. Fatty Acids 315-325 insulin Homo sapiens 216-223 25899581-11 2015 Insulin mediated inhibition of lipolysis was decreased in patients, reflected by increased non-esterified fatty acid levels. Fatty Acids 106-116 insulin Homo sapiens 0-7 26085100-5 2015 The development of hepatic steatosis and insulin resistance in CBA/J mice on a sucrose-enriched diet was paralleled by increased hepatic expression of the transcription factor Ppargamma and its target gene Cd36 whereas that of genes implicated in lipogenesis, fatty acid oxidation, and VLDL secretion was unaltered. Fatty Acids 260-270 insulin Homo sapiens 41-48 26039731-8 2015 The present study therefore suggested that BCG administration suppressed development of nonalcoholic fatty liver disease, at least partly, by alleviating fatty acid-induced insulin resistance in the liver. Fatty Acids 154-164 insulin Homo sapiens 173-180 26243517-1 2015 Increased accumulation and/or impaired utilization of fatty acid in extra-adipose tissues are implicated in the pathogenesis of insulin resistance and type 2 diabetes. Fatty Acids 54-64 insulin Homo sapiens 128-135 26273324-1 2015 BACKGROUND: Evidence from several recent metabolomic studies suggests that increased concentrations of triacylglycerols with shorter (14-16 carbon atoms), saturated fatty acids are associated with insulin resistance and the risk of type 2 diabetes. Fatty Acids 155-176 insulin Homo sapiens 197-204 26085904-2 2015 The first hit is represented by the action of hyperinsulinemia and insulin resistance, accompanying obesity, that leads to liver steatosis increasing the absolute non esterified fatty acids uptake in the liver and the esterification to form triacylglycerol. Fatty Acids 178-189 insulin Homo sapiens 51-58 25921849-0 2015 Endothelial function and insulin sensitivity during acute non-esterified fatty acid elevation: Effects of fat composition and gender. Fatty Acids 73-83 insulin Homo sapiens 25-32 25921849-1 2015 BACKGROUND AND AIMS: We have reported that adverse effects on flow-mediated dilation of an acute elevation of non-esterified fatty acids rich in saturated fat (SFA) are reversed following addition of long-chain (LC) n-3 polyunsaturated fatty acids (PUFA), and hypothesised that these effects may be mediated through alterations in insulin signalling pathways. Fatty Acids 125-136 insulin Homo sapiens 331-338 25921849-1 2015 BACKGROUND AND AIMS: We have reported that adverse effects on flow-mediated dilation of an acute elevation of non-esterified fatty acids rich in saturated fat (SFA) are reversed following addition of long-chain (LC) n-3 polyunsaturated fatty acids (PUFA), and hypothesised that these effects may be mediated through alterations in insulin signalling pathways. Fatty Acids 145-158 insulin Homo sapiens 331-338 25367746-8 2015 Saturated fatty acids can be regarded as the most detrimental of FFA, being capable of inducing insulin resistance and inflammation through lipid mediators such as ceramide, which can increase risk of developing atherosclerosis. Fatty Acids 0-21 insulin Homo sapiens 96-103 25964336-7 2015 Interestingly, large-scale expression data, target analysis, and metabolic flux assays suggest this let-7-driven CM maturation could be a result of down-regulation of the phosphoinositide 3 kinase (PI3K)/AKT protein kinase/insulin pathway and an up-regulation of fatty acid metabolism. Fatty Acids 263-273 insulin Homo sapiens 223-230 25439266-4 2015 Compared to baseline concentrations (at 0 min), insulin infusion decreased (P < 0.05) plasma concentrations of glucagon, non-esterified fatty acids (NEFA), lactate, nonessential amino acids (NEAA), branched-chain amino acids (BCAA), total amino acids (TAA) and urea nitrogen (UN). Fatty Acids 139-150 insulin Homo sapiens 48-55 25367746-9 2015 Elevated FFA, in particular saturated fatty acids, maybe a driving factor for both the increased insulin resistance, cardiovascular disease risk and inflammation in older adults. Fatty Acids 28-49 insulin Homo sapiens 97-104 25733449-5 2015 Mutations in GLUD1 and HADH lead to leucine-induced HH, and these two genes encode the key enzymes glutamate dehydrogenase and short chain 3-hydroxyacyl-CoA dehydrogenase which play a key role in amino acid and fatty acid regulation of insulin secretion respectively. Fatty Acids 211-221 insulin Homo sapiens 236-243 25702040-2 2015 Elevation of circulating non-esterified (i.e. free) fatty acid (NEFA) concentrations can lead to insulin resistance and plays a central role in the development of metabolic diseases. Fatty Acids 52-62 insulin Homo sapiens 97-104 25793412-0 2015 Lipid mixtures containing a very high proportion of saturated fatty acids only modestly impair insulin signaling in cultured muscle cells. Fatty Acids 52-73 insulin Homo sapiens 95-102 25793412-4 2015 In contrast, the fatty acid mixtures only modestly impaired insulin-stimulated pAktThr308M/Akt, and we found no differences between NORM and HSFA. Fatty Acids 17-27 insulin Homo sapiens 60-67 25601634-7 2015 We hypothesize that lipid metabolism alterations in subjects with the PROX1 CC genotype may be a primary cause of higher glucose levels after glucose load, since the fatty acids can inhibit insulin-stimulated glucose uptake by decreasing carbohydrate oxidation. Fatty Acids 166-177 insulin Homo sapiens 190-197 25793412-6 2015 Therefore, the robust impairment in insulin signaling found with palmitate exposure was attenuated with physiologic mixtures of fatty acids, even with a very high proportion of saturated fatty acids. Fatty Acids 128-139 insulin Homo sapiens 36-43 25793412-6 2015 Therefore, the robust impairment in insulin signaling found with palmitate exposure was attenuated with physiologic mixtures of fatty acids, even with a very high proportion of saturated fatty acids. Fatty Acids 177-198 insulin Homo sapiens 36-43 25758824-8 2015 Several significant pathways relate to metabolizing sugars and fatty acids; others relate to insulin signaling. Fatty Acids 63-74 insulin Homo sapiens 93-100 25441706-2 2015 Dietary macronutrient composition has been examined in a number of articles, and diets enriched in saturated fatty acids, and possibly in fructose, appear to be most consistently associated with the development of insulin resistance. Fatty Acids 99-120 insulin Homo sapiens 214-221 25459884-6 2015 Similarly, the maternal intake of saturated fatty acids seems to trigger alterations in the liver and adipose tissue function associated with insulin resistance and diabetes. Fatty Acids 34-55 insulin Homo sapiens 142-149 25486510-6 2015 These regulations may participate in the fatty acid-related pathophysiology of insulin resistance. Fatty Acids 41-51 insulin Homo sapiens 79-86 25445050-1 2015 Elevated fatty acid levels play a pathogenic role in the development of insulin resistance, associated with type 2 diabetes. Fatty Acids 9-19 insulin Homo sapiens 72-79 25281561-21 2015 It was found that the body fat level was low in AS due to high fatty acid oxidation, suggesting that insulin signaling may play an important role in the metabolic switch from predominant to fatty acid metabolism that characterizes the ligament of AS. Fatty Acids 63-73 insulin Homo sapiens 101-108 25281561-21 2015 It was found that the body fat level was low in AS due to high fatty acid oxidation, suggesting that insulin signaling may play an important role in the metabolic switch from predominant to fatty acid metabolism that characterizes the ligament of AS. Fatty Acids 190-200 insulin Homo sapiens 101-108 25445050-2 2015 Interventions with ability to ameliorate fatty acid-induced insulin resistance might be useful for the management of diabetes. Fatty Acids 41-51 insulin Homo sapiens 60-67 26663182-23 2015 Defects in mitochondrial function, namely related to oxidation of fatty acids, have been linked to diet-induced obesity and the development of insulin resistance in adipose tissue and skeletal muscle. Fatty Acids 66-77 insulin Homo sapiens 143-150 25565210-3 2015 Beta-cell lines expressing this construct cosecrete luciferase and insulin in close correlation, under both standard conditions or when stressed by cytokines, fatty acids, or ER toxins. Fatty Acids 159-170 insulin Homo sapiens 67-74 25814122-2 2015 Excess circulating fatty acids (FAs), which characterize obesity, induce insulin resistance, steatosis, beta cells dysfunction and apoptosis. Fatty Acids 32-35 insulin Homo sapiens 73-80 25874297-5 2015 Under insulin resistance secretion of insulin increases up to 8 times and decreasing of content of fatty acids is less expressed. Fatty Acids 99-110 insulin Homo sapiens 6-13 24785103-0 2015 Relatively low endogenous fatty acid mobilization and uptake helps preserve insulin sensitivity in obese women. Fatty Acids 26-36 insulin Homo sapiens 76-83 24785103-2 2015 OBJECTIVES: The primary aim of this study was to determine whether alterations in fatty acid mobilization and uptake underlie differences in insulin sensitivity (Si) among a seemingly homogeneous cohort of obese women. Fatty Acids 82-92 insulin Homo sapiens 141-148 24785103-10 2015 CONCLUSION: These findings suggest that obese women who maintain a relatively low rate of endogenous fatty acid uptake may be somewhat "protected" against the development of insulin resistance potentially by less activation of inflammatory pathways within skeletal muscle. Fatty Acids 101-111 insulin Homo sapiens 174-181 25342132-1 2015 Insulin resistance may be linked to incomplete fatty acid beta-oxidation and the subsequent increase in acylcarnitine species in different tissues including skeletal muscle. Fatty Acids 47-57 insulin Homo sapiens 0-7 25874297-3 2015 In patients with different resistance to insulin content of non-etherized fatty acids decreased approximatively up to 3 times. Fatty Acids 74-85 insulin Homo sapiens 41-48 25874297-5 2015 Under insulin resistance secretion of insulin increases up to 8 times and decreasing of content of fatty acids is less expressed. Fatty Acids 99-110 insulin Homo sapiens 38-45 24752559-0 2014 Clustering effects on postprandial insulin secretion and sensitivity in response to meals with different fatty acid compositions. Fatty Acids 105-115 insulin Homo sapiens 35-42 25195818-1 2014 Lipotoxicity resulting from a high concentration of saturated fatty acids is closely linked to development of insulin resistance, as well as apoptosis in skeletal muscle. Fatty Acids 52-73 insulin Homo sapiens 110-117 25364776-3 2014 Insulin resistance resulting from high fat diet is associated with skeletal muscle mitochondrial dysfunction, leading to alterations in lipid accumulation and specific species of intracellular fatty acids; whereas, exercise training augments insulin resistance while improving skeletal muscle mitochondrial function and producing beneficial fatty acid profiles. Fatty Acids 193-204 insulin Homo sapiens 0-7 25364776-3 2014 Insulin resistance resulting from high fat diet is associated with skeletal muscle mitochondrial dysfunction, leading to alterations in lipid accumulation and specific species of intracellular fatty acids; whereas, exercise training augments insulin resistance while improving skeletal muscle mitochondrial function and producing beneficial fatty acid profiles. Fatty Acids 193-203 insulin Homo sapiens 0-7 25172378-0 2014 High saturated fatty acid intake induces insulin secretion by elevating gastric inhibitory polypeptide levels in healthy individuals. Fatty Acids 5-25 insulin Homo sapiens 41-48 25172378-12 2014 These results suggest that a high saturated fatty acid content stimulates postprandial insulin release via increased GIP secretion. Fatty Acids 34-54 insulin Homo sapiens 87-94 25262585-0 2014 Associations between erythrocyte membrane fatty acid compositions and insulin resistance in obese adolescents. Fatty Acids 42-52 insulin Homo sapiens 70-77 25262585-1 2014 BACKGROUND/OBJECTIVE: Cytokines released from the adipose tissue and fatty acids (FAs) derived from lipolysis or uptake of fats go in to competition with glucose to be uptaken from the liver leads to insulin resistance (IR). Fatty Acids 69-80 insulin Homo sapiens 200-207 25262585-1 2014 BACKGROUND/OBJECTIVE: Cytokines released from the adipose tissue and fatty acids (FAs) derived from lipolysis or uptake of fats go in to competition with glucose to be uptaken from the liver leads to insulin resistance (IR). Fatty Acids 82-85 insulin Homo sapiens 200-207 25519064-5 2014 Accumulation of fatty acids in a cell and resulting lipotoxicity include resistance to insulin and leptin, endoplasmic reticulum stress, uncoupling of oxidation and phosphorylation, and dysfunction of biological membranes. Fatty Acids 16-27 insulin Homo sapiens 87-94 25884071-8 2014 The higher number of double bonds is in the pool of unesterified fatty acids the more active is the effect of insulin. Fatty Acids 65-76 insulin Homo sapiens 110-117 25884071-10 2014 According the phylogenetic theory of general pathology, the effect of insulin on metabolism of glucose is mediated by fatty acids. Fatty Acids 118-129 insulin Homo sapiens 70-77 25884071-12 2014 The insulin is depriving all cells of possibility to absorb unesterified fatty acids and "forces" them to absorb glucose increasing hereby number of GLUT4 on cell membrane. Fatty Acids 73-84 insulin Homo sapiens 4-11 25884071-13 2014 The resistance to insulin is manifested in high concentration of unesterfied fatty acids, hyperinsulinemia, hyperalbuminemia and increasing of concentration of C-reactive protein-monomer. Fatty Acids 77-88 insulin Homo sapiens 18-25 25335398-9 2014 The specialized adipocytes with receptors to insulin and glucose transporter type 4 are the cells of subcutaneous depot of fatty acids. Fatty Acids 123-134 insulin Homo sapiens 45-52 24821967-1 2014 The SLC13 transporter family, whose members play key physiological roles in the regulation of fatty acid synthesis, adiposity, insulin resistance, and other processes, catalyzes the transport of Krebs cycle intermediates and sulfate across the plasma membrane of mammalian cells. Fatty Acids 94-104 insulin Homo sapiens 127-134 24700885-2 2014 Although inhibition of fatty acid oxidation has been proposed as a novel approach to treat ischemic heart disease and heart failure, reduced muscle fatty acid oxidation rates may contribute to the development of obesity-associated insulin resistance. Fatty Acids 148-158 insulin Homo sapiens 231-238 24962347-1 2014 BACKGROUND: Elevated fatty acids contribute to the development of type 2 diabetes and affect skeletal muscle insulin sensitivity. Fatty Acids 21-32 insulin Homo sapiens 109-116 24703492-1 2014 The worldwide prevalence of diabetes type 2 is increasing and intramuscular accumulation of fatty acid metabolites is gradually becoming recognized as core features of this condition as lipotoxicity induces insulin resistance. Fatty Acids 92-102 insulin Homo sapiens 207-214 24641631-9 2014 Phosphorylation sites detected more often or exclusively in insulin-stimulated samples include multiple sites in mitochondrial proteins involved in oxidative phosphorylation, tricarboxylic acid cycle, and fatty acid metabolism, as well as several components of the newly defined mitochondrial inner membrane organizing system (MINOS). Fatty Acids 205-215 insulin Homo sapiens 60-67 24892004-3 2014 Fatty acid induced synthesis of ceramide is considered to be one of the major causes for insulin resistance. Fatty Acids 0-10 insulin Homo sapiens 89-96 24892004-11 2014 CONCLUSION: In this study, we provide evidences that inhibition of nSMase can protect skeletal muscles from saturated fatty acid induced insulin