PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 20385503-3 2010 However, data from animal and clinical studies have suggested that catecholamines can induce insulin resistance. Catecholamines 67-81 insulin Homo sapiens 93-100 16527823-6 2006 This association was controlled by insulin and catecholamine: perilipin B was specifically depleted from the plasma membrane in response to the catecholamine isoproterenol, while insulin increased the amount of threonine phosphorylated perilipin at the plasma membrane. Catecholamines 47-60 insulin Homo sapiens 179-186 18537611-2 2008 Its function is primarily controlled by the anabolic hormone insulin and its counterparts glucagon, catecholamines and glucocorticoids. Catecholamines 100-114 insulin Homo sapiens 61-68 17713401-3 2007 Under physiologic conditions, infusing catecholamine is associated with enhanced rates of aerobic glycolysis (resulting in adenosine triphosphate production), glucose release (both from glycogenolysis and gluconeogenesis), and inhibition of insulin-mediated glycogenesis. Catecholamines 39-52 insulin Homo sapiens 241-248 17148734-2 2006 These stimuli, acting both on the central control stations of the stress system and its final effectors, catecholamines and glucocorticoids, and on the peripheral target tissues, can modulate insulin action in the body. Catecholamines 105-119 insulin Homo sapiens 192-199 20184923-10 2010 Increased pancreastatin plasma levels, correlating with catecholamines levels, have been found in insulin resistance states, such as gestational diabetes or essential hypertension. Catecholamines 56-70 insulin Homo sapiens 98-105 15889114-6 2005 CONCLUSION: Subjects born SGA demonstrated a hyperlipolytic reactivity to catecholamines, which might be regarded as an additional deleterious component of the insulin resistance associated with SGA. Catecholamines 74-88 insulin Homo sapiens 160-167 15977304-5 2005 These may include insulin-antagonistic action of hormones like catecholamines, glucocorticoids, sex steroids and adipokines as well as dysregulation of autonomic nervous activity and they could contribute to the early development of insulin resistance. Catecholamines 63-77 insulin Homo sapiens 18-25 15388645-1 2005 Insulin counterregulates catecholamine action in part by inducing the sequestration of beta2-adrenergic receptors. Catecholamines 25-38 insulin Homo sapiens 0-7 15736119-10 2005 By showing a dose-dependent increasing influence of insulin on systolic BP and circulating catecholamine levels, the present study provides experimental evidence for the notion that hyperinsulinemia contributes to the development of hypertension. Catecholamines 91-104 insulin Homo sapiens 52-59 15457373-8 2004 The impossibility of demonstrating ex vivo the mechanism of catecholamine-mediated regulation that is evident in vitro is perhaps due to our experimental conditions or to substances which in vivo inhibit the action of the catecholamines on magnesium, such as insulin and/or glucose. Catecholamines 60-73 insulin Homo sapiens 259-266 15256333-0 2004 Catecholamine excess in pheochromocytoma inducing insulin resistance. Catecholamines 0-13 insulin Homo sapiens 50-57 15898827-7 2004 In several life-threatening poisonings in humans, the administration of high-dose insulin produced cardiovascular stabilisation, decreased the catecholamine vasopressor infusion rate and improved the survival rate. Catecholamines 143-156 insulin Homo sapiens 82-89 14693408-9 2004 However, increased sensitivity to catecholamine-induced lipolysis of the Gly allele promotes higher free fatty acids concentrations in the portal system, which could enhance the higher levels of fasting insulin. Catecholamines 34-47 insulin Homo sapiens 203-210 14592784-1 2003 Increased free intracellular calcium ([Ca(2+)](i)) in adipocytes blunts the lipolytic response to catecholamines by activating phosphodiesterase 3B - the same enzyme that mediates the antilipolytic effect of insulin - while also compromising the efficiency of insulin-stimulated glucose uptake. Catecholamines 98-112 insulin Homo sapiens 208-215 14610262-5 2003 However, intense exercise provokes the release of insulin-counter regulatory hormones such as glucagons and catecholamines, which ultimately cause a reduction in the insulin action. Catecholamines 108-122 insulin Homo sapiens 50-57 14610262-5 2003 However, intense exercise provokes the release of insulin-counter regulatory hormones such as glucagons and catecholamines, which ultimately cause a reduction in the insulin action. Catecholamines 108-122 insulin