resistance, metabolic dysfunction, cellular stress and inflammation. Fatty Acids 108-128 insulin Homo sapiens 137-144 25080793-10 2014 It is assumed that under post-prandial hyperglycemia insulin regulates metabolism of fatty acids, blocks lipolysis, decreases in cytosol of cells content of oleic and palmitic fatty acids inform of acetyl-KoA and forces mitochondrions intensively oxidate acetyl-KoA formed from pyruvate, from GLU. Fatty Acids 85-96 insulin Homo sapiens 53-60 24353137-8 2014 Total fatty acids and unsaturated fatty acids such as oleic acid and linoleic acid showed an inverse significant correlation with insulin resistance. Fatty Acids 6-17 insulin Homo sapiens 130-137 24591340-13 2014 Reduced insulin suppression of subcutaneous adipocyte lipolysis may increase the burden of plasma fatty acids that the mother has to process in preeclampsia. Fatty Acids 98-109 insulin Homo sapiens 8-15 25080793-12 2014 Hypoglycemic effect of insulin is mediated by regulation first of all of metabolism of fatty acids. Fatty Acids 87-98 insulin Homo sapiens 23-30 25080798-0 2014 [Insulin: initiation of pool of insulin-dependent cells, targeted transfer of triglycerides and increase of kinetic parameters of oxidation of fatty acids]. Fatty Acids 143-154 insulin Homo sapiens 1-8 25080798-3 2014 These occurrences confirm that syndrome of insulin resistance primarily is the pathology of metabolism of fatty acids and only secondary the pathology metabolism of glucose. Fatty Acids 106-117 insulin Homo sapiens 43-50 24632852-1 2014 AIMS/HYPOTHESIS: Reduced skeletal muscle insulin sensitivity is a feature associated with sustained exposure to excess saturated fatty acids (SFA), whereas mono and polyunsaturated fatty acids (MUFA and PUFA) not only improve insulin sensitivity but blunt SFA-induced insulin resistance. Fatty Acids 256-259 insulin Homo sapiens 41-48 24315620-5 2014 Modern research approaches have helped to establish the important role that hexoses, aminoacids, and fatty acids have in insulin resistance and beta-cell dysfunction, and the potential role of changes in the microbiome. Fatty Acids 101-112 insulin Homo sapiens 121-128 24632852-1 2014 AIMS/HYPOTHESIS: Reduced skeletal muscle insulin sensitivity is a feature associated with sustained exposure to excess saturated fatty acids (SFA), whereas mono and polyunsaturated fatty acids (MUFA and PUFA) not only improve insulin sensitivity but blunt SFA-induced insulin resistance. Fatty Acids 119-140 insulin Homo sapiens 41-48 24310562-0 2014 Reduction of non-esterified fatty acids improves insulin sensitivity and lowers oxidative stress, but fails to restore oxidative capacity in type 2 diabetes: a randomised clinical trial. Fatty Acids 28-39 insulin Homo sapiens 49-56 24632852-1 2014 AIMS/HYPOTHESIS: Reduced skeletal muscle insulin sensitivity is a feature associated with sustained exposure to excess saturated fatty acids (SFA), whereas mono and polyunsaturated fatty acids (MUFA and PUFA) not only improve insulin sensitivity but blunt SFA-induced insulin resistance. Fatty Acids 142-145 insulin Homo sapiens 41-48 24323910-4 2014 This review summarises the evidence for these mechanisms in the context of excess dietary FAs generating insulin resistance in muscle, the major tissue involved in insulin-stimulated disposal of blood glucose. Fatty Acids 90-93 insulin Homo sapiens 105-112 24378016-0 2014 Treatment with omega-3 fatty acid ethyl-ester alters fatty acid composition of lipoproteins in overweight or obese adults with insulin resistance. Fatty Acids 23-33 insulin Homo sapiens 127-134 24323910-4 2014 This review summarises the evidence for these mechanisms in the context of excess dietary FAs generating insulin resistance in muscle, the major tissue involved in insulin-stimulated disposal of blood glucose. Fatty Acids 90-93 insulin Homo sapiens 164-171 24323910-5 2014 It also outlines potential problems with models and measurements that may hinder as well as help improve our understanding of the links between FAs and insulin action. Fatty Acids 144-147 insulin Homo sapiens 152-159 24153346-2 2014 OBJECTIVE: We determined whether certain phospholipid species and fatty acids that are associated with full-fat dairy consumption may also be linked to diminished insulin resistance. Fatty Acids 66-77 insulin Homo sapiens 163-170 24262853-4 2014 Stimulation of mitochondrial oxidative metabolism by mild dissipation of the mitochondrial potential is thought to increase fatty acid utilization and thereby prevent insulin resistance. Fatty Acids 124-134 insulin Homo sapiens 167-174 24977487-4 2014 Numerous studies in humans and rodents have shown that insulin resistance is associated with elevations of non-esterified fatty acids (NEFA) in the plasma. Fatty Acids 122-133 insulin Homo sapiens 55-62 24211519-0 2014 Role of NADPH oxidase-4 in saturated fatty acid-induced insulin resistance in SK-Hep-1 cells. Fatty Acids 27-47 insulin Homo sapiens 56-63 24211519-2 2014 The results showed that Akt phosphorylation was increased in SK-Hep-1 cells treated with insulin in a time- and concentration-dependent manner, which was inhibited by saturated fatty acids, but not by unsaturated fatty acids. Fatty Acids 167-188 insulin Homo sapiens 89-96 24320032-8 2014 The appearance of NAFLD is mainly dependent on increased flow of fatty acids derived from an excess of lipolysis from insulin-resistant adipose tissue. Fatty Acids 65-76 insulin Homo sapiens 118-125 25371775-6 2014 Decreased ETC function combined with increased rates of fatty acid beta-oxidation leads to the accumulation of incomplete products of beta-oxidation, which combined with increased levels of ROS contribute to insulin resistance. Fatty Acids 56-66 insulin Homo sapiens 208-215 25428743-1 2014 Dietary composition and metabolism of fatty acids (FA) influence insulin resistance, atherogenic dyslipidemia and other components of the metabolic syndrome (MS). Fatty Acids 38-49 insulin Homo sapiens 65-72 23820633-0 2013 Fatty acids differentially regulate insulin resistance through endoplasm reticulum stress-mediated induction of tribbles homologue 3: a potential link between dietary fat composition and the pathophysiological outcomes of obesity. Fatty Acids 0-11 insulin Homo sapiens 36-43 24278393-7 2013 RESULTS: A close linear relationship between acute and chronic changes could be demonstrated for insulin concentration (p=0.001; r=0.83), the fasting indicator of insulin sensitivity HOMA-IR (p<0.001; r=0.78) and non-esterified fatty acid concentration (p=0.001; r=0.88). Fatty Acids 231-241 insulin Homo sapiens 97-104 24064340-1 2013 The development of insulin resistance has been associated with impaired mitochondrial fatty acid oxidation (FAO), but the exact relationship between FAO capacity and glucose metabolism continues to be debated. Fatty Acids 86-96 insulin Homo sapiens 19-26 24640105-6 2013 Insulin through expressing stearil-coenzymeA-desaturase 2 transforms energetically non-optimal palmitinic variation of metabolism of substrates into highly effective oleic variation for cells" groundwork of energy (saturated fatty acid and mono fatty acid). Fatty Acids 215-235 insulin Homo sapiens 0-7 23792672-0 2013 Redox regulation of insulin sensitivity due to enhanced fatty acid utilization in the mitochondria. Fatty Acids 56-66 insulin Homo sapiens 20-27 23792672-3 2013 Paradoxically, regulatory mechanisms that promote utilization of fatty acids appear to initiate diet-induced insulin insensitivity. Fatty Acids 65-76 insulin Homo sapiens 109-116 23792672-6 2013 However, with prolonged consumption of high dietary fat and ensuing obesity, the near exclusive dependence on fatty acid oxidation for production of energy by the mitochondria drives insulin resistance, diabetes, and cardiovascular disease. Fatty Acids 110-120 insulin Homo sapiens 183-190 23757424-9 2013 Importantly, the change in fatty acid uptake after exercise compared with CON was negatively correlated with the change in insulin sensitivity for all trials (r = -0.60, P = 0.003). Fatty Acids 27-37 insulin Homo sapiens 123-130 23989724-1 2013 AIMS/HYPOTHESIS: An accumulation of ceramides has been implicated in the generation of insulin resistance in skeletal muscle upon an oversupply of fatty acid. Fatty Acids 147-157 insulin Homo sapiens 87-94 23989724-9 2013 The fatty acid also inhibited insulin-stimulated Akt phosphorylation and glycogen synthesis. Fatty Acids 4-14 insulin Homo sapiens 30-37 23954331-6 2013 The inability of AT to expand further to store excess nutrients, rather than obesity per se, induces a diabetogenic milieu by promoting the overflow and the ectopic deposition of fatty acids in insulin-dependent organs (i.e., lipotoxicity), the secretion of various metabolically detrimental adipose-derived hormones (i.e., adipokines and lipokines), and the occurrence of local and systemic inflammation and oxidative stress. Fatty Acids 179-190 insulin Homo sapiens 194-201 23756914-5 2013 The results showed that (a) the serum insulin level measured at the time of hypoglycaemia had no correlation with the severity of hypoglycaemia, (b) the serum insulin level was undetectable despite severe hypoglycaemia in a significant proportion of patients, (c) there was no correlation between the birth weight and the insulin level at the time of hypoglycaemia, (d) the suppression of ketogenesis was more marked than that of the non-esterified fatty acids. Fatty Acids 449-460 insulin Homo sapiens 159-166 23756914-5 2013 The results showed that (a) the serum insulin level measured at the time of hypoglycaemia had no correlation with the severity of hypoglycaemia, (b) the serum insulin level was undetectable despite severe hypoglycaemia in a significant proportion of patients, (c) there was no correlation between the birth weight and the insulin level at the time of hypoglycaemia, (d) the suppression of ketogenesis was more marked than that of the non-esterified fatty acids. Fatty Acids 449-460 insulin Homo sapiens 159-166 23512750-1 2013 OBJECTIVE: The link between a reduced capacity for skeletal muscle mitochondrial fatty acid oxidation (FAO) and lipotoxicity in human insulin resistance has been the subject of intense debate. Fatty Acids 81-91 insulin Homo sapiens 134-141 23643711-12 2013 The catalase overexpression improved mitochondrial respiration protecting the cells from fatty acid-induced, insulin resistance. Fatty Acids 89-99 insulin Homo sapiens 109-116 23643711-13 2013 This effect indicates that control of hydrogen peroxide production regulates the mitochondrial respiration preventing the insulin resistance in skeletal muscle cells by a mechanism associated with CREB phosphorylation and beta-oxidation of fatty acids. Fatty Acids 240-251 insulin Homo sapiens 122-129 23979843-7 2013 Fatty acid-induced ER enlargement was associated with proinsulin retention in the ER, together with increased proinsulin/insulin ratio. Fatty Acids 0-10 insulin Homo sapiens 54-64 23979843-7 2013 Fatty acid-induced ER enlargement was associated with proinsulin retention in the ER, together with increased proinsulin/insulin ratio. Fatty Acids 0-10 insulin Homo sapiens 110-120 23979843-7 2013 Fatty acid-induced ER enlargement was associated with proinsulin retention in the ER, together with increased proinsulin/insulin ratio. Fatty Acids 0-10 insulin Homo sapiens 57-64 27335827-3 2013 Insulin regulates metabolism, at least in part, via the control of the expression of the hepatic genes involved in glucose and fatty acid metabolism. Fatty Acids 127-137 insulin Homo sapiens 0-7 27335827-10 2013 This paper also summarizes the effects of VA status and RA treatments on the glucose and lipid metabolism in vivo and the effects of retinoid treatments on the expression of insulin-regulated genes involved in the glucose and fatty acid metabolism in the primary hepatocytes. Fatty Acids 226-236 insulin Homo sapiens 174-181 23774280-10 2013 Physical activity partially protects myocytes from fatty acid-induced insulin resistance and inactivity is associated with dysregulation of metabolism in satellite cells challenged with palmitate. Fatty Acids 51-61 insulin Homo sapiens 70-77 23535137-1 2013 Circulating NEFAs (non-esterified fatty acids) from adipose tissue lipolysis lead to endothelial dysfunction and insulin resistance in patients with the metabolic syndrome or Type 2 diabetes mellitus. Fatty Acids 34-45 insulin Homo sapiens 113-120 23820633-1 2013 AIMS/HYPOTHESIS: Previous studies have shown that saturated fatty acids cause insulin resistance (IR) that is prevented by unsaturated fatty acids. Fatty Acids 50-71 insulin Homo sapiens 78-85 23743348-0 2013 Fatty acid transport proteins chronically relocate to the transverse-tubules in muscle from obese Zucker rats but are resistant to further insulin-induced translocation. Fatty Acids 0-10 insulin Homo sapiens 139-146 23807942-1 2013 Insulin degludec is, like insulin detemir, a product of coupling of Des-B30 threonine insulin to fatty acid side chains. Fatty Acids 97-107 insulin Homo sapiens 0-7 23562819-10 2013 We suggest a regulatory role for miR-204-5p which was predicted to inhibit acetyl coenzyme A carboxylase beta, a key fatty acid oxidation enzyme that has been shown to play a role in regulating body fat and insulin resistance in adipose tissue. Fatty Acids 117-127 insulin Homo sapiens 207-214 23866690-0 2013 Saturated fatty acid palmitate-induced insulin resistance is accompanied with myotube loss and the impaired expression of health benefit myokine genes in C2C12 myotubes. Fatty Acids 0-20 insulin Homo sapiens 39-46 23866690-1 2013 BACKGROUND: Excessive circular fatty acid, particlarly saturated fatty acid, can result in insulin resistance in skeletal muscle, but other adverse effects of fatty acid accumulation in myocytes remain unclear. Fatty Acids 55-75 insulin Homo sapiens 91-98 23866690-1 2013 BACKGROUND: Excessive circular fatty acid, particlarly saturated fatty acid, can result in insulin resistance in skeletal muscle, but other adverse effects of fatty acid accumulation in myocytes remain unclear. Fatty Acids 31-41 insulin Homo sapiens 91-98 23826383-6 2013 Exposure of insulin-secreting cells to proinflammatory cytokines, fatty acids or oxidized low-density lipoproteins, mimicking physiopathological conditions that favor the development of diabetes, resulted in a decrease in Rab37 expression. Fatty Acids 66-77 insulin Homo sapiens 12-19 23773230-0 2013 Ethnic- and sex-specific associations between plasma fatty acids and markers of insulin resistance in healthy young adults. Fatty Acids 53-64 insulin Homo sapiens 80-87 23773230-1 2013 BACKGROUND: Although evidence indicates that fatty acids (FA) can affect insulin resistance (IR), not all FA contribute equally to the process. Fatty Acids 45-56 insulin Homo sapiens 73-80 24341187-5 2013 The syndrome of resistance to insulin consists in the derangement of humoral regulation of metabolism of fatty acids and glucose at the phylogenetically different levels in vivo both in paracrine cells cenosis and at the level of organism. Fatty Acids 105-116 insulin Homo sapiens 30-37 24341187-7 2013 The exogenous resistance to insulin is formed under physiologic function of insulin system when hormone effect is prevented by derangement of biologic function of trophology (nutrition)--the formation of such palmitinic mode of metabolism of fatty acids as substrates for oxidation in mitochondria. Fatty Acids 242-253 insulin Homo sapiens 28-35 24341187-7 2013 The exogenous resistance to insulin is formed under physiologic function of insulin system when hormone effect is prevented by derangement of biologic function of trophology (nutrition)--the formation of such palmitinic mode of metabolism of fatty acids as substrates for oxidation in mitochondria. Fatty Acids 242-253 insulin Homo sapiens 76-83 24341187-10 2013 Primarily, insulin regulates metabolism of fatty acids and only secondly metabolic transformations of glucose. Fatty Acids 43-54 insulin Homo sapiens 11-18 23807942-1 2013 Insulin degludec is, like insulin detemir, a product of coupling of Des-B30 threonine insulin to fatty acid side chains. Fatty Acids 97-107 insulin Homo sapiens 26-33 23642261-1 2013 BACKGROUND: Circulating adipocyte fatty acid-binding protein (FABP4) levels are considered to be a link between obesity, insulin resistance, diabetes, and cardiovascular (CV) diseases. Fatty Acids 34-44 insulin Homo sapiens 121-128 23515281-0 2013 A novel JNK2/SREBP-1c pathway involved in insulin-induced fatty acid synthesis in human adipocytes. Fatty Acids 58-68 insulin Homo sapiens 42-49 23515281-9 2013 Furthermore, depletion of JNK2 attenuated insulin-induced upregulation of SREBP-1c target lipogenic enzymes, leading to reduced de novo fatty acid synthesis. Fatty Acids 136-146 insulin Homo sapiens 42-49 23515281-11 2013 These results suggest that SREBP-1c is a novel insulin/JNK2-regulated gene and that the JNK2/SREBP-1c pathway mediates insulin-induced fatty acid synthesis, which may lead to enlargement of LDs in human adipocytes. Fatty Acids 135-145 insulin Homo sapiens 47-54 23515281-11 2013 These results suggest that SREBP-1c is a novel insulin/JNK2-regulated gene and that the JNK2/SREBP-1c pathway mediates insulin-induced fatty acid synthesis, which may lead to enlargement of LDs in human adipocytes. Fatty Acids 135-145 insulin Homo sapiens 119-126 23817228-0 2013 Fatty acid-binding protein 2 Ala54Thr genotype is associated with insulin resistance and leptin levels changes after a high monounsaturated fat diet in obese non-diabetic patients. Fatty Acids 0-10 insulin Homo sapiens 66-73 23723111-9 2013 Next we focus on the detrimental roles of proinflammatory cytokines and fatty acids on insulin signalling and beta-cell function. Fatty Acids 72-83 insulin Homo sapiens 87-94 23397118-5 2013 Greater uptake rates of plasma non-esterified fatty acids are attributable to increased release from an expanded mass of adipose tissue as a consequence of diminished insulin responsiveness. Fatty Acids 35-57 insulin Homo sapiens 167-174 23416068-0 2013 Mitochondrial dysfunction caused by saturated fatty acid loading induces myocardial insulin-resistance in differentiated H9c2 myocytes: a novel ex vivo myocardial insulin-resistance model. Fatty Acids 36-56 insulin Homo sapiens 84-91 23416068-0 2013 Mitochondrial dysfunction caused by saturated fatty acid loading induces myocardial insulin-resistance in differentiated H9c2 myocytes: a novel ex vivo myocardial insulin-resistance model. Fatty Acids 36-56 insulin Homo sapiens 163-170 23584084-7 2013 An important link between obesity, the metabolic syndrome and dyslipidemia, seems to be the development of insulin resistance in peripheral tissues leading to an enhanced hepatic flux of fatty acids from dietary sources, intravascular lipolysis and from adipose tissue resistant to the antilipolytic effects of insulin. Fatty Acids 187-198 insulin Homo sapiens 107-114 23584084-7 2013 An important link between obesity, the metabolic syndrome and dyslipidemia, seems to be the development of insulin resistance in peripheral tissues leading to an enhanced hepatic flux of fatty acids from dietary sources, intravascular lipolysis and from adipose tissue resistant to the antilipolytic effects of insulin. Fatty Acids 187-198 insulin Homo sapiens 311-318 23238293-0 2013 A lipidomics analysis of the relationship between dietary fatty acid composition and insulin sensitivity in young adults. Fatty Acids 58-68 insulin Homo sapiens 85-92 25278764-5 2013 Deregulation of fatty acid metabolism is the main culprit for developing insulin resistance and type 2 diabetes. Fatty Acids 16-26 insulin Homo sapiens 73-80 23139355-8 2013 Elevated levels of fatty acids are known to associate with beta-cell dysfunction, insulin resistance, and increased incidence of late complications. Fatty Acids 19-30 insulin Homo sapiens 82-89 23375099-0 2013 Serum adipocyte fatty acid-binding protein levels in patients with critical illness are associated with insulin resistance and predict mortality. Fatty Acids 16-26 insulin Homo sapiens 104-111 22936679-8 2013 Finally, non-esterified fatty acids levels were ~2.5 times higher in patients during steady state clamp conditions (150 +- 26 vs 58 +- 4 pmol/L, p = 0.01), reflecting decreased insulin sensitivity of lipolysis. Fatty Acids 24-35 insulin Homo sapiens 177-184 23401297-6 2013 RESULTS AND CONCLUSION: IL-1beta inhibited insulin-induced activation of Akt phosphorylation, glucose transport, and fatty acid uptake. Fatty Acids 117-127 insulin Homo sapiens 43-50 23118029-8 2013 In vitro C5a and C3a (100 nM) exhibited novel insulin-like effects on 3T3-L1 adipocytes, promoting energy conservation by increasing glucose and fatty acid uptake while inhibiting cAMP signaling and lipolysis, and induced PGE(2) release from macrophages, effects all blocked by each respective antagonist (10 muM). Fatty Acids 145-155 insulin Homo sapiens 46-53 23219531-1 2013 Fatty acid and triglyceride synthesis is induced in response to feeding and insulin. Fatty Acids 0-10 insulin Homo sapiens 76-83 23509418-1 2013 The ingestion of excessive amounts of saturated fatty acids (SFAs) and transfatty acids (TFAs) is considered to be a risk factor for cardiovascular diseases, insulin resistance, dyslipidemia, and obesity. Fatty Acids 38-59 insulin Homo sapiens 158-165 23357262-4 2013 In b-cell, intracellular calcium concentration elevates when GPR40 is binding to fatty acid, thereby promoting the release of insulin. Fatty Acids 81-91 insulin Homo sapiens 126-133 26052434-4 2012 Considerable evidence has accumulated to suggest that the cytosolic ectopic accumulation of fatty acid metabolites, including diacylglycerol and ceramides, underlies the development of insulin resistance in skeletal muscle. Fatty Acids 92-102 insulin Homo sapiens 185-192 22891212-1 2012 Increased lipid availability reduces insulin-stimulated glucose disposal in skeletal muscle, which is generally explained by fatty acid-mediated inhibition of insulin signaling. Fatty Acids 125-135 insulin Homo sapiens 37-44 22891212-1 2012 Increased lipid availability reduces insulin-stimulated glucose disposal in skeletal muscle, which is generally explained by fatty acid-mediated inhibition of insulin signaling. Fatty Acids 125-135 insulin Homo sapiens 159-166 23168281-3 2012 Some hormones like insulin, thyroid hormones and adipokines (e.g., leptin, adiponectin) have positive effects on muscle mitochondrial bioenergetics through their direct or indirect effects on mitochondrial biogenesis, mitochondrial protein expression, mitochondrial enzyme activities and/or AMPK pathway activation--all of which can improve fatty acid oxidation. Fatty Acids 341-351 insulin Homo sapiens 19-26 23142675-3 2012 Ligands for PPARgamma regulate adipocyte production and secretion of fatty acids as well as glucose metabolism, resulting in increased insulin sensitivity in adipose tissue, liver, and skeletal muscle. Fatty Acids 69-80 insulin Homo sapiens 135-142 27152152-4 2012 Both catecholamine-induced nonesterified fatty acid mobilization and insulin-stimulated storage of meal fatty acids are impaired in many WAT depots of insulin-resistant individuals. Fatty Acids 104-115 insulin Homo sapiens 69-76 27152152-4 2012 Both catecholamine-induced nonesterified fatty acid mobilization and insulin-stimulated storage of meal fatty acids are impaired in many WAT depots of insulin-resistant individuals. Fatty Acids 104-115 insulin Homo sapiens 151-158 25414798-8 2012 CONCLUSION: These observations indicate that the fatty acid changes associated with type 2 diabetes follow the onset of the disease as opposed to being a causative factor of poor glucose control and insulin insensitivity. Fatty Acids 49-59 insulin Homo sapiens 199-206 23079398-4 2012 Additionally, evidence from recent studies demonstrate that a combination of protein containing high levels of leucine with nutrients containing saturated fatty acids or an excess of leucine are capable of inducing insulin resistance. Fatty Acids 145-166 insulin Homo sapiens 215-222 22977275-0 2012 Effect of insulin infusion on spillover of meal-derived fatty acids. Fatty Acids 56-67 insulin Homo sapiens 10-17 23089338-8 2012 CONCLUSIONS: These studies reveal a heightened adipose inflammatory response to increased FFA and insulin availability in middle-aged individuals relative to younger adults, suggesting that increased susceptibility to the effects of fatty acid excess may contribute to the pathogenesis of age-related diseases. Fatty Acids 233-243 insulin Homo sapiens 98-105 23011062-8 2012 The results of the present study indicate an important role for a decreased transport and metabolism of fatty acids, which provides a link between physical activity levels and insulin signaling. Fatty Acids 104-115 insulin Homo sapiens 176-183 22898765-1 2012 AIMS/HYPOTHESIS: Fatty acid entrapment in femoral adipose tissue has been proposed to prevent ectopic fat deposition and visceral fat accumulation, resulting in protection from insulin resistance. Fatty Acids 17-27 insulin Homo sapiens 177-184 23039070-4 2012 Inclusion of insulin in the treatment medium increased total fatty acid amount by 50% and increased the concentration of monounsaturated fatty acids by 12% while decreasing that of saturated fatty acids by 35%. Fatty Acids 61-71 insulin Homo sapiens 13-20 23176795-8 2012 Using gene-set enrichment analysis (GSEA) of microarray data, we found that a number of gene sets of fatty acid metabolism, insulin resistance, and oxidative stress were differentially expressed by OVX and reversed by genistein. Fatty Acids 101-111 insulin Homo sapiens 124-131 23039070-4 2012 Inclusion of insulin in the treatment medium increased total fatty acid amount by 50% and increased the concentration of monounsaturated fatty acids by 12% while decreasing that of saturated fatty acids by 35%. Fatty Acids 127-148 insulin Homo sapiens 13-20 22796147-1 2012 Development of insulin resistance is positively associated with dietary saturated fatty acids and negatively associated with monounsaturated fatty acids. Fatty Acids 72-93 insulin Homo sapiens 15-22 22810223-1 2012 Insulin controls fatty acid (FA) release from white adipose tissue (WAT) through direct effects on adipocytes and indirectly through hypothalamic signaling by reducing sympathetic nervous system outflow to WAT. Fatty Acids 17-27 insulin Homo sapiens 0-7 22742515-11 2012 In contrast, saturated fatty acid exposure caused insulin resistance, reducing PI3K (phosphoinositide 3-kinase) and ERK (extracellular-signal-regulated kinase) activation while increasing activation of stress kinases JNK (c-Jun N-terminal kinase) and p38. Fatty Acids 13-33 insulin Homo sapiens 50-57 22742515-15 2012 Taken together, our findings indicate that chronic insulin and fatty acid-induced insulin resistance differentially affect mitochondrial function. Fatty Acids 63-73 insulin Homo sapiens 82-89 22672330-9 2012 This review summarizes the Dorothy Hodgkin lecture given by the author at the 2012 Diabetes UK annual scientific conference, proposing that fatty acid fluxes through the liver are crucial for the pathogenesis of non-alcoholic fatty liver disease and for increasing insulin resistance. Fatty Acids 140-150 insulin Homo sapiens 265-272 21712806-0 2012 Impaired insulin sensitivity is accompanied by disturbances in skeletal muscle fatty acid handling in subjects with impaired glucose metabolism. Fatty Acids 79-89 insulin Homo sapiens 9-16 22693206-0 2012 High insulin levels are required for FAT/CD36 plasma membrane translocation and enhanced fatty acid uptake in obese Zucker rat hepatocytes. Fatty Acids 89-99 insulin Homo sapiens 5-12 22723441-8 2012 Activation of fatty acid uptake is consistent with the human data, has mechanistic precedent in cell culture, and highlights a new potential target for therapies aimed at improving the control of fatty acid metabolism in insulin-resistant disease states. Fatty Acids 14-24 insulin Homo sapiens 221-228 22723441-8 2012 Activation of fatty acid uptake is consistent with the human data, has mechanistic precedent in cell culture, and highlights a new potential target for therapies aimed at improving the control of fatty acid metabolism in insulin-resistant disease states. Fatty Acids 196-206 insulin Homo sapiens 221-228 22547568-8 2012 Female adipose tissue treated with androgens displayed elevated basal but reduced insulin-dependent fatty acid uptake. Fatty Acids 100-110 insulin Homo sapiens 82-89 22271091-6 2012 We found that activation of insulin signaling triggers a strong induction of the AKT/mTOR cascade that is paralleled by increased synthesis of fatty acids, cholesterol, and triglycerides, induction of glycolysis, and decrease of fatty acid oxidation and gluconeogenesis in rat preneoplastic and neoplastic liver lesions, when compared with the healthy liver. Fatty Acids 143-154 insulin Homo sapiens 28-35 22271091-6 2012 We found that activation of insulin signaling triggers a strong induction of the AKT/mTOR cascade that is paralleled by increased synthesis of fatty acids, cholesterol, and triglycerides, induction of glycolysis, and decrease of fatty acid oxidation and gluconeogenesis in rat preneoplastic and neoplastic liver lesions, when compared with the healthy liver. Fatty Acids 143-153 insulin Homo sapiens 28-35 22761459-0 2012 Effects of acute and one-week fatty acid lowering on cardiac function and insulin sensitivity in relation with myocardial and muscle fat and adiponectin levels. Fatty Acids 30-40 insulin Homo sapiens 74-81 22723441-1 2012 OBJECTIVE: Insulin control of fatty acid metabolism has long been deemed dominated by suppression of adipose lipolysis. Fatty Acids 30-40 insulin Homo sapiens 11-18 22723441-6 2012 The observed insulin K(m) for nonesterified fatty acid uptake was inversely correlated with both insulin sensitivity of glucose uptake (intravenous glucose tolerance test insulin sensitivity; r=-0.626; P=0.01) and whole body fat oxidation after the meal (r=-0.538; P=0.05). Fatty Acids 44-54 insulin Homo sapiens 13-20 22723441-6 2012 The observed insulin K(m) for nonesterified fatty acid uptake was inversely correlated with both insulin sensitivity of glucose uptake (intravenous glucose tolerance test insulin sensitivity; r=-0.626; P=0.01) and whole body fat oxidation after the meal (r=-0.538; P=0.05). Fatty Acids 44-54 insulin Homo sapiens 97-104 22723441-6 2012 The observed insulin K(m) for nonesterified fatty acid uptake was inversely correlated with both insulin sensitivity of glucose uptake (intravenous glucose tolerance test insulin sensitivity; r=-0.626; P=0.01) and whole body fat oxidation after the meal (r=-0.538; P=0.05). Fatty Acids 44-54 insulin Homo sapiens 97-104 22723441-7 2012 CONCLUSIONS: These results support insulin regulation of fatty acid turnover by both release and uptake mechanisms. Fatty Acids 57-67 insulin Homo sapiens 35-42 22270906-1 2012 The fatty-acid-binding protein-2 (FABP2) gene has been proposed as a candidate gene for diabetes because the encoded protein is involved in fatty acid absorption and therefore may affect insulin sensitivity and glucose metabolism. Fatty Acids 140-150 insulin Homo sapiens 187-194 22586279-4 