Homo sapiens 166-173 14592784-1 2003 Increased free intracellular calcium ([Ca(2+)](i)) in adipocytes blunts the lipolytic response to catecholamines by activating phosphodiesterase 3B - the same enzyme that mediates the antilipolytic effect of insulin - while also compromising the efficiency of insulin-stimulated glucose uptake. Catecholamines 98-112 insulin Homo sapiens 260-267 12107377-4 2002 Among the most detailed mediators studied are corticotropin-releasing factor and serotonin which, via the hypothalamic-pituitary-adrenal axis and the sympathetic and parasympathetic nervous system, stimulate catecholamines and cortisol and inhibit anabolic hormones, insulin, leptin, ghrelin, including neuropeptide Y and other neuropeptides, among them the paracrine-acting cytokines. Catecholamines 208-222 insulin Homo sapiens 267-274 12450763-2 2003 This paper proposes that post-prandial insulin resistance, in association with raised levels of cortisol and catecholamines, plays the major role, and may even be the primary causative factor. Catecholamines 109-123 insulin Homo sapiens 39-46 12915647-2 2003 Data from animal and evidence from clinical studies suggest that catecholamines can induce insulin resistance. Catecholamines 65-79 insulin Homo sapiens 91-98 12915647-10 2003 CONCLUSION: Our data provide evidence that endogenous catecholamine excess in patients with pheochromocytoma can induce or aggravate insulin resistance both in patients with type 2 diabetes and patients with normal glucose tolerance. Catecholamines 54-67 insulin Homo sapiens 133-140 11815511-4 2002 We hypothesized that caffeine reduces insulin sensitivity, either due to catecholamines and/or as a result of blocking adenosine-mediated stimulation of peripheral glucose uptake. Catecholamines 73-87 insulin Homo sapiens 38-45 11809767-1 2002 The counterregulation of catecholamine action by insulin includes insulin-stimulated sequestration of the beta(2)-adrenergic receptor. Catecholamines 25-38 insulin Homo sapiens 49-56 11809767-1 2002 The counterregulation of catecholamine action by insulin includes insulin-stimulated sequestration of the beta(2)-adrenergic receptor. Catecholamines 25-38 insulin Homo sapiens 66-73 11893370-4 2002 An immediate response to the angor animi and initial symptoms of an acute coronary syndrome is a rapid and marked increase in catecholamine release, which leads to adipose tissue lipolysis with an acute increase in plasma free fatty acid concentrations, suppression of insulin activity, and a reduction in glucose uptake by the myocardium. Catecholamines 126-139 insulin Homo sapiens 269-276 11932285-11 2002 Finally, catecholamine-induced HSL activation can be inhibited by insulin in a similar manner in both FCHL and controls. Catecholamines 9-22 insulin Homo sapiens 66-73 11465683-7 2001 An increase of catecholamines appears to increase glucose while both reducing insulin release and reducing sensitivity to insulin that is available. Catecholamines 15-29 insulin Homo sapiens 78-85 11465683-7 2001 An increase of catecholamines appears to increase glucose while both reducing insulin release and reducing sensitivity to insulin that is available. Catecholamines 15-29 insulin Homo sapiens 122-129 9453333-3 1998 In conscious chronically instrumented rats, we measured plasma concentrations of catecholamines during acute insulin-induced hypoglycemia in groups of rats pretreated with the AT1 receptor antagonist losartan (10 mg/kg i.v. Catecholamines 81-95 insulin Homo sapiens 109-116 11118030-6 2000 We demonstrate defects in insulin action on 2-deoxy-D-glucose transport (SHRSP 3.3 +/- 1.5 vs. 21.0 +/- 7.4 pmol x min(-1) x [20 microl packed cells](-1), SHRSP vs. WKY, respectively, P = 0.01) and inhibition of catecholamine-stimulated lipolysis (P < 0.05 at all concentrations of insulin) in adipocytes isolated from SHRSP. Catecholamines 212-225 insulin Homo sapiens 26-33 11117672-3 2000 Insulin resistance in PCOS adipocytes was manifested as a reduction in insulin sensitivities for stimulation of glucose transport and suppression of catecholamine-activated lipolysis with no impact on final hormone responsiveness. Catecholamines 149-162 insulin Homo sapiens 0-7 11117672-3 2000 Insulin resistance in PCOS adipocytes was manifested as a reduction in insulin sensitivities for stimulation of glucose transport and suppression of catecholamine-activated lipolysis with no impact on final hormone responsiveness. Catecholamines 149-162 insulin Homo sapiens 71-78 9918386-8 1998 In conclusion, during insulin-induced hypoglycemia, PDE 3 activation clearly counteracts the lipolytic effect of catecholamines. Catecholamines 113-127 insulin Homo sapiens 22-29 10940302-2 2000 The counterregulatory actions of insulin on catecholamine action are well known and include phosphorylation of the beta(2)-adrenergic receptor on Tyr(350), Tyr(354), and Tyr(364) in the C-terminal cytoplasmic domain, as well as enhanced sequestration of the beta(2)-adrenergic receptor. Catecholamines 44-57 insulin Homo sapiens 33-40 10877211-4 2000 These data suggest that the primary mechanism by which insulin stimulates leptin release is to blunt the inhibitory effects of beta1-adrenergic receptor agonists, and low concentrations of catecholamines actually enhance the stimulation of leptin release by insulin. Catecholamines 189-203 insulin Homo sapiens 258-265 10232719-7 1999 Plasma concentrations of cortisol and catecholamines increased after hysterectomy (cortisol from 6 +/- 2 to 31 +/- 7 microg x dl(-1), epinephrine from 25 +/- 14 to 205 +/- 132 pg x ml(-1), norepinephrine from 182 +/- 82 to 377 +/- 132 pg x ml(-1), P < 0.05), whereas plasma lactate, insulin and glucagon concentrations remained unchanged. Catecholamines 38-52 insulin Homo sapiens 286-293 9342538-8 1997 Insulin and glucocorticoids increase leptin expression, whereas catecholamines, via beta-adrenergic receptors and cAMP, and long-chain fatty acids (and thiazolidinediones), via PPARy, inhibit leptin expression. Catecholamines 64-78 insulin Homo sapiens 0-7 9350634-12 1997 In response to insulin infusion, catecholamines increased on day 2 (noradrenaline and adrenaline) and day 7 (adrenaline), but not at sea level. Catecholamines 33-47 insulin Homo sapiens 15-22 8897002-2 1996 In the present study, we aimed at investigation in hVSMC: 1) the interrelationships between insulin-induced increases of cGMP and cAMP; 2) the insulin effect on the catecholamine modulation of cAMP. Catecholamines 165-178 insulin Homo sapiens 143-150 8914428-4 1996 Several mechanisms mediated by hyperinsulinemia can be entertained as follows: 1) sodium and water retention, 2) increased sympathetic nerve activity and reduced catecholamine clearance, 3) increased intracellular calcium concentration and reduced magnesium concentration, 4) increased coagulant activity and impaired fibrinolytic activity, 5) impaired endothelium-dependent NO synthesis and release, 6) increased vascular responsiveness for the vasoactive substrates, 7) increased proliferation of vascular smooth muscle cell by activation of protein kinase C or mediated by insulin and IGF-1 action. Catecholamines 162-175 insulin Homo sapiens 36-43 8664455-1 1995 OBJECTIVE: The purpose was to study whether the hemodynamic benefit of a catabolic catecholamine (dobutamine) induces a certain oxygen cost for the myocardial energy demand and whether this effect would be less pronounced if an anabolic intervention, such as the administration of insulin, was used. Catecholamines 83-96 insulin Homo sapiens 281-288 8891519-7 1996 We propose that catecholamines prevent hypoglycaemia during exercise when changes in insulin and C-peptide do not occur. Catecholamines 16-30 insulin Homo sapiens 85-92 8891519-7 1996 We propose that catecholamines prevent hypoglycaemia during exercise when changes in insulin and C-peptide do not occur. Catecholamines 16-30 insulin Homo sapiens 97-106 8737076-8 1996 The presence of insulin receptors in human red blood cells, and the relationship between insulin and catecholamine levels in the plasma led us to investigate the effect of insulin on catecholamine transport. Catecholamines 101-114 insulin Homo sapiens 89-96 8737076-8 1996 The presence of insulin receptors in human red blood cells, and the relationship between insulin and catecholamine levels in the plasma led us to investigate the effect of insulin on catecholamine transport. Catecholamines 101-114 insulin Homo sapiens 89-96 8737076-10 1996 Furthermore, the addition of exogenous insulin to red blood cells from fasting subjects significantly reduced the influx of catecholamines while no effect was observed when insulin was added to red blood cells obtained from fed subjects. Catecholamines 124-138 insulin Homo sapiens 39-46 8742566-1 1996 OBJECTIVE: To evaluate the effects of captopril on circulating catecholamine levels in NIDDM patients and the possible relationship between captopril-related changes in circulating catecholamine levels and insulin sensitivity. Catecholamines 181-194 insulin Homo sapiens 206-213 8742566-10 1996 CONCLUSIONS: The reduction of circulating catecholamines could contribute, at least in part, to the captopril-related amelioration of insulin sensitivity. Catecholamines 42-56 insulin Homo sapiens 134-141 8557631-2 1996 Cross-regulation among members of both receptor superfamilies has been reported, including the counter-regulatory effects of insulin on beta-adrenergic catecholamine action. Catecholamines 152-165 insulin Homo sapiens 125-132 9162435-4 1996 Insulin resistance was characterized by higher body mass index (p = 0.002, analysis of variance), triglycerides (p = 0.001), total cholesterol/high density lipoprotein cholesterol ratio (p = 0.002), haemoglobin (p = 0.013), haematocrit (p = 0.017) and resting heart rate (p = 0.041) but not resting blood pressure or catecholamines in arterialized blood. Catecholamines 317-331 insulin Homo sapiens 0-7 8563461-9 1995 As catecholamines antagonize insulin effects, one possible explanation for insulin resistance in amputees is hyperglycaemia-induced sympathoneural activation and a failure of hyperglycaemia to decrease adrenomedullary secretion. Catecholamines 3-17 insulin Homo sapiens 29-36 8563461-9 1995 As catecholamines antagonize insulin effects, one possible explanation for insulin resistance in amputees is hyperglycaemia-induced sympathoneural activation and a failure of hyperglycaemia to decrease adrenomedullary secretion. Catecholamines 3-17 insulin Homo sapiens 75-82 8535550-1 1995 The aim of the present study was to compare insulin sensitivity and catecholamine responses to insulin in lean, hypertensive (HT) and normotensive (NT) premenopausal women. Catecholamines 68-81 insulin Homo sapiens 95-102 8568012-5 1995 Also, insulin can augment catecholamine release, increase vascular sensitivity to vasoconstrictor substances, and decrease vascular sensitivity to vasodilator substances. Catecholamines 26-39 insulin Homo sapiens 6-13 7553077-7 1995 Altered membrane lipid composition and increased levels of free fatty acids; 2. long-lasting hyperinsulinemia; 3. increased plasma levels of insulin counteracting hormones such as growth hormone, glucagon, catecholamines and possibly cytokines; 4. a lack of liver-derived humoral factors with insulin-like activity, i.e. insulin-like growth factors I and II. Catecholamines 206-220 insulin Homo sapiens 141-148 7556372-9 1995 In the whole group of hypertensive patients (n = 26), partial correlations showed left ventricular mass index (LVMI) associated with fasting plasma insulin levels (r = 0.44 P < 0.005), insulin-mediated whole body glucose disposal (r = -0.41 P < 0.01) and nonoxidative glucose metabolism (r = -0.33 P < 0.04) independently of age, body weight, systolic blood pressure and plasma catecholamines levels. Catecholamines 387-401 insulin Homo sapiens 188-195 7838011-5 1994 Conversely, promoting brain insulin activity with chromium picolinate may help to maintain the hypothalamus in a more functionally youthful state; increased hypothalamic catecholamine activity, sensitization of insulin-responsive central mechanisms regulating appetite and thermogenesis, and perhaps trophic effects on brain neurons may play a role in this regard. Catecholamines 170-183 insulin Homo sapiens 28-35 7902002-3 1993 We hypothesized that insulin-induced catecholamine-mediated beta-adrenergic stimulation supports some of these hemodynamic changes in the hyperinsulinemic ovine fetus. Catecholamines 37-50 insulin Homo sapiens 21-28 7902002-8 1993 We conclude that in the hyperinsulinemic-hypoglycemic normoxemic ovine fetus, insulin-induced catecholamine-mediated hemodynamic changes are modulated in part by beta-adrenergic receptor stimulation. Catecholamines 94-107 insulin Homo sapiens 29-36 8419906-4 1993 Since alpha 2-adrenoceptor stimulation suppresses insulin secretion, catecholamines from intrapancreatic nerve terminals may be involved in the mechanism behind the marked impairment of the glucose-stimulated insulin response in the intact pancreas. Catecholamines 69-83 insulin Homo sapiens 209-216 8400589-9 1993 Anabolic IGF-1 and insulin levels showed significant negative correlation with the catabolic indicators 3-methylhistidine and catecholamine excretion. Catecholamines 126-139 insulin Homo sapiens 19-26 8425662-10 1993 In summary, the 6-fold higher insulin level resulted in significantly greater increases in catecholamine and cortisol secretion, HGP, lipolysis, heart rate, and sBP despite equivalent hypoglycemia. Catecholamines 91-104 insulin Homo sapiens 30-37 1547683-0 1992 Catecholamine response during human and pork insulin-induced hypoglycemia in IDDM patients. Catecholamines 0-13 insulin Homo sapiens 45-52 1474052-5 1992 On the other hand, insulin-induced hypoglycemia during HDT produced increases in ADH, cortisol, PRA, aldosterone, and catecholamine levels. Catecholamines 118-131 insulin Homo sapiens 19-26 1628451-0 1992 [Effects of insulin-induced hypoglycemia on catecholamine secretion and blood pressure in neurological disorders affecting autonomic nervous system]. Catecholamines 44-57 insulin Homo sapiens 12-19 1628451-1 1992 The effects of insulin-induced hypoglycemia on catecholamine secretion were investigated in patients with various neurological disorders affecting the autonomic nervous system. Catecholamines 47-60 insulin Homo sapiens 15-22 1445172-3 1992 On the other hand, phaeochromocytoma and hyperaldosteronism, via the respective actions of catecholamines and hypokalaemia on the pancreatic beta-cell, impair glucose tolerance primarily by inhibiting insulin release. Catecholamines 91-105 insulin Homo sapiens 201-208 1547683-1 1992 OBJECTIVE: To evaluate the catecholamine response during human and pork insulin-induced hypoglycemia. Catecholamines 27-40 insulin Homo sapiens 72-79 1283768-5 1992 Catecholamines may raise total cholesterol, triglycerides, and insulin, decrease HDL cholesterol, and cause insulin resistance and glucose intolerance, and recent evidence supports an in vivo influence of epinephrine on blood platelets, causing dysfunction in hypertensive subjects. Catecholamines 0-14 insulin Homo sapiens 63-70 1311009-0 1992 High plasma levels of catecholamines during insulin-induced hypoglycemic stress do not cause beta-adrenergic receptor sequestration. Catecholamines 22-36 insulin Homo sapiens 44-51 1283768-5 1992 Catecholamines may raise total cholesterol, triglycerides, and insulin, decrease HDL cholesterol, and cause insulin resistance and glucose intolerance, and recent evidence supports an in vivo influence of epinephrine on blood platelets, causing dysfunction in hypertensive subjects. Catecholamines 0-14 insulin Homo sapiens 108-115 2012249-4 1991 Total catecholamine secretion during insulin-induced hypoglycemia was significantly lower in the RO. Catecholamines 6-19 insulin Homo sapiens 37-44 1936584-2 1991 Physiological concentrations of insulin decrease the catecholamine-induced production of prostaglandin I2 (PGI2; prostacyclin) and PGE2, two potent vasodilators, in adipose tissue, one of the largest organs in the body. Catecholamines 53-66 insulin Homo sapiens 32-39 8577141-3 1991 The subjects with a higher insulin in plasma and renal excretion of catecholamines showed a longer time of tolerance to the above exposure which varied from 50 to 120 min. Catecholamines 68-82 insulin Homo sapiens 27-34 1674642-7 1991 Thus we conclude that sympathochromaffin activation plays a minor role when insulin and glucagon are operative, but a catecholamine, probably epinephrine, becomes critical to the prevention of hypoglycemia during exercise when changes in insulin and glucagon do not occur. Catecholamines 118-131 insulin Homo sapiens 238-245 1648157-3 1991 Thus, alpha 2-adrenoceptor activation by circulating or neuronally released catecholamines inhibits the release of insulin from pancreatic islet beta-cells and, by inhibiting this response, alpha 2-adrenoceptor antagonists have been shown to have an antihyperglycemic effect. Catecholamines 76-90 insulin Homo sapiens 115-122 2060427-7 1991 RESULTS: Basal plasma catecholamine levels were lower in diabetic subjects after intensive insulin therapy than in control subjects (P = 0.008). Catecholamines 22-35 insulin Homo sapiens 91-98 2060427-8 1991 The peak and incremental catecholamine responses after insulin withdrawal and intensive insulin therapy in IDDM subjects were significantly decreased compared with control subjects (P less than 0.001). Catecholamines 25-38 insulin Homo sapiens 55-62 2060427-8 1991 The peak and incremental catecholamine responses after insulin withdrawal and intensive insulin therapy in IDDM subjects were significantly decreased compared with control subjects (P less than 0.001). Catecholamines 25-38 insulin Homo sapiens 88-95 2060427-9 1991 Peak catecholamine responses to hypoglycemia in IDDM were decreased after intensive insulin therapy (P = 0.002). Catecholamines 5-18 insulin Homo sapiens 84-91 2060427-11 1991 The diminished catecholamine responses were primarily due to decreased peak epinephrine responses after intensive insulin therapy compared with insulin withdrawal (P = 0.011). Catecholamines 15-28 insulin Homo sapiens 114-121 2060427-13 1991 CONCLUSIONS: These results suggest that children and adolescents with IDDM after insulin withdrawal have diminished catecholamine response to hypoglycemia compared with control subjects and indicate that short-term intensive insulin therapy diminishes this response further. Catecholamines 116-129 insulin Homo sapiens 81-88 2060427-13 1991 CONCLUSIONS: These results suggest that children and adolescents with IDDM after insulin withdrawal have diminished catecholamine response to hypoglycemia compared with control subjects and indicate that short-term intensive insulin therapy diminishes this response further. Catecholamines 116-129 insulin Homo sapiens 225-232 1664342-4 1991 Catecholamines seem to be more regulator than originator of the insulin secretory process. Catecholamines 0-14 insulin Homo sapiens 64-71 2243613-0 1990 Neural influence on the action of insulin in the adrenomedullary catecholamine content in the pigeon. Catecholamines 65-78 insulin Homo sapiens 34-41 2260723-1 1990 The present studies were designed to determine the fetal catecholamine and metabolic responses to insulin-induced maternal hypoglycemia. Catecholamines 57-70 insulin Homo sapiens 98-105 2076856-5 1990 It has been suggested that hyperinsulinism and insulin resistance may lead to hypertension through altered intracellular calcium metabolism, enhanced renal sodium reabsorption, or through an effect of insulin upon lipid and/or catecholamine metabolism. Catecholamines 227-240 insulin Homo sapiens 32-39 2076856-5 1990 It has been suggested that hyperinsulinism and insulin resistance may lead to hypertension through altered intracellular calcium metabolism, enhanced renal sodium reabsorption, or through an effect of insulin upon lipid and/or catecholamine metabolism. Catecholamines 227-240 insulin Homo sapiens 47-54 2195784-7 1990 These observations suggest that endogenous insulin secretion is suppressed by increase plasma catecholamines, and that excessive rebound secretion of insulin after removal of a pheochromocytoma is a rather common phenomenon. Catecholamines 94-108 insulin Homo sapiens 43-50 1975832-11 1990 It is well known that catecholamine, especially noradrenaline has an inhibiting action on insulin secretion from beta cell. Catecholamines 22-35 insulin Homo sapiens 90-97 1975832-14 1990 We think an inhibiting action on insulin secretion of catecholamine was diminished through its action as adrenoceptor antagonist. Catecholamines 54-67 insulin Homo sapiens 33-40 2203383-2 1990 It is possible that these factors may play a role in changes in insulin sensitivity in vivo produced by such diverse conditions as treatment with furosemide, thyroid status or catecholamine status. Catecholamines 176-189 insulin Homo sapiens 64-71 2203383-3 1990 In particular, there is evidence that chronic elevation of catecholamine or sympathetic stimulation improves insulin sensitivity. Catecholamines 59-72 insulin Homo sapiens 109-116 2203383-5 1990 Consequently, insulin resistance and decreased thermogenesis may be explained by decreased levels of catecholamines and/or a decreased sensitivity of skeletal muscle and perhaps other tissues to catecholamines or a decreased activity of the sympathetic nervous system. Catecholamines 101-115 insulin Homo sapiens 14-21 2203383-5 1990 Consequently, insulin resistance and decreased thermogenesis may be explained by decreased levels of catecholamines and/or a decreased sensitivity of skeletal muscle and perhaps other tissues to catecholamines or a decreased activity of the sympathetic nervous system. Catecholamines 195-209 insulin Homo sapiens 14-21 35124671-3 2022 Psychological stress leads to an increase of serum glucocorticoid concentrations and catecholamines release increasing the insulin need and the insulin resistance. Catecholamines 85-99 insulin Homo sapiens 123-130 2192764-0 1990 Chronic and endogenous regulation of insulin receptors by catecholamines in adipocytes from patients with a phaeochromocytoma. Catecholamines 58-72 insulin Homo sapiens 37-44 2192764-5 1990 This was accompanied by a catecholamine-desensitization of the adipocytes to the antilipolytic action of insulin. Catecholamines 26-39 insulin Homo sapiens 105-112 2192764-6 1990 These events could represent a final situation of a chronic and endogenous regulation by high levels of catecholamines of insulin receptors in human adipose tissue. Catecholamines 104-118 insulin Homo sapiens 122-129 2281657-0 1990 [Catecholamine excretion in diabetics on insulin treatment]. Catecholamines 1-14 insulin Homo sapiens 41-48 34576151-6 2021 Insulin is known to regulate glucose metabolism, support cognition, enhance the outgrowth of neurons, modulate the release and uptake of catecholamine, and regulate the expression and localization of gamma-aminobutyric acid (GABA). Catecholamines 137-150 insulin Homo sapiens 0-7 35124671-3 2022 Psychological stress leads to an increase of serum glucocorticoid concentrations and catecholamines release increasing the insulin need and the insulin resistance. Catecholamines 85-99 insulin Homo sapiens 144-151 2459120-0 1988 Insulin antagonism of catecholamine stimulation of fatty acid transport in the adipocyte. Catecholamines 22-35 insulin Homo sapiens 0-7 35070058-11 2022 CONCLUSION: High doses of catecholamines exert insulin-like actions on glucose transport in human adipocytes. Catecholamines 26-40 insulin Homo sapiens 47-54 2647559-0 1989 Abnormal action of catecholamines on lipolysis in adipocytes of type I diabetic patients treated with insulin. Catecholamines 19-33 insulin Homo sapiens 102-109 2647559-1 1989 Catecholamine-induced lipolysis was investigated in adipocytes obtained before and after 30 min of exercise from 10 insulin-treated type I (insulin-dependent) diabetic men and 10 male matched control subjects. Catecholamines 0-13 insulin Homo sapiens 116-123 2647559-1 1989 Catecholamine-induced lipolysis was investigated in adipocytes obtained before and after 30 min of exercise from 10 insulin-treated type I (insulin-dependent) diabetic men and 10 male matched control subjects. Catecholamines 0-13 insulin Homo sapiens 140-147 2646946-9 1989 This effect is due to the exquisite sensitivity of lipolysis to insulin and is overcome by catecholamine release during hypoglycemia. Catecholamines 91-104 insulin Homo sapiens 64-71 2688232-5 1989 Thus, smoking stimulates the secretion of the antiinsulin hormones, particularly catecholamines, resulting in subcutaneous vasoconstriction which may be unfortunate as it influences insulin absorption. Catecholamines 81-95 insulin Homo sapiens 50-57 2560726-0 1989 Beta-adrenoceptors desensitization may modulate catecholamine induced insulin resistance in human pheochromocytoma. Catecholamines 48-61 insulin Homo sapiens 70-77 2560726-1 1989 Catecholamines acutely exert a pronounced insulin-antagonistic effect, which is mediated by beta-adrenergic receptors stimulation. Catecholamines 0-14 insulin Homo sapiens 42-49 2853087-1 1988 Insulin-induced hypoglycaemia causes profound haemodynamic changes, commonly ascribed to catecholamine increase. Catecholamines 89-102 insulin Homo sapiens 0-7 2844816-1 1988 The mechanisms by which insulin inhibits catecholamine-induced lipolysis in fat cells are unknown. Catecholamines 41-54 insulin Homo sapiens 24-31 2459120-2 1988 Insulin at physiological concentrations can suppress catecholamine activation of the membrane transport of long chain fatty acids in the adipocyte. Catecholamines 53-66 insulin Homo sapiens 0-7 2820811-6 1987 Catecholamine and phorbol ester induced insulin resistance of isolated rat fat cells as well as human fat cells was associated with a decreased activity of the insulin receptor tyrosine kinase which was apparently due to a modulation of the ATP binding site of the insulin receptor tyrosine kinase; 3. Catecholamines 0-13 insulin Homo sapiens 40-47 2898127-1 1988 The gene for the catecholamine biosynthetic enzyme, tyrosine hydroxylase (TH), has been previously mapped to human chromosome 11 p15.5 in the vicinity of the loci for insulin (INS) and for the oncogene Harvey Ras 1 (HRAS). Catecholamines 17-30 insulin Homo sapiens 167-174 3359794-2 1988 Hypoglycemia after resection of pheochromocytoma may be due to release of insulin from the beta cells of the pancreas due to sudden withdrawal of catecholamines. Catecholamines 146-160 insulin Homo sapiens 74-81 3287952-2 1988 Our previous data indicated that changes in pancreatic islet hormones are not normally critical but decrements in insulin, increments in glucagon, or both become critical when catecholamine actions are blocked pharmacologically. Catecholamines 176-189 insulin Homo sapiens 114-121 3036595-0 1987 Catecholamine inhibition of Ca2+-induced insulin secretion from electrically permeabilised islets of Langerhans. Catecholamines 0-13 insulin Homo sapiens 41-48 2820811-6 1987 Catecholamine and phorbol ester induced insulin resistance of isolated rat fat cells as well as human fat cells was associated with a decreased activity of the insulin receptor tyrosine kinase which was apparently due to a modulation of the ATP binding site of the insulin receptor tyrosine kinase; 3. Catecholamines 0-13 insulin Homo sapiens 160-167 2820811-6 1987 Catecholamine and phorbol ester induced insulin resistance of isolated rat fat cells as well as human fat cells was associated with a decreased activity of the insulin receptor tyrosine kinase which was apparently due to a modulation of the ATP binding site of the insulin receptor tyrosine kinase; 3. Catecholamines 0-13 insulin Homo sapiens 160-167 3109862-0 1987 Differential effects of insulin- and proinsulin-induced hypoglycemia on pituitary hormone and catecholamine secretion. Catecholamines 94-107 insulin Homo sapiens 24-47 3109862-6 1987 Peak and integrated cortisol, GH, and catecholamine responses to insulin and proinsulin were similar, but those of prolactin were reduced after proinsulin when compared with insulin by 42% (P less than .01) and 34% (P less than .05), respectively. Catecholamines 38-51 insulin Homo sapiens 65-72 2439067-2 1987 Two antibodies which reacted with receptor alpha-subunit and completely inhibited 125I-insulin binding mimicked the actions of insulin to stimulate lipogenesis from [14C]glucose and to inhibit catecholamine-induced lipolysis. Catecholamines 193-206 insulin Homo sapiens 87-94 2439067-2 1987 Two antibodies which reacted with receptor alpha-subunit and completely inhibited 125I-insulin binding mimicked the actions of insulin to stimulate lipogenesis from [14C]glucose and to inhibit catecholamine-induced lipolysis. Catecholamines 193-206 insulin Homo sapiens 127-134 3032719-0 1987 Catecholamines and tumour promoting phorbolesters inhibit insulin receptor kinase and induce insulin resistance in isolated human adipocytes. Catecholamines 0-14 insulin Homo sapiens 58-65 3032719-0 1987 Catecholamines and tumour promoting phorbolesters inhibit insulin receptor kinase and induce insulin resistance in isolated human adipocytes. Catecholamines 0-14 insulin Homo sapiens 93-100 3032719-7 1987 We conclude from the data that catecholamine and phorbolester treatment of human adipocytes modulates the kinase activity of the insulin receptor by increasing its Michaelis constant for adenosine-triphosphate, and propose that this modulation of receptor kinase is a mechanism that can contribute to the pathogenesis of insulin resistance in human fat cells. Catecholamines 31-44 insulin Homo sapiens 129-136 3032719-7 1987 We conclude from the data that catecholamine and phorbolester treatment of human adipocytes modulates the kinase activity of the insulin receptor by increasing its Michaelis constant for adenosine-triphosphate, and propose that this modulation of receptor kinase is a mechanism that can contribute to the pathogenesis of insulin resistance in human fat cells. Catecholamines 31-44 insulin Homo sapiens 321-328 3538108-4 1986 After 3 weeks of administration of therapeutic doses of lithium carbonate, healthy volunteers showed a differential response of catecholamines to insulin stimulation. Catecholamines 128-142 insulin Homo sapiens 146-153 3542342-2 1987 However, hypomagnesaemia has been reported in patients in clinical situations where circulating catecholamines are raised including myocardial infarction, cardiac surgery and insulin-induced hypoglycaemia stress tests. Catecholamines 96-110 insulin Homo sapiens 175-182 6398261-2 1984 When the insulin dose delivered is adjusted to achieve a near match of the peripheral plasma glucose profile, the 24 h profiles of free fatty acids, glycerol, lactate and beta-hydroxybutyrate and the hormones, insulin, glucagon, cortisol and catecholamines were identical. Catecholamines 242-256 insulin Homo sapiens 9-16 3532664-5 1986 The IDM"s are able to respond to both physiologic and metabolic stress with an increased catecholamine secretion during the first hours of life, and the catecholamines seem to counteract the inhibitory effect of insulin on lipolysis and, at least partly, to oppose the blood glucose lowering effect of insulin. Catecholamines 153-167 insulin Homo sapiens 212-219 3532664-5 1986 The IDM"s are able to respond to both physiologic and metabolic stress with an increased catecholamine secretion during the first hours of life, and the catecholamines seem to counteract the inhibitory effect of insulin on lipolysis and, at least partly, to oppose the blood glucose lowering effect of insulin. Catecholamines 153-167 insulin Homo sapiens 302-309 3946504-4 1986 Mean amniotic fluid catecholamine concentrations were lower, although not statistically so, in both insulin-dependent and gestational diabetic women than in control women. Catecholamines 20-33 insulin Homo sapiens 100-107 3936737-3 1985 Met-enkephalin, catecholamines