2012 Systemic insulin resistance in heart failure was accompanied by decreased myocardial triglyceride and overall fatty acid content but increased toxic lipid intermediates, diacylglycerol, and ceramide. Fatty Acids 110-120 insulin Homo sapiens 9-16 22337228-5 2012 Fatty acids stimulate IL1beta expression and may promote inflammation, causing hyperglycemia and insulin resistance. Fatty Acids 0-11 insulin Homo sapiens 97-104 22560213-1 2012 Fatty acids (FA) and FA-derived metabolites have long been implicated in the development of insulin resistance and type 2 diabetes. Fatty Acids 0-11 insulin Homo sapiens 92-99 22374970-1 2012 Chronically elevated fatty acids contribute to insulin resistance through poorly defined mechanisms. Fatty Acids 21-32 insulin Homo sapiens 47-54 22173574-1 2012 Excessive metabolism of glucose and/or fatty acids may impair insulin signaling by increasing oxidative stress. Fatty Acids 39-50 insulin Homo sapiens 62-69 22834149-4 2012 To "force" the mitochondria starting to oxidize glucose first of all the insulin is to inhibit the biochemical reactions in all cells where releasing of polar non-etherified fatty acids and formation of their polar metabolites occurs. Fatty Acids 174-185 insulin Homo sapiens 73-80 22147666-6 2012 CONCLUSION: The rs2289046 polymorphism at the IRS2 gene locus may influence insulin sensitivity by interacting with certain plasma fatty acids in MetS subjects. Fatty Acids 131-142 insulin Homo sapiens 76-83 22834149-8 2012 It is possible to be validly of opinion that the same philogenically ancient principles as inhibition of activity of carnitine-palmitoilacylaminotrsansferase, decrease of formation of fatty acid metabolites C4 (ketone bodies), short-chained metabolites of palmitic fatty acid and olein mono fatty acid are applied in realization of philogenically late insulin effect. Fatty Acids 184-194 insulin Homo sapiens 352-359 22834149-9 2012 The first insulin effect in the hypoglycemia and biologic exotrophy reaction conditions is targeted to the regulation of fatty acids metabolism. Fatty Acids 121-132 insulin Homo sapiens 10-17 21988496-9 2012 Model-derived non-esterified fatty acid parameters were lower in subjects with impaired glucose metabolism than in control subjects, particularly sensitivity of non-esterified fatty acid inhibition to insulin (2.50 +- 0.52 vs. 1.06 +- 0.20 10(-2) ml/muU). Fatty Acids 176-186 insulin Homo sapiens 201-208 22360800-0 2012 Mechanisms underlying skeletal muscle insulin resistance induced by fatty acids: importance of the mitochondrial function. Fatty Acids 68-79 insulin Homo sapiens 38-45 22360800-3 2012 Accordantly, in vivo and in vitro exposure of skeletal muscle and myocytes to physiological concentrations of saturated fatty acids is associated with insulin resistance condition. Fatty Acids 110-131 insulin Homo sapiens 151-158 22360800-4 2012 Several mechanisms have been postulated to account for fatty acids-induced muscle insulin resistance, including Randle cycle, oxidative stress, inflammation and mitochondrial dysfunction. Fatty Acids 55-66 insulin Homo sapiens 82-89 22360800-5 2012 Here we reviewed experimental evidence supporting the involvement of each of these propositions in the development of skeletal muscle insulin resistance induced by saturated fatty acids and propose an integrative model placing mitochondrial dysfunction as an important and common factor to the other mechanisms. Fatty Acids 164-185 insulin Homo sapiens 134-141 22108437-1 2012 Pancreatic beta-cells secrete insulin in response to fluctuations in blood fuel concentrations, in particular glucose and fatty acids. Fatty Acids 122-133 insulin Homo sapiens 30-37 22374408-1 2012 BACKGROUND: Activation of free fatty acid receptor 1 (FFAR1; also known as G-protein-coupled receptor 40) by fatty acids stimulated glucose-dependent beta-cell insulin secretion in preclinical models. Fatty Acids 109-120 insulin Homo sapiens 160-167 22326434-4 2012 The release of fatty acids from dysfunctional and insulin-resistant adipocytes results in lipotoxicity, caused by the accumulation of triglyceride-derived toxic metabolites in ectopic tissues (liver, muscle, pancreatic beta cells) and subsequent activation of inflammatory pathways, cellular dysfunction, and lipoapoptosis. Fatty Acids 15-26 insulin Homo sapiens 50-57 22308370-1 2012 The G protein-coupled free fatty acid receptor-1 (FFA1/GPR40) plays a major role in the regulation of insulin secretion by fatty acids. Fatty Acids 123-134 insulin Homo sapiens 102-109 22863834-1 2012 AIMS: Plasma fatty acid composition can change with age, reflecting diet and levels of desaturating enzymes such as stearoyl-CoA desaturase (SCD), delta-6 desaturase (D6D) and delta-5 desaturase (D5D), which contribute to the development of insulin resistance. Fatty Acids 13-23 insulin Homo sapiens 241-248 23393681-2 2012 Absence of insulin or insensitivity of tissues to insulin leads to hyperglycaemia and elevated plasma fatty acid concentration. Fatty Acids 102-112 insulin Homo sapiens 11-18 23393681-5 2012 Elevated plasma fatty acid concentration impairs insulin signalling in skeletal muscle and reduce nitric oxide production in muscle. Fatty Acids 16-26 insulin Homo sapiens 49-56 22876922-2 2012 The main insulin-sensitizing action of adiponectin results from decrease in hepatic gluconeogenesis and increase in muscle glucose transport and, secondly from enhancement of energy consumption and fatty acid oxidation in peripheral tissues with the aim of increasing ATP production. Fatty Acids 198-208 insulin Homo sapiens 9-16 22450341-8 2012 Adiponectin increases fatty acids oxidation, which lowers circulating free fatty acids and prevents insulin resistance. Fatty Acids 22-33 insulin Homo sapiens 100-107 23183516-0 2012 Plasma fatty acid profile in depressive disorder resembles insulin resistance state. Fatty Acids 7-17 insulin Homo sapiens 59-66 23183516-2 2012 Insulin resistance (IR), connected with altered fatty acid (FA) composition, namely with decreased proportion of polyunsaturated FA could participate in these associations. Fatty Acids 48-58 insulin Homo sapiens 0-7 22834331-4 2012 This involves a) beta-oxidation of fatty acids in the mitochondria, b) synthesis of C 16:0 palmitic saturated fatty acid, c) glucose metabolism in pro- and eukaryotes, d) regulation of biochemical reactions in insulin-independent cells, e) humoral effects of mediators at the level of paracrine cell communities which are structural and functional units of all internal organs, and f) hormonal regulation at the entire organism level. Fatty Acids 35-46 insulin Homo sapiens 210-217 22275878-0 2012 Insulin signaling regulates fatty acid catabolism at the level of CoA activation. Fatty Acids 28-38 insulin Homo sapiens 0-7 22275878-8 2012 In sum, we identify fatty acid activation onto CoA as an important, regulated step in triglyceride catabolism, and we identify a mechanistic link through which insulin regulates lipid homeostasis. Fatty Acids 20-30 insulin Homo sapiens 160-167 22396741-0 2012 Common variants of the liver fatty acid binding protein gene influence the risk of type 2 diabetes and insulin resistance in Spanish population. Fatty Acids 29-39 insulin Homo sapiens 103-110 22834331-8 2012 Insulin resistance is a pathophysiological disparity between humoral regulation of metabolism at the level of phylogenetically earlier paracrine cell communities and at the level of phylogenetically late total organism, on the one hand, and successive phylogenetic formation of passive cellular uptake of fatty acids as unesterified fatty acids and later triglycerides, on the other. Fatty Acids 305-316 insulin Homo sapiens 0-7 22834331-8 2012 Insulin resistance is a pathophysiological disparity between humoral regulation of metabolism at the level of phylogenetically earlier paracrine cell communities and at the level of phylogenetically late total organism, on the one hand, and successive phylogenetic formation of passive cellular uptake of fatty acids as unesterified fatty acids and later triglycerides, on the other. Fatty Acids 333-344 insulin Homo sapiens 0-7 21877927-11 2011 CONCLUSIONS: The influence of physical activity during a 3-h interruption of insulin pump treatment is evident, especially in the increase in plasma levels of non-esterified fatty acids and ketone bodies. Fatty Acids 174-185 insulin Homo sapiens 77-84 22336648-0 2011 Adipocyte fatty acid binding protein and C-reactive protein levels as indicators of insulin resistance development. Fatty Acids 10-20 insulin Homo sapiens 84-91 21793541-6 2011 Interestingly, differentiation to adipocytes is greatly suppressed on G because insulin, which is a key regulator for the synthesis of fatty acids, is denatured upon pi-pi adsorption on G; in contrast, GO does not interfere with adipogenesis due to electrostatic binding with insulin. Fatty Acids 135-146 insulin Homo sapiens 80-87 21596547-4 2011 Thus fatty acids relocalize SNAP23 from the plasma membrane (and the translocation of GLUT 4) to the interior of the cell giving rise to insulin resistance. Fatty Acids 5-16 insulin Homo sapiens 137-144 21802492-1 2011 Elevated fatty acid levels have been thought to contribute to insulin resistance. Fatty Acids 9-19 insulin Homo sapiens 62-69 21802492-2 2011 Repression of the glucose transporter 4 (GLUT4) gene as well as impaired GLUT4 translocation may be a mediator for fatty acid-induced insulin resistance. Fatty Acids 115-125 insulin Homo sapiens 134-141 21663979-0 2011 Targeting GPR120 and other fatty acid-sensing GPCRs ameliorates insulin resistance and inflammatory diseases. Fatty Acids 27-37 insulin Homo sapiens 64-71 21713385-2 2011 However, uncontrolled fatty acid release from WAT during non-fasting states causes lipotoxicity and promotes inflammation and insulin resistance, which can lead to and worsen type 2 diabetes (DM2). Fatty Acids 22-32 insulin Homo sapiens 126-133 21713385-3 2011 WAT is also a source for insulin sensitizing fatty acids such as palmitoleate produced during de novo lipogenesis. Fatty Acids 45-56 insulin Homo sapiens 25-32 21893042-3 2011 For instance, a key mechanism involved in the development of insulin resistance is lipotoxicity, through increased circulating saturated fatty acids. Fatty Acids 127-148 insulin Homo sapiens 61-68 21269264-2 2011 A wide range of evidence suggests that defective muscle mitochondrial metabolism, and subsequent impaired ability to oxidize fatty acids, may be a causative factor in the accumulation of intramuscular lipid and the development of insulin resistance. Fatty Acids 125-136 insulin Homo sapiens 230-237 21778123-4 2011 Increased adipose tissue has been related to an increased production of pro-inflammatory cytokines which, together with fatty acids, appear to be responsible for the development of insulin resistance. Fatty Acids 120-131 insulin Homo sapiens 181-188 21599616-4 2011 Fatty acid levels are elevated in obesity and induce inflammatory pathways by yet a mostly unknown mechanism, leading to the development of insulin and leptin resistance. Fatty Acids 0-10 insulin Homo sapiens 140-147 21413848-1 2011 Increasing evidence suggests that fatty acid desaturases, rate-limiting enzymes in unsaturated fatty acid biosynthesis, are important factors in the pathogenesis of lipid-induced insulin resistance. Fatty Acids 34-44 insulin Homo sapiens 179-186 23646067-2 2011 The failure to respond and resulting increase in plasma fatty acids could contribute to the development of insulin resistance and perturbations in the fuel homeostasis in the whole body. Fatty Acids 56-67 insulin Homo sapiens 107-114 21602515-9 2011 In contrast, when exposed to lipolytically active adipocytes, cocultured myotubes shifted substrate use in favor of fatty acids, which was accompanied by intracellular accumulation of triacylglycerol and even-chain acylcarnitines, decreased glucose oxidation, and modest attenuation of insulin signaling. Fatty Acids 116-127 insulin Homo sapiens 286-293 21331063-0 2011 Skeletal muscle fatty acid handling in insulin resistant men. Fatty Acids 16-26 insulin Homo sapiens 39-46 21331063-2 2011 In this study, we examined fasting and postprandial skeletal muscle fatty acid (FA) handling in insulin resistant (IR) men. Fatty Acids 68-78 insulin Homo sapiens 96-103 21411512-5 2011 Multiorgan insulin sensitivity before and after treatment was evaluated by using the hyperinsulinemic-euglycemic clamp procedure in conjunction with stable isotopically labeled tracer infusions to measure glucose, glycerol, and fatty acid kinetics. Fatty Acids 228-238 insulin Homo sapiens 11-18 21494141-5 2011 Some recent studies have suggested that, contrary to expectations, hepatic fatty acid oxidation is upregulated in insulin-resistant individuals. Fatty Acids 75-85 insulin Homo sapiens 114-121 21494141-9 2011 Insulin undoubtedly regulates the supply of fatty acids to the liver from adipose tissue; however, whether insulin has a direct intrahepatic effect on hepatic fatty acid partitioning, in humans, remains unclear. Fatty Acids 44-55 insulin Homo sapiens 0-7 21508840-7 2011 These receptors act also as nutrient sensors, and in the presence of fatty acids will induce an inflammatory cascade that affects insulin signaling with development of insulin resistance. Fatty Acids 69-80 insulin Homo sapiens 130-137 21386858-8 2011 Plasma triglycerides, leptin and glucose combined predicted about 60% of variation in insulin level whereas insulin was the only component that predicted the membrane fatty acids. Fatty Acids 167-178 insulin Homo sapiens 108-115 21386858-9 2011 CONCLUSIONS: We postulate that membrane phospholipids fatty acids have an indirect role in determining insulin concentration but insulin has a major role in determining membrane fatty acid composition. Fatty Acids 54-65 insulin Homo sapiens 103-110 21386858-9 2011 CONCLUSIONS: We postulate that membrane phospholipids fatty acids have an indirect role in determining insulin concentration but insulin has a major role in determining membrane fatty acid composition. Fatty Acids 54-64 insulin Homo sapiens 103-110 21389182-9 2011 CONCLUSION: The rs2953171 polymorphism at the CAPN10 gene locus may influence insulin sensitivity by interacting with the plasma fatty acid composition in subjects with MetS. Fatty Acids 129-139 insulin Homo sapiens 78-85 21508840-7 2011 These receptors act also as nutrient sensors, and in the presence of fatty acids will induce an inflammatory cascade that affects insulin signaling with development of insulin resistance. Fatty Acids 69-80 insulin Homo sapiens 168-175 20938439-2 2011 Dietary saturated fatty acids (SFAs) may be particularly detrimental on insulin sensitivity (SI) and on other components of the MetS. Fatty Acids 8-29 insulin Homo sapiens 72-79 21389182-0 2011 Calpain-10 interacts with plasma saturated fatty acid concentrations to influence insulin resistance in individuals with the metabolic syndrome. Fatty Acids 33-53 insulin Homo sapiens 82-89 21389182-6 2011 RESULTS: The rs2953171 SNP interacted with plasma total saturated fatty acid (SFA) concentrations, which were significantly associated with insulin sensitivity (P < 0.031 for fasting insulin, P < 0.028 for HOMA-IR, and P < 0.012 for glucose effectiveness). Fatty Acids 56-76 insulin Homo sapiens 140-147 21389182-6 2011 RESULTS: The rs2953171 SNP interacted with plasma total saturated fatty acid (SFA) concentrations, which were significantly associated with insulin sensitivity (P < 0.031 for fasting insulin, P < 0.028 for HOMA-IR, and P < 0.012 for glucose effectiveness). Fatty Acids 56-76 insulin Homo sapiens 186-193 21389182-6 2011 RESULTS: The rs2953171 SNP interacted with plasma total saturated fatty acid (SFA) concentrations, which were significantly associated with insulin sensitivity (P < 0.031 for fasting insulin, P < 0.028 for HOMA-IR, and P < 0.012 for glucose effectiveness). Fatty Acids 78-81 insulin Homo sapiens 140-147 21389182-6 2011 RESULTS: The rs2953171 SNP interacted with plasma total saturated fatty acid (SFA) concentrations, which were significantly associated with insulin sensitivity (P < 0.031 for fasting insulin, P < 0.028 for HOMA-IR, and P < 0.012 for glucose effectiveness). Fatty Acids 78-81 insulin Homo sapiens 186-193 21277757-1 2011 We analyse how chronic overfeeding, by increasing circulating fatty acids, might lead to inflammation, insulin resistance (IR) and injury in the liver. Fatty Acids 62-73 insulin Homo sapiens 103-110 21892559-6 2011 However, metabolic changes such as insulin resistance (IR) are developed, being a common factor in the retention of fatty acids (FA) within the hepatocytes with oxidation and production of free radicals at the mitochondrial level, which are capable of causing lipid peroxidation, cytokine production, and necrosis. Fatty Acids 116-127 insulin Homo sapiens 35-42 21677348-6 2011 In either case as a result insulin resistance develops, enhancing hyperglycemia and subsequent hyperinsulinemia, which in turn aggravate liver lipogenesis and fatty acid accumulation. Fatty Acids 159-169 insulin Homo sapiens 27-34 21478880-0 2011 Fatty acid-induced NLRP3-ASC inflammasome activation interferes with insulin signaling. Fatty Acids 0-10 insulin Homo sapiens 69-76 21333978-1 2011 Elevation in non-esterified fatty acids (NEFA) has been shown to modulate insulin secretion and it is considered as a risk factor for the development of type 2 diabetes. Fatty Acids 28-39 insulin Homo sapiens 74-81 21211036-2 2011 Chronic exposure to fatty acids due to an impaired beta-oxidation may down-regulate the glucose-stimulated insulin release and result in an increased risk of type 2 diabetes (T2D). Fatty Acids 20-31 insulin Homo sapiens 107-114 21211036-10 2011 CONCLUSIONS: In glucose-tolerant individuals the minor C-allele of rs2014355 of ACADS was associated with reduced measures of glucose-stimulated insulin release during an OGTT, a finding which in part may be mediated through an impaired beta-oxidation of fatty acids. Fatty Acids 255-266 insulin Homo sapiens 145-152 20978091-0 2011 Insulin resistance, defective insulin-mediated fatty acid suppression, and coronary artery calcification in subjects with and without type 1 diabetes: The CACTI study. Fatty Acids 47-57 insulin Homo sapiens 30-37 21059654-8 2011 Metabolic profiling of beta-cells treated with siRNAs against the ARNT/HIF-1beta gene revealed that glycolysis, anaplerosis, and glucose-induced fatty acid production were down-regulated, and all are key events involved in glucose-stimulated insulin secretion. Fatty Acids 145-155 insulin Homo sapiens 242-249 20711693-4 2010 However, replacement of saturated fat by carbohydrates, particularly refined carbohydrates and added sugars, increases levels of triglyceride and small LDL particles and reduces high-density lipoprotein cholesterol, effects that are of particular concern in the context of the increased prevalence of obesity and insulin resistance. Fatty Acids 24-37 insulin Homo sapiens 313-320 20460954-0 2011 Relationship of adipokines and non-esterified fatty acid to the insulin resistance in non-diabetic individuals. Fatty Acids 35-56 insulin Homo sapiens 64-71 20460954-1 2011 BACKGROUND: Altered secretion of adipokines and non-esterified fatty acid (NEFA) seems to play a pivotal role in the abdominal obesity-related insulin resistance (IR). Fatty Acids 63-73 insulin Homo sapiens 143-150 22164267-9 2011 Adipocyte fatty acid binding protein in the entire cohort (r = -0.625, p = 0.04) and controls (r = -0.869, p = 0.046) correlated best with insulin resistance, independent of BMI. Fatty Acids 10-20 insulin Homo sapiens 139-146 22164267-11 2011 Adipocyte fatty acid binding protein, strongly associated with insulin resistance, independent of adiposity in the young Asian American population, may potentially serve as a biomarker to identify at-risk individuals. Fatty Acids 10-20 insulin Homo sapiens 63-70 21152018-7 2010 CONCLUSIONS/SIGNIFICANCE: These data indicate that reduced oxidative capacity and capacity for fatty acid utilisation at the whole body level are key features of the insulin resistant phenotype observed in South Asians, but that this is not the consequence of reduced skeletal muscle expression of oxidative and lipid metabolism genes. Fatty Acids 95-105 insulin Homo sapiens 166-173 21484574-10 2011 This is that by increasing fatty acid oxidation fatty acid oxidation more than fatty acid supply, drugs lower the concentrations of fatty acid metabolites that cause insulin resistance. Fatty Acids 27-37 insulin Homo sapiens 166-173 21484574-10 2011 This is that by increasing fatty acid oxidation fatty acid oxidation more than fatty acid supply, drugs lower the concentrations of fatty acid metabolites that cause insulin resistance. Fatty Acids 48-58 insulin Homo sapiens 166-173 21484574-10 2011 This is that by increasing fatty acid oxidation fatty acid oxidation more than fatty acid supply, drugs lower the concentrations of fatty acid metabolites that cause insulin resistance. Fatty Acids 48-58 insulin Homo sapiens 166-173 21484574-10 2011 This is that by increasing fatty acid oxidation fatty acid oxidation more than fatty acid supply, drugs lower the concentrations of fatty acid metabolites that cause insulin resistance. Fatty Acids 48-58 insulin Homo sapiens 166-173 22472280-9 2011 Even in an insulin-resistant state, insulin is able to stimulate fatty acid synthesis in liver, activate lipoprotein lipase, and prevent lipolysis in adipose tissues, which all facilitate adipose tissue enlargement. Fatty Acids 65-75 insulin Homo sapiens 36-43 20943795-1 2010 BACKGROUND: Animal experiments suggest that circulating palmitoleic acid (cis-16:1n-7) from adipocyte de novo fatty acid synthesis may directly regulate insulin resistance and metabolic dysregulation. Fatty Acids 110-120 insulin Homo sapiens 153-160 21130299-1 2010 The levels of circulating nonesterified fatty acids increase during obesity and contribute to insulin resistance by inhibiting insulin-stimulated glucose transport and phosphorylation in human muscles. Fatty Acids 40-51 insulin Homo sapiens 94-101 20811782-2 2010 This enzyme is activated by insulin and T(3), and inhibited by fatty acids. Fatty Acids 63-74 insulin Homo sapiens 28-35 20850803-7 2010 Insulin"s effect on substrate oxidation was significantly impaired for both the decrease in fatty acid oxidation and the increase in glucose oxidation. Fatty Acids 92-102 insulin Homo sapiens 0-7 20850803-9 2010 The impaired oxidative response to insulin was associated with reduced mRNA expression of the genes regulating fatty acid oxidation (long-chain-acyl-coenzyme A dehydrogenase, carnitine palmitoyltransferase 1, peroxisome proliferator-activated receptor-alpha) and mitochondrial biogenesis (mitochondrial transcription factor A). Fatty Acids 111-121 insulin Homo sapiens 35-42 21130299-1 2010 The levels of circulating nonesterified fatty acids increase during obesity and contribute to insulin resistance by inhibiting insulin-stimulated glucose transport and phosphorylation in human muscles. Fatty Acids 40-51 insulin Homo sapiens 127-134 20920650-1 2010 Fatty acid-binding proteins (FABPs) 4 and 5 play coordinated roles in rodent models of inflammation, insulin resistance, and atherosclerosis, but little is known of their role in human disease. Fatty Acids 0-10 insulin Homo sapiens 101-108 20687888-5 2010 Thus, fatty acids that cannot be properly stored as triglycerides in subcutaneous adipose tissue are expected to accumulate in visceral fat as well as in organs and tissues, such as the pancreas, muscle and liver, leading to the pattern of metabolic alterations associated with abnormal ectopic fat accumulation, mainly insulin resistance. Fatty Acids 6-17 insulin Homo sapiens 320-327 20682693-9 2010 Tandem mass spectrometry identified protein abundance differences per mitochondrial mass in insulin resistance, including lower abundance of complex I subunits and enzymes involved in the oxidation of branched-chain amino acids (BCAA) and fatty acids (e.g., carnitine palmitoyltransferase 1B). Fatty Acids 239-250 insulin Homo sapiens 92-99 20719107-0 2010 Individual saturated fatty acids are associated with different components of insulin resistance and glucose metabolism: the GOCADAN study. Fatty Acids 11-32 insulin Homo sapiens 77-84 20354806-7 2010 Evidence for the effects of SFA consumption on vascular function, insulin resistance, diabetes, and stroke is mixed, with many studies showing no clear effects, highlighting a need for further investigation of these endpoints. Fatty Acids 28-31 insulin Homo sapiens 66-73 20570821-0 2010 Single-cell analysis of insulin-regulated fatty acid uptake in adipocytes. Fatty Acids 42-52 insulin Homo sapiens 24-31 20570821-7 2010 We propose that, when cell size approaches a critical boundary, adipocytes lose insulin-dependent fatty acid transport. Fatty Acids 98-108 insulin Homo sapiens 80-87 20719107-9 2010 CONCLUSIONS: These results strongly support the hypothesis that saturated fatty acids are associated with insulin resistance and glucose intolerance and that saturated fatty acids are significant risk factors for type 2 diabetes. Fatty Acids 64-85 insulin Homo sapiens 106-113 20697199-6 2010 And finally, we have defined key mechanisms involved in the etiology of cellular insulin resistance in hypothalamic neurons that may play a fundamental role in cases of high levels of insulin or saturated fatty acids, often linked to the exacerbation of obesity and diabetes. Fatty Acids 195-216 insulin Homo sapiens 81-88 20111019-1 2010 Dysregulation of fatty acid oxidation (FAO) is recognized as important in the pathophysiology of obesity and insulin resistance (IR). Fatty Acids 17-27 insulin Homo sapiens 109-116 20373917-3 2010 The limited evidence available suggests that the enzymes responsible for skeletal muscle lipolysis and IMTG synthesis play an important role in determining the fate of fatty acids and therefore the concentration of lipid metabolites and insulin sensitivity of skeletal muscle. Fatty Acids 168-179 insulin Homo sapiens 237-244 21437093-7 2010 Although the exact mechanism of these relationships are complex and not completely understood, the ability to store and limit fatty acid deposition to adipose tissue is a common component to remaining insulin sensitive, controlling the inflammatory cascade and reducing the risk of developing obesity-related comorbidities. Fatty Acids 126-136 insulin Homo sapiens 201-208 20534879-1 2010 The intestinal fatty acid binding protein (FABP2) is involved in lipid metabolism whereby variations in the promoter (haplotypes A/B) and exon 2 (Ala54Thr) are associated with dyslipidemia and insulin resistance. Fatty Acids 15-25 insulin Homo sapiens 193-200 20495453-1 2010 PURPOSE OF REVIEW: The present review outlines possible mechanisms by which high fatty acids, associated with high-fat diet and obesity, impose insulin resistance on glucose uptake into skeletal muscle. Fatty Acids 81-92 insulin Homo sapiens 144-151 20390405-2 2010 Acylcoenzyme A dehydrogenase 10 (ACAD10) catalyses mitochondrial fatty acid beta-oxidation, which plays a pivotal role in developing insulin resistance and type 2 diabetes. Fatty Acids 65-75 insulin Homo sapiens 133-140 21537430-2 2010 It has been postulated that an increase in the intracellular concentration of fatty acid metabolites activates a serine kinase cascade, which leads to defects in insulin signaling downstream to the insulin receptor. Fatty Acids 78-88 insulin Homo sapiens 162-169 20495453-8 2010 Recent evidence also shows proinflammatory macrophages infiltrating muscle tissue and/or intermuscular adipose tissue, and there is growing evidence that fatty acids trigger macrophages to secrete factors that directly impair insulin actions. Fatty Acids 154-165 insulin Homo sapiens 226-233 20427507-1 2010 CONTEXT: Intracellular lipid partitioning toward storage and the incomplete oxidation of fatty acids (FA) have been linked to insulin resistance. Fatty Acids 89-100 insulin Homo sapiens 126-133 20185414-1 2010 Dietary fatty acids are major contributors to the development and progression of insulin resistance and nonalcoholic fatty liver disease (NAFLD). Fatty Acids 8-19 insulin Homo sapiens 81-88 20089366-2 2010 Since insulin signals adipocytes to take up and retain fatty acids, a high dietary saturate-to-unsaturate ratio would be expected to promote obesity. Fatty Acids 55-66 insulin Homo sapiens 6-13 20526369-9 2010 Other metabolites from this global analysis that significantly correlated to insulin sensitivity included certain organic acid, amino acid, lysophospholipid, acylcarnitine and fatty acid species. Fatty Acids 176-186 insulin Homo sapiens 77-84 19875212-0 2010 Inactivity-mediated insulin resistance is associated with upregulated pro-inflammatory fatty acids in human cell membranes. Fatty Acids 87-98 insulin Homo sapiens 20-27 19875212-2 2010 We hypothesize that inactivity-induced insulin resistance could affect levels of pro-inflammatory fatty acids in cell membranes. Fatty Acids 98-109 insulin Homo sapiens 39-46 19228266-4 2010 Physiologically, L4 acts as an insulin-sensitizing agent that is able to enhance hepatocellular glycogen and fatty acid biosynthesis. Fatty Acids 109-119 insulin Homo sapiens 31-38 19948081-4 2010 Peripheral insulin resistance seems to be related to skeletal muscle fatty acid (FA) accumulation and oxidation imbalance. Fatty Acids 69-79 insulin Homo sapiens 11-18 19715772-5 2010 Recent studies from our laboratory have identified several pathways implicated in fatty acid inhibition of insulin gene expression, including the extracellular-regulated kinase (ERK1/2) pathway, the metabolic sensor Per-Arnt-Sim kinase (PASK), and the ATF6 branch of the unfolded protein response. Fatty Acids 82-92 insulin Homo sapiens 107-114 20127308-1 2010 AIMS/HYPOTHESIS: Dietary fatty acids may affect insulin sensitivity. Fatty Acids 25-36 insulin Homo sapiens 48-55 20127308-3 2010 We aimed to determine the association between adipose tissue fatty acids and insulin sensitivity in elderly Swedish men. Fatty Acids 61-72 insulin Homo sapiens 77-84 20336586-2 2010 GPR43 is a GPCR that has been implicated in the regulation of fatty-acid and glucose homeostasis in adipose tissue and the intestines, thus having potential therapeutic relevance in the treatment of type 2 diabetes, insulin resistance and obesity. Fatty Acids 62-72 insulin Homo sapiens 216-223 19846171-2 2010 Functional studies suggest that TNFalpha acts through pathways involving adipokines and fatty acids to induce insulin resistance. Fatty Acids 88-99 insulin Homo sapiens 110-117 20032495-0 2010 Gene-nutrient interactions in the metabolic syndrome: single nucleotide polymorphisms in ADIPOQ and ADIPOR1 interact with plasma saturated fatty acids to modulate insulin resistance. Fatty Acids 129-150 insulin Homo sapiens 163-170 20166804-7 2010 These were unravelled by the parallel losses of these two activities in a subset of glimepiride derivatives and the impairment in the insulin-releasing activity in parallel with elevation in the fatty acid-metabolizing activity in a different subset. Fatty Acids 195-205 insulin Homo sapiens 134-141 20032495-7 2010 Minor allele homozygotes for both of these SNPs were identified as having degrees of insulin resistance, as measured by the homeostasis model assessment of insulin resistance, that were highly responsive to differences in plasma saturated fatty acids (SFAs). Fatty Acids 229-250 insulin Homo sapiens 85-92 20032495-7 2010 Minor allele homozygotes for both of these SNPs were identified as having degrees of insulin resistance, as measured by the homeostasis model assessment of insulin resistance, that were highly responsive to differences in plasma saturated fatty acids (SFAs). Fatty Acids 229-250 insulin Homo sapiens 156-163 20032495-10 2010 Personalized dietary advice to decrease SFA consumption in these individuals may be recommended as a possible therapeutic measure to improve insulin sensitivity. Fatty Acids 40-43 insulin Homo sapiens 141-148 21099306-0 2010 Targeting triglyceride/fatty acid cycling in beta-cells as a therapy for augmenting glucose-stimulated insulin secretion. Fatty Acids 23-33 insulin Homo sapiens 103-110 20166804-3 2010 However, a moderate insulin-independent regulation of fatty acid esterification and release in adipose tissue cells has been reported for certain sulphonylureas, in particular for glimepiride. Fatty Acids 54-64 insulin Homo sapiens 20-27 19818872-1 2010 Although the underlying causes of insulin resistance have not been completely delineated, in most analyses, a recurring theme is dysfunctional metabolism of fatty acids. Fatty Acids 157-168 insulin Homo sapiens 34-41 19915461-2 2010 RECENT FINDINGS: Studies in humans have shown that beta-cell function and insulin sensitivity improve progressively in the postprandial period as the proportion of monounsaturated fatty acids (MUFAs) with respect to saturated fatty acids (SFAs) in dietary fats increases. Fatty Acids 170-191 insulin Homo sapiens 74-81 20041406-5 2010 It is likely that abnormalities in fatty acid metabolism, in conjunction with adipose tissue, hepatic, and systemic inflammation, are key factors involved in the development of insulin resistance, dyslipidemia, and other cardiometabolic risk factors associated with NAFLD. Fatty Acids 35-45 insulin Homo sapiens 177-184 19952270-3 2010 One key mechanism involved in the development of insulin resistance is lipotoxicity, through increased circulating saturated fatty acids. Fatty Acids 115-136 insulin Homo sapiens 49-56 20093718-2 2010 Insulin resistance drives the increase in the three main sources of TG for VLDL synthesis: fatty-acid flux from adipose tissue, de novo lipogenesis, and uptake of remnant lipoproteins. Fatty Acids 91-101 insulin Homo sapiens 0-7 19949414-0 2010 Metabolic endotoxemia and saturated fat contribute to circulating NGAL concentrations in subjects with insulin resistance. Fatty Acids 26-39 insulin Homo sapiens 103-110 20148112-2 2010 Just like PPARgamma, fatty acid synthesis enzymes such as FASN have been implicated in almost all aspects of human metabolic alterations such as obesity, insulin resistance or dyslipemia. Fatty Acids 21-31 insulin Homo sapiens 154-161 20699619-2 2010 Disturbances in fatty acid (FA) metabolism may underlie this reduced insulin sensitivity. Fatty Acids 16-26 insulin Homo sapiens 69-76 19782765-0 2010 Role of fatty acid uptake and fatty acid beta-oxidation in mediating insulin resistance in heart and skeletal muscle. Fatty Acids 8-18 insulin Homo sapiens 69-76 19782765-0 2010 Role of fatty acid uptake and fatty acid beta-oxidation in mediating insulin resistance in heart and skeletal muscle. Fatty Acids 30-40 insulin Homo sapiens 69-76 19782765-5 2010 Accumulation of fatty acids and lipid metabolites (such as long chain acyl CoA, diacylglycerol, triacylglycerol, and/or ceramide) can lead to alterations in this insulin signaling pathway. Fatty Acids 16-27 insulin Homo sapiens 162-169 19782765-6 2010 An imbalance between fatty acid uptake and oxidation is believed to be responsible for this lipid accumulation, and is thought to be a major cause of insulin resistance in obesity and diabetes, due to lipid accumulation and inhibition of one or more steps in the insulin-signaling cascade. Fatty Acids 21-31 insulin Homo sapiens 150-157 19782765-6 2010 An imbalance between fatty acid uptake and oxidation is believed to be responsible for this lipid accumulation, and is thought to be a major cause of insulin resistance in obesity and diabetes, due to lipid accumulation and inhibition of one or more steps in the insulin-signaling cascade. Fatty Acids 21-31 insulin Homo sapiens 263-270 19782765-7 2010 As a result, decreasing muscle fatty acid uptake can improve insulin sensitivity. Fatty Acids 31-41 insulin Homo sapiens 61-68 19782765-8 2010 However, the potential role of increasing fatty acid beta-oxidation in the heart or skeletal muscle in order to prevent cytoplasmic lipid accumulation and decrease insulin resistance is controversial. Fatty Acids 42-52 insulin Homo sapiens 164-171 19782765-10 2010 In this review, we discuss the proposed mechanisms by which alterations in fatty acid uptake and oxidation contribute to insulin resistance, and how targeting fatty acid uptake and oxidation is a potential therapeutic approach to treat insulin resistance. Fatty Acids 75-85 insulin Homo sapiens 121-128 19782765-10 2010 In this review, we discuss the proposed mechanisms by which alterations in fatty acid uptake and oxidation contribute to insulin resistance, and how targeting fatty acid uptake and oxidation is a potential therapeutic approach to treat insulin resistance. Fatty Acids 75-85 insulin Homo sapiens 236-243 19782765-10 2010 In this review, we discuss the proposed mechanisms by which alterations in fatty acid uptake and oxidation contribute to insulin resistance, and how targeting fatty acid uptake and oxidation is a potential therapeutic approach to treat insulin resistance. Fatty Acids 159-169 insulin Homo sapiens 121-128 19782765-10 2010 In this review, we discuss the proposed mechanisms by which alterations in fatty acid uptake and oxidation contribute to insulin resistance, and how targeting fatty acid uptake and oxidation is a potential therapeutic approach to treat insulin resistance. Fatty Acids 159-169 insulin Homo sapiens 236-243 20445742-3 2010 Dysregulation of fatty acid metabolism plays a pivotal role in the pathogenesis of insulin resistance in skeletal muscle. Fatty Acids 17-27 insulin Homo sapiens 83-90 19697961-5 2009 The insulin resistance statuses were closely associated with the serum metabonomic changes in terms of glucose, fatty acid and protein/amino acid metabolisms. Fatty Acids 112-122 insulin Homo sapiens 4-11 20829623-4 2010 In particular, glucocorticoid excess stimulates the expression of several key enzymes involved in the process of gluconeogenesis, with a consequent increase of glucose production, and induces an impairment of insulin sensitivity either directly by interfering with the insulin receptor signaling pathway or indirectly, through the stimulation of lipolysis and proteolysis and the consequent increase of fatty acids and amino acids, which contribute to the development of insulin resistance. Fatty Acids 403-414 insulin Homo sapiens 209-216 19851294-1 2009 BACKGROUND: Fatty acid (FA) synthesis enzymes (FA synthase (FASN) and acetyl-CoA carboxylase (ACC)) are related to metabolic alterations such as obesity, insulin resistance, or dyslipidemia. Fatty Acids 12-22 insulin Homo sapiens 154-161 19796990-6 2009 However, recent work by Nair and coworkers has demonstrated that mitochondrial activity may actually be higher in persons exposed to high-calorie diet leading to obesity, suggesting that the accumulation of intramuscular fat and associated fatty acid metabolites may be directly responsible for the development of insulin resistance, independent of mitochondrial function. Fatty Acids 240-250 insulin Homo sapiens 314-321 20086080-6 2010 Thus, following an acute stimulus, particularly insulin or muscle contraction, specific fatty acid transporters translocate from intracellular stores to the plasma membrane to facilitate fatty acid uptake, just as these same stimuli recruit glucose transporters to increase glucose uptake. Fatty Acids 88-98 insulin Homo sapiens 48-55 20021538-4 2009 Alterations in adipose tissue fatty acid and adipokine metabolism are involved in the pathogenesis of insulin resistance. Fatty Acids 30-40 insulin Homo sapiens 102-109 20021538-5 2009 Excessive rates of fatty acid release into the bloodstream can impair the ability of insulin to stimulate muscle glucose uptake and suppress hepatic glucose production. Fatty Acids 19-29 insulin Homo sapiens 85-92 19927142-6 2009 We also discuss how impaired fatty acid oxidation (FAO) in skeletal muscle may be related to both insulin resistance and a contributor to weight gain. Fatty Acids 29-39 insulin Homo sapiens 98-105 19664593-2 2009 Elevated saturated fatty acids promote insulin resistance, hyperglycaemia and associated atherosclerotic complications, but their effect on "metabolic memory" is unknown. Fatty Acids 9-30 insulin Homo sapiens 39-46 19556298-0 2009 Saturated fatty acids induce insulin resistance in human podocytes: implications for diabetic nephropathy. Fatty Acids 0-21 insulin Homo sapiens 29-36 20455448-0 2009 [Features of fatty-acid spectrum of triglycerides in patients with insulin resistance and metabolic syndrome]. Fatty Acids 13-23 insulin Homo sapiens 67-74 19671019-0 2009 Direct and macrophage-mediated actions of fatty acids causing insulin resistance in muscle cells. Fatty Acids 42-53 insulin Homo sapiens 62-69 19671019-3 2009 Elevated levels of fatty acids in the plasma and interstitial fluids lead to whole-body insulin resistance by disrupting normal insulin-regulated glucose uptake and glycogen storage in skeletal muscle. Fatty Acids 19-30 insulin Homo sapiens 88-95 19671019-3 2009 Elevated levels of fatty acids in the plasma and interstitial fluids lead to whole-body insulin resistance by disrupting normal insulin-regulated glucose uptake and glycogen storage in skeletal muscle. Fatty Acids 19-30 insulin Homo sapiens 128-135 19671019-6 2009 This review summarizes our observations that fatty acids evoke the release of pro-inflammatory factors from macrophages that consequently induce insulin resistance in muscle cells. Fatty Acids 45-56 insulin Homo sapiens 145-152 19754436-5 2009 Fatty acids induce a missorting of SNAP-23, from the plasma membrane to the interior of the cell, resulting in cellular insulin resistance that can be overcome by increasing the levels of SNAP-23. Fatty Acids 0-11 insulin Homo sapiens 120-127 20455448-1 2009 The article presents results of the study of fatty-acid spectrum of triglycerides in insulin resistance patients with metabolic syndrome. Fatty Acids 45-55 insulin Homo sapiens 85-92 19502541-7 2009 A factor containing fatty acids was inversely related to the acute insulin response to glucose (R(2) = 0.12). Fatty Acids 20-31 insulin Homo sapiens 67-74 19560442-3 2009 Insulin-stimulated fatty acid influx (palmitate or arachidonate) into cultured adipocytes resulted in an increase in the phosphorylation of AMPK and its downstream target acetyl-CoA carboxylase. Fatty Acids 19-29 insulin Homo sapiens 0-7 19560442-6 2009 Taken together, these results demonstrate that, in adipocytes, insulin-stimulated fatty acid influx mediated by FATP1 regulates AMPK and provides a potential regulatory mechanism for balancing de novo production of fatty acids from glucose metabolism with influx of preformed fatty acids via phosphorylation of acetyl-CoA carboxylase. Fatty Acids 82-92 insulin Homo sapiens 63-70 19560442-6 2009 Taken together, these results demonstrate that, in adipocytes, insulin-stimulated fatty acid influx mediated by FATP1 regulates AMPK and provides a potential regulatory mechanism for balancing de novo production of fatty acids from glucose metabolism with influx of preformed fatty acids via phosphorylation of acetyl-CoA carboxylase. Fatty Acids 215-226 insulin Homo sapiens 63-70 19560442-6 2009 Taken together, these results demonstrate that, in adipocytes, insulin-stimulated fatty acid influx mediated by FATP1 regulates AMPK and provides a potential regulatory mechanism for balancing de novo production of fatty acids from glucose metabolism with influx of preformed fatty acids via phosphorylation of acetyl-CoA carboxylase. Fatty Acids 276-287 insulin Homo sapiens 63-70 19502541-12 2009 Both large neutral amino acids and fatty acids were related to an appropriate pancreatic response, suggesting that these metabolic intermediates might play a role in the progression to type 2 diabetes, one by contributing to insulin resistance and the other to pancreatic failure. Fatty Acids 35-46 insulin Homo sapiens 225-232 19478146-2 2009 Saturated fatty acids (SFAs) such as palmitate especially have lipotoxic effects leading to endoplasmatic reticulum (ER) stress, inflammation, and insulin resistance. Fatty Acids 0-21 insulin Homo sapiens 147-154 19439328-1 2009 The Thr54 allele of the intestinal fatty acid-binding protein Ala54Thr functional polymorphism (FABP2) is associated with increased fat oxidation and insulin resistance. Fatty Acids 35-45 insulin Homo sapiens 150-157 19478146-2 2009 Saturated fatty acids (SFAs) such as palmitate especially have lipotoxic effects leading to endoplasmatic reticulum (ER) stress, inflammation, and insulin resistance. Fatty Acids 23-27 insulin Homo sapiens 147-154 19763019-5 2009 Proinflammatory factors and saturated fatty acids secreted into the bloodstream from white adipose tissue impair insulin signaling in non-adipose tissues, which causes whole-body insulin resistance. Fatty Acids 28-49 insulin Homo sapiens 113-120 19763019-5 2009 Proinflammatory factors and saturated fatty acids secreted into the bloodstream from white adipose tissue impair insulin signaling in non-adipose tissues, which causes whole-body insulin resistance. Fatty Acids 28-49 insulin Homo sapiens 179-186 19349201-2 2009 However, there is a strong association between insulin resistance and lipid accumulation - and, in particular, lipotoxic fatty acid metabolites - in insulin-target tissues. Fatty Acids 121-131 insulin Homo sapiens 149-156 19277946-1 2009 Saturated fatty acids (SFAs) are known to induce inflammation and insulin resistance in adipocytes through toll-like receptor-4 (Tlr4) signaling, but the mechanisms are not well delineated. Fatty Acids 0-21 insulin Homo sapiens 66-73 19336660-0 2009 Muscle inflammatory response and insulin resistance: synergistic interaction between macrophages and fatty acids leads to impaired insulin action. Fatty Acids 101-112 insulin Homo sapiens 33-40 19364109-6 2009 These results suggested that c9,t11-CLA induced an insulin-independent enhancement of glucose and fatty acid metabolism. Fatty Acids 98-108 insulin Homo sapiens 51-58 19486592-3 2009 The rise in obesity and type 2 diabetes with associated insulin resistance results in abnormal glucose and fatty acid metabolism of the myocardium and the entire body, serving to highlight the fact that deranged metabolism may provide a therapeutic target beyond existing neuroendocrine inhibition. Fatty Acids 107-117 insulin Homo sapiens 56-63 19252892-5 2009 RESULTS: We found strong positive relationships between adipose tissue TG content of the fatty acids myristic acid (14:0) and stearic acid (18:0) with insulin sensitivity (HOMA model) (p < 0.01 for each), and inverse relationships with adipocyte size (p < 0.01, p < 0.05, respectively). Fatty Acids 89-100 insulin Homo sapiens 151-158 19245657-5 2009 Understanding how these secreted signalling proteins regulate AMPK activity to control fatty acid oxidation, glucose uptake, gluconeogenesis and appetite may yield therapeutic treatments for metabolic disorders such as diabetes, insulin resistance and obesity. Fatty Acids 87-97 insulin Homo sapiens 229-236 19252892-1 2009 AIMS/HYPOTHESIS: Previous studies have shown relationships between fatty acid ratios in adipose tissue triacylglycerol (TG), adipocyte size and measures of insulin sensitivity. Fatty Acids 67-77 insulin Homo sapiens 156-163 19675375-8 2009 Dietary saturated fatty acids intake is positively associated with insulin resistance. Fatty Acids 8-29 insulin Homo sapiens 67-74 19337955-1 2009 Insulin suppresses the release of non-esterified fatty acids from adipocytes and suppresses glucose production from hepatocytes, but stimulates glucose uptake by skeletal muscle, liver and adipose tissue. Fatty Acids 38-60 insulin Homo sapiens 0-7 18804984-0 2009 Relationship between n-3 and n-6 plasma fatty acid levels and insulin resistance in coronary patients with and without metabolic syndrome. Fatty Acids 40-50 insulin Homo sapiens 62-69 19233843-3 2009 Incubating primary hepatocyte cultures with recombinant FGF-19 suppressed the ability of insulin to stimulate fatty acid synthesis. Fatty Acids 110-120 insulin Homo sapiens 89-96 19337955-7 2009 In this review, recent in vitro and in vivo data that implicate the IKK (inhibitor of kappaB kinase)/NFkappaB pathway, a component of both fatty acid and inflammatory cytokine signaling cascades, in the regulation of insulin sensitivity are discussed, and the value of this pathway as a therapeutic target in T2D is evaluated. Fatty Acids 139-149 insulin Homo sapiens 217-224 19066312-1 2009 OBJECTIVE: Increased availability of fatty acids is important for accumulation of intracellular lipids and development of insulin resistance in human myotubes. Fatty Acids 37-48 insulin Homo sapiens 122-129 19214471-0 2009 Serum saturated fatty acids containing triacylglycerols are better markers of insulin resistance than total serum triacylglycerol concentrations. Fatty Acids 6-27 insulin Homo sapiens 78-85 19192424-1 2009 In humans, insulin sensitivity is relatively impaired by diets that are low in oleic acid (OA), a cis monounsaturated fatty acid (MUFA), or rich in trans MUFA or palmitic acid (PA), a saturated fatty acid (FA). Fatty Acids 108-128 insulin Homo sapiens 11-18 19207879-4 2009 Fatty acid availability, uptake and oxidation all play a role in metabolic flexibility and insulin resistance. Fatty Acids 0-10 insulin Homo sapiens 91-98 19192421-4 2009 This loss of insulin sensitivity within AT can lead to uncontrolled release of fatty acids, secretion of inflammatory cytokines, and alterations in the balance of adipokines, which ultimately impact lipoprotein metabolism and insulin sensitivity systemically. Fatty Acids 79-90 insulin Homo sapiens 13-20 18472252-12 2009 A reduction in insulin sensitivity and its impact on adiponectin concentration could be linked to high non-esterified fatty acid levels, increased triglyceride synthesis in the liver and impaired catabolism of triglyceride-rich lipoproteins. Fatty Acids 118-128 insulin Homo sapiens 15-22 19154947-0 2009 The association of desaturase 9 and plasma fatty acid composition with insulin resistance-associated factors in female adolescents. Fatty Acids 43-53 insulin Homo sapiens 71-78 19217762-4 2009 Moreover, we investigated the effects of insulin and several adipokines on the fatty acid uptake by these cells as obesity and insulin resistance syndrome have been suggested to affect breast cancer risk. Fatty Acids 79-89 insulin Homo sapiens 127-134 19217762-0 2009 Fatty acid uptake by breast cancer cells (MDA-MB-231): effects of insulin, leptin, adiponectin, and TNFalpha. Fatty Acids 0-10 insulin Homo sapiens 66-73 19056574-2 2009 It has been hypothesized that this "deficiency" of mitochondria mediates insulin resistance by impairing the ability of muscle to oxidize fatty acids (FAs). Fatty Acids 138-149 insulin Homo sapiens 73-80 18599191-2 2009 Insulin-antagonistic effects of hormones, cytokines and excess metabolic substrates such as glucose and fatty acids may be exerted via common mechanisms involving for example reactive oxygen species (ROS) accumulation and associated inflammatory responses. Fatty Acids 104-115 insulin Homo sapiens 0-7 19056574-2 2009 It has been hypothesized that this "deficiency" of mitochondria mediates insulin resistance by impairing the ability of muscle to oxidize fatty acids (FAs). Fatty Acids 151-154 insulin Homo sapiens 73-80 18957619-1 2009 The saturated fatty acid (SFA) palmitate induces insulin resistance in cultured skeletal muscle cells, which may be related to NF-kappaB activation. Fatty Acids 4-24 insulin Homo sapiens 49-56 18957619-1 2009 The saturated fatty acid (SFA) palmitate induces insulin resistance in cultured skeletal muscle cells, which may be related to NF-kappaB activation. Fatty Acids 26-29 insulin Homo sapiens 49-56 18957619-7 2009 Collectively, these results demonstrate that SFA-induced NF-kappaB activation coincides with insulin resistance and depends on FA chain length. Fatty Acids 45-48 insulin Homo sapiens 93-100 19273380-3 2009 Compelling evidence links insulin resistance with an excess fatty acid supply over energy need, resulting in lipid accumulation in non-adipose tissues. Fatty Acids 60-70 insulin Homo sapiens 26-33 19120431-6 2009 The two basal insulin analogues, glargine and detemir, developed by adjusting the isoelectric point and adding a fatty acid residue, respectively, have a protracted duration of action and a relatively smooth profile. Fatty Acids 113-123 insulin Homo sapiens 14-21 21694920-3 2009 Insulin resistance from excess fatty acids is exacerbated by decreased secretion of high molecular weight adiponectin from adipose cells in the obese state. Fatty Acids 31-42 insulin Homo sapiens 0-7 20530934-0 2009 Relationship between carnitine, fatty acids and insulin resistance. Fatty Acids 32-43 insulin Homo sapiens 48-55 21694920-10 2009 Fatty acid accumulation and resistin inhibit insulin and adiponectin. Fatty Acids 0-10 insulin Homo sapiens 45-52 18198986-1 2009 Recent studies have demonstrated that adipocyte fatty acid binding proteins (FABP) may play a role in the etiopathogenesis of insulin resistance. Fatty Acids 48-58 insulin Homo sapiens 126-133 18839419-3 2009 These defects are thought to play a role in the reduced skeletal muscle fatty acid oxidation and increased intramuscular lipid (IMCL) accumulation that is apparent with obesity and other insulin-resistant states such as type 2 diabetes. Fatty Acids 72-82 insulin Homo sapiens 187-194 19299910-3 2009 In response to an increase in circulating glucose levels, insulin is secreted by pancreatic beta cells to cause an increase in the uptake of glucose, fatty acids and amino acids into adipose tissue, muscle and the liver to subsequently promote the storage of these nutrients in the form of glycogen, lipids and protein, respectively, as well as suppress hepatic glucose release. Fatty Acids 150-161 insulin Homo sapiens 58-65 19195626-4 2008 Insulin signals in the liver through its tyrosine-kinase receptors to negatively control hepatic glucose production (HGP), replenish glycogen stores and synthesize fatty acids (FA), leading to TG exported as VLDL. Fatty Acids 164-175 insulin Homo sapiens 0-7 19032965-2 2009 Dietary fat is of particular interest because fatty acids influence glucose metabolism by altering cell membrane function, enzyme activity, insulin signaling, and gene expression. Fatty Acids 46-57 insulin Homo sapiens 140-147 19251040-8 2009 However, FAs in the presence of glucose produce high concentration of malonyl-CoA that repress FA oxidation and increase the formation of LC-CoA amplifying the insulin release. Fatty Acids 9-12 insulin Homo sapiens 160-167 18809633-3 2008 Insulin stimulation of glucose disposal, and insulin suppression of endogenous glucose production (EGP) and nonesterified fatty acids (NEFAs), was studied using a 200-min two-step (10 mU x m(-2) body surface x min(-1) and 80 mU x m(-2) x min (-1) insulin infusion rates) euglycemic clamp with [6,6-(2)H(2)]glucose as the tracer. Fatty Acids 122-133 insulin Homo sapiens 45-52 18929494-2 2008 Triglyceride turnover determines the availability of fatty acids for utilization by mammalian tissues, and any dysfunction in this process can lead to alterations in glucose metabolism, insulin resistance and type 2 diabetes. Fatty Acids 53-64 insulin Homo sapiens 186-193 19047536-5 2008 Activation of FFA1 has been proposed to mediate fatty acid augmentation of glucose-stimulated insulin secretion although it is unclear whether the known long-term detrimental effects of beta-cell exposure to high levels of fatty acids are also mediated through this receptor. Fatty Acids 48-58 insulin Homo sapiens 94-101 18949388-11 2008 Expression of genes related to fatty acid oxidation and ROS elimination were higher in the non-obese group than in the obese group, which contributes to the trend of more severe liver injury, insulin resistance and steatosis in obese patients. Fatty Acids 31-41 insulin Homo sapiens 192-199 18853969-9 2008 There is considerable evidence to suggest that different types of fatty acids, independent of the total amount of fat consumption, affect insulin sensitivity and cholesterol gallstone disease differently. Fatty Acids 66-77 insulin Homo sapiens 138-145 18801860-4 2008 Thus, aerobic exercise training may prevent insulin resistance by correcting a mismatch between fatty acid uptake and fatty acid oxidation in skeletal muscle. Fatty Acids 96-106 insulin Homo sapiens 44-51 18801860-4 2008 Thus, aerobic exercise training may prevent insulin resistance by correcting a mismatch between fatty acid uptake and fatty acid oxidation in skeletal muscle. Fatty Acids 118-128 insulin Homo sapiens 44-51 18805083-3 2008 (2008) now take this concept a step further by identifying a fatty acid metabolite generated in adipose tissue that regulates insulin sensitivity in liver and muscle. Fatty Acids 61-71 insulin Homo sapiens 126-133 18956297-6 2008 The eventual development of insulin resistance leads to continuous lipolysis within these depots, releasing fatty acids into the portal circulation, where they are rapidly translocated to the liver and reassembled into triglycerides. Fatty Acids 108-119 insulin Homo sapiens 28-35 18793158-4 2008 In vitro, prolonged exposure of insulin-secreting cells or isolated islets to concomitantly elevated levels of fatty acids and glucose impairs insulin secretion, inhibits insulin gene expression and, under certain circumstances, induces beta-cell death by apoptosis. Fatty Acids 111-122 insulin Homo sapiens 32-39 18793158-4 2008 In vitro, prolonged exposure of insulin-secreting cells or isolated islets to concomitantly elevated levels of fatty acids and glucose impairs insulin secretion, inhibits insulin gene expression and, under certain circumstances, induces beta-cell death by apoptosis. Fatty Acids 111-122 insulin Homo sapiens 143-150 18793168-0 2008 Saturated and unsaturated (including arachidonic acid) non-esterified fatty acid modulation of insulin secretion from pancreatic beta-cells. Fatty Acids 70-80 insulin Homo sapiens 95-102 18727921-1 2008 SREBP1c (sterol regulatory element-binding protein 1c) is a metabolic-syndrome-associated transcription factor that controls fatty acid biosynthesis under glucose/insulin stimulation. Fatty Acids 125-135 insulin Homo sapiens 163-170 18826455-0 2008 Role of fatty acids in the development of insulin resistance and type 2 diabetes mellitus. Fatty Acids 8-19 insulin Homo sapiens 42-49 18826455-5 2008 Further support for the lipocentric hypothesis of the pathogenesis of insulin resistance was provided by knocking out the gene coding for ACC2 in mice; this led to greater fatty acid oxidation, reduced fat mass and, in consequence, greatly enhanced insulin sensitivity. Fatty Acids 172-182 insulin Homo sapiens 70-77 18769626-4 2008 We then discuss how obesity leads to insulin resistance via a complex interplay among systemic fatty acid excess, microhypoxia in adipose tissue, ER stress, and inflammation. Fatty Acids 95-105 insulin Homo sapiens 37-44 18556566-1 2008 OBJECTIVE: Insulin resistant states are associated with increased fatty acid flux to liver and intestine, which stimulates the production of triglyceride-rich lipoproteins (TRL). Fatty Acids 66-76 insulin Homo sapiens 11-18 18394213-4 2008 Obesity, type 2 diabetes and insulin resistance are highly prevalent, and both are strongly related to disorders of lipid metabolism characterized by an increased plasma and intracellular fatty acid availability. Fatty Acids 188-198 insulin Homo sapiens 29-36 18505832-0 2008 The lowering of hepatic fatty acid uptake improves liver function and insulin sensitivity without affecting hepatic fat content in humans. Fatty Acids 24-34 insulin Homo sapiens 70-77 18673007-9 2008 One possible mechanism is that abnormal levels of metabolites, such as lipids, fatty acids, and various cytokines from the adipose tissue, activate monocytes and increase the secretion of inflammatory cytokines, enhancing insulin resistance. Fatty Acids 79-90 insulin Homo sapiens 222-229 18504545-0 2008 Adipose tissue fatty acid metabolism in insulin-resistant men. Fatty Acids 15-25 insulin Homo sapiens 40-47 18654640-1 2008 The sterol regulatory element-binding protein (SREBP) family member SREBP1 is a critical transcriptional regulator of cholesterol and fatty acid metabolism and has been implicated in insulin resistance, diabetes, and other diet-related diseases. Fatty Acids 134-144 insulin Homo sapiens 183-190 18535477-1 2008 Impaired fatty acid oxidation occurs with type 2 diabetes and is associated with accumulations of intracellular lipids, which may increase diacylglycerol (DAG), stimulate protein kinase C activity, and inactivate insulin signaling. Fatty Acids 9-19 insulin Homo sapiens 213-220 18542013-6 2008 Nevertheless, there are consistent data indicating that women are protected against fatty acid-induced insulin resistance. Fatty Acids 84-94 insulin Homo sapiens 103-110 18349111-1 2008 Reduced skeletal muscle mitochondrial content and fatty acid oxidation are associated with obesity and insulin resistance. Fatty Acids 50-60 insulin Homo sapiens 103-110 18430774-6 2008 The secretion pattern of nonesterified fatty acids, IL-6, adiponectin, leptin, and monocyte chemotactic protein-1 was in keeping with the changes in insulin sensitivity during differentiation. Fatty Acids 39-50 insulin Homo sapiens 149-156 18509062-2 2008 Efficient sequestration of fat in adipocytes also prevents fatty acid overload in skeletal muscle and liver, which can impair insulin signaling. Fatty Acids 59-69 insulin Homo sapiens 126-133 18481955-4 2008 Western diets rich in saturated fats cause obesity and insulin resistance, and increase levels of circulating NEFAs [non-esterified ("free") fatty acids]. Fatty Acids 22-36 insulin Homo sapiens 55-62 18571119-4 2008 On the other hand, the decrease of fatty acid oxidation increases the level of free fatty acid (FFA), which increases the insulin resistance, and then decreases the glucose uptake, which ultimately causes increased plasma glucose and type 2 diabetes (T2D). Fatty Acids 35-45 insulin Homo sapiens 122-129 18062827-1 2008 Altered fatty acid (FA) composition is related to insulin resistance and CVD. Fatty Acids 8-18 insulin Homo sapiens 50-57 18460913-1 2008 PURPOSE OF REVIEW: Acute exposure to fatty acids causes insulin resistance in muscle, and excess dietary lipid and obesity are also strongly associated with muscle insulin resistance. Fatty Acids 37-48 insulin Homo sapiens 56-63 18460913-6 2008 Several animal models with gene deletions in pathways of fatty acid synthesis and storage also show increased metabolic rate, reduced intramuscular lipid storage and improved insulin action when challenged with a high lipid load. Fatty Acids 57-67 insulin Homo sapiens 175-182 18460913-7 2008 SUMMARY: Studies in genetic and dietary obese animal models, genetically modified animals and humans with obesity or type 2 diabetes suggest plausible mechanisms for effects of fatty acids, lipid metabolites, inflammatory pathways and mitochondrial dysfunction on insulin action in muscle. Fatty Acids 177-188 insulin Homo sapiens 264-271 18460341-5 2008 Via reduced release of fatty acids into the circulation, the anti-lipolytic effect could be a mechanism through which FGF21 promotes insulin sensitivity in man. Fatty Acids 23-34 insulin Homo sapiens 133-140 18207474-5 2008 Hence it is believed that intermediates in fatty acid metabolism, such as fatty acyl-CoA, ceramides or diacylglycerol (DAG) link fat deposition in the muscle to compromised insulin signaling. Fatty Acids 43-53 insulin Homo sapiens 173-180 18342897-4 2008 Furthermore, type 2 diabetes is associated with impaired metabolic flexibility, i.e. an impaired switching from fatty acid to glucose oxidation in response to insulin. Fatty Acids 112-122 insulin Homo sapiens 159-166 18048763-3 2008 In addition to their contribution to the deterioration of beta-cell function after the onset of the disease, elevations of plasma fatty acid levels that often accompany insulin resistance may, as glucose levels begin to rise outside of the normal range, also play a pathogenic role in the early stages of the disease. Fatty Acids 130-140 insulin Homo sapiens 169-176 18317722-0 2008 Fatty acid-induced mitochondrial uncoupling in adipocytes as a key protective factor against insulin resistance and beta cell dysfunction: do adipocytes consume sufficient amounts of oxygen to oxidise fatty acids? Fatty Acids 0-10 insulin Homo sapiens 93-100 18360697-12 2008 These data indicate that, in NAFLD, insulin signaling via IRS-1 causes the up-regulation of SREBP1-c, leading to the increased synthesis of fatty acids by the hepatocytes; negative feedback regulation via AMPK does not occur and the activation of Foxa2, following a decrease of IRS-2, up-regulates fatty acid oxidation. Fatty Acids 140-151 insulin Homo sapiens 36-43 18355813-5 2008 The ability of insulin to suppress fatty acid release from adipose tissue and to stimulate glucose uptake by skeletal muscle were also inversely correlated with IHTG content (adipose tissue: r = -0.590, P < .001; skeletal muscle: r = -0.656, P < .001). Fatty Acids 35-45 insulin Homo sapiens 15-22 18401346-2 2008 In skeletal muscle, insulin resistance can result from high levels of circulating fatty acids that disrupt insulin signalling pathways. Fatty Acids 82-93 insulin Homo sapiens 20-27 18401346-2 2008 In skeletal muscle, insulin resistance can result from high levels of circulating fatty acids that disrupt insulin signalling pathways. Fatty Acids 82-93 insulin Homo sapiens 107-114 18309299-1 2008 OBJECTIVE: An impaired fatty acid handling in skeletal muscle may be involved in the development of insulin resistance and diabetes mellitus type 2 (DM2). Fatty Acids 23-33 insulin Homo sapiens 100-107 18360697-12 2008 These data indicate that, in NAFLD, insulin signaling via IRS-1 causes the up-regulation of SREBP1-c, leading to the increased synthesis of fatty acids by the hepatocytes; negative feedback regulation via AMPK does not occur and the activation of Foxa2, following a decrease of IRS-2, up-regulates fatty acid oxidation. Fatty Acids 140-150 insulin Homo sapiens 36-43 18405640-8 2008 Subsequent fatty acid re-esterification participates in the reduction in blood NEFA and insulin resistance. Fatty Acids 11-21 insulin Homo sapiens 88-95 18198225-0 2008 Abdominal obesity in older women: potential role for disrupted fatty acid reesterification in insulin resistance. Fatty Acids 63-73 insulin Homo sapiens 94-101 18198225-10 2008 Importantly, fatty acid reesterification was significantly (P < 0.01) associated with abdominal circumference and hepatic and peripheral insulin resistance, regardless of total body fat. Fatty Acids 13-23 insulin Homo sapiens 140-147 18301083-2 2008 The effects of different types of dietary fatty acids on insulin sensitivity in humans are discussed, with focus on recent controlled studies. Fatty Acids 42-53 insulin Homo sapiens 57-64 17708582-1 2008 Fatty acid (FA) and glucose transport into insulin-dependent cells are impaired in insulin resistance (IR; type 2 diabetes mellitus). Fatty Acids 0-10 insulin Homo sapiens 83-90 18301083-3 2008 RECENT FINDINGS: Observational studies assessing fatty acid composition in serum or tissues suggest that insulin resistance is associated with relatively high intakes of saturated fat (e.g. palmitic acid) and low intakes of polyunsaturated fat (e.g. linoleic acid), findings that are supported by recent clinical data. Fatty Acids 49-59 insulin Homo sapiens 105-112 18097647-5 2008 The major locus of control of fatty acid release beyond the stimulation of lipolysis is the pathway of fatty acid esterification, already probably targeted by the thiazolidinedione insulin-sensitising agents. Fatty Acids 30-40 insulin Homo sapiens 181-188 18097647-5 2008 The major locus of control of fatty acid release beyond the stimulation of lipolysis is the pathway of fatty acid esterification, already probably targeted by the thiazolidinedione insulin-sensitising agents. Fatty Acids 103-113 insulin Homo sapiens 181-188 18097647-9 2008 We conclude that prevention or treatment of insulin resistance through alteration of adipocyte fatty acid handling will require more than a simple alteration of the activity of mitochondrial beta-oxidation within normal limits. Fatty Acids 95-105 insulin Homo sapiens 44-51 18301083-3 2008 RECENT FINDINGS: Observational studies assessing fatty acid composition in serum or tissues suggest that insulin resistance is associated with relatively high intakes of saturated fat (e.g. palmitic acid) and low intakes of polyunsaturated fat (e.g. linoleic acid), findings that are supported by recent clinical data. Fatty Acids 170-183 insulin Homo sapiens 105-112 18301083-3 2008 RECENT FINDINGS: Observational studies assessing fatty acid composition in serum or tissues suggest that insulin resistance is associated with relatively high intakes of saturated fat (e.g. palmitic acid) and low intakes of polyunsaturated fat (e.g. linoleic acid), findings that are supported by recent clinical data. Fatty Acids 224-243 insulin Homo sapiens 105-112 18301083-4 2008 Most controlled studies have hitherto examined the effect of monounsaturated fat on insulin sensitivity, several indicating that it has beneficial effects when substituted for saturated fat. Fatty Acids 61-80 insulin Homo sapiens 84-91 18301083-4 2008 Most controlled studies have hitherto examined the effect of monounsaturated fat on insulin sensitivity, several indicating that it has beneficial effects when substituted for saturated fat. Fatty Acids 67-80 insulin Homo sapiens 84-91 18301083-7 2008 Finally, we and others hypothesize that dietary fatty acids may partly mediate their effects on insulin action by regulating the activity of lipogenic enzymes and desaturases. Fatty Acids 48-59 insulin Homo sapiens 96-103 17906687-4 2008 PPAR-gamma receptor activation by TZDs improves insulin sensitivity by promoting fatty acid uptake into adipose tissue, increasing production of adiponectin and reducing levels of inflammatory mediators such as tumour necrosis factor-alpha (TNF-alpha), plasminogen activator inhibitor-1(PAI-1) and interleukin-6 (IL-6). Fatty Acids 81-91 insulin Homo sapiens 48-55 18180399-7 2008 In vitro gene expression analysis in human coronary endothelial cells revealed that resistin induced fatty acid binding protein, a key molecule of insulin resistance, diabetes, and atherosclerosis. Fatty Acids 101-111 insulin Homo sapiens 147-154 18358420-3 2008 In the uncontrolled diabetic state, because of the combined effects of insulin resistance and high circulating fatty acids, cardiac myocytes use fatty acids almost exclusively to support ATP synthesis. Fatty Acids 145-156 insulin Homo sapiens 71-78 18358420-5 2008 Fatty acids also play a critical role in triggering the development of cellular insulin resistance through derangements in insulin signalling cascade. Fatty Acids 0-11 insulin Homo sapiens 80-87 18358420-5 2008 Fatty acids also play a critical role in triggering the development of cellular insulin resistance through derangements in insulin signalling cascade. Fatty Acids 0-11 insulin Homo sapiens 123-130 18177719-1 2008 Elevated fatty acids promote inflammation and insulin resistance. Fatty Acids 9-20 insulin Homo sapiens 46-53 18177719-3 2008 (2008) explore a novel paradigm suggesting that beta-oxidation of fatty acids exceeding the capacity of the tricarboxylic acid cycle yields incomplete fat oxidation and mitochondrial distress, obligatory events in the pathogenesis of insulin resistance. Fatty Acids 66-77 insulin Homo sapiens 234-241 18166818-1 2008 OBJECTIVE: In obese subjects, chronically elevated plasma concentrations of non-esterified fatty acids (NEFAs) exert a marked risk to contract insulin resistance and subsequently type 2 diabetes. Fatty Acids 80-102 insulin Homo sapiens 143-150 17914030-7 2008 Increasing plasma insulin levels decreased myocardial fatty acid esterification rates but increased the percentage of fatty acids going into esterification. Fatty Acids 54-64 insulin Homo sapiens 18-25 17914030-7 2008 Increasing plasma insulin levels decreased myocardial fatty acid esterification rates but increased the percentage of fatty acids going into esterification. Fatty Acids 118-129 insulin Homo sapiens 18-25 17914030-9 2008 However, its myocardial glucose and fatty acid metabolism still responds to changes in plasma insulin and plasma FFA levels. Fatty Acids 36-46 insulin Homo sapiens 94-101 17914030-10 2008 Moreover, insulin and plasma FFA levels can regulate the intramyocardial fate of fatty acids in humans with type 1 diabetes. Fatty Acids 81-92 insulin Homo sapiens 10-17 17970749-1 2007 Fatty acids can stimulate the secretory activity of insulin-producing beta-cells. Fatty Acids 0-11 insulin Homo sapiens 52-59 18154600-4 2008 The 2007 Stock Conference focused on the role of fatty acids and other lipid signals in initiating insulin resistance and the consequences of central insulin resistance to the regulation of energy balance and peripheral metabolism. Fatty Acids 49-60 insulin Homo sapiens 99-106 17804680-2 2007 How fatty acids affect postprandial insulin, glucose, and triglyceride concentrations, however, remains unclear. Fatty Acids 4-15 insulin Homo sapiens 36-43 17804680-3 2007 The objective of this study was to study the effect of fatty acids on postprandial insulin, glucose, and triglyceride responses. Fatty Acids 55-66 insulin Homo sapiens 83-90 18055661-0 2007 Fasting nonesterified fatty acid profiles in childhood and their relationship with adiposity, insulin sensitivity, and lipid levels. Fatty Acids 22-32 insulin Homo sapiens 94-101 18055661-1 2007 OBJECTIVE: The objective of this study was to examine the major constituent of nonesterified fatty acids in children with respect to auxologic parameters, insulin sensitivity, and lipid levels, because nonesterified fatty acid levels are elevated in obesity and are important in the development of comorbidities. Fatty Acids 93-103 insulin Homo sapiens 155-162 18516264-4 2007 Insulin resistance, predisposing to lipolysis of peripheral fat with mobilization to and uptake of fatty acids by the liver, is the most consistent underlying pathogenic factor. Fatty Acids 99-110 insulin Homo sapiens 0-7 17956338-1 2007 SREBP-1c (sterol-regulatory-element-binding protein 1c) is a transcription factor that regulates genes associated with glucose and fatty acid metabolism and exhibits responsiveness to insulin and exercise. Fatty Acids 131-141 insulin Homo sapiens 184-191 17725635-1 2007 AIMS: The aims of our study were to determine if insulin resistance is associated with increased plasma levels of non-esterified fatty acids (NEFA), glycerol, 3-hydroxybutyrate and triglycerides in obese children. Fatty Acids 129-140 insulin Homo sapiens 49-56 17704301-0 2007 Genes involved in fatty acid partitioning and binding, lipolysis, monocyte/macrophage recruitment, and inflammation are overexpressed in the human fatty liver of insulin-resistant subjects. Fatty Acids 18-28 insulin Homo sapiens 162-169 17922004-8 2007 Thus, SNAP23 might be a link between insulin sensitivity and the inflow of fatty acids to the cell. Fatty Acids 75-86 insulin Homo sapiens 37-44 17921407-1 2007 BACKGROUND: The intestinal fatty acid-binding protein (FABP2) is involved in the intracellular transport and metabolism of fatty acids and may affect insulin sensitivity and glucose metabolism. Fatty Acids 27-37 insulin Homo sapiens 150-157 17921407-1 2007 BACKGROUND: The intestinal fatty acid-binding protein (FABP2) is involved in the intracellular transport and metabolism of fatty acids and may affect insulin sensitivity and glucose metabolism. Fatty Acids 123-134 insulin Homo sapiens 150-157 17712547-0 2007 Fatty acid-induced mitochondrial uncoupling in adipocytes as a key protective factor against insulin resistance and beta cell dysfunction: a new concept in the pathogenesis of obesity-associated type 2 diabetes mellitus. Fatty Acids 0-10 insulin Homo sapiens 93-100 17601988-9 2007 CONCLUSIONS: In the postprandial period, the only sources of fatty acids for VLDL TG production to differ in the insulin-resistant compared with the insulin-sensitive men are those derived from splanchnic sources. Fatty Acids 61-72 insulin Homo sapiens 113-120 17712547-11 2007 Unless these released fatty acids are removed by mitochondrial oxidation in active muscles, these fatty acids result in ectopic triacylglycerol deposits, induction of insulin resistance, beta cell damage and diabetes. Fatty Acids 22-33 insulin Homo sapiens 167-174 17601988-9 2007 CONCLUSIONS: In the postprandial period, the only sources of fatty acids for VLDL TG production to differ in the insulin-resistant compared with the insulin-sensitive men are those derived from splanchnic sources. Fatty Acids 61-72 insulin Homo sapiens 149-156 17712547-11 2007 Unless these released fatty acids are removed by mitochondrial oxidation in active muscles, these fatty acids result in ectopic triacylglycerol deposits, induction of insulin resistance, beta cell damage and diabetes. Fatty Acids 98-109 insulin Homo sapiens 167-174 17712547-13 2007 Thus, the number and activity of mitochondria within adipocytes contribute to the threshold at which fatty acids are released into the circulation, leading to insulin resistance and type 2 diabetes. Fatty Acids 101-112 insulin Homo sapiens 159-166 17921788-2 2007 This review addresses the effect of chronic and acute endurance exercise on insulin action in obesity and the role of exercise-induced alterations in fatty acid partitioning within the muscle cell on insulin sensitivity. Fatty Acids 150-160 insulin Homo sapiens 200-207 18348079-0 2008 Enhanced protection against cytokine- and fatty acid-induced apoptosis in pancreatic beta cells by combined treatment with glucagon-like peptide-1 receptor agonists and insulin analogues. Fatty Acids 42-52 insulin Homo sapiens 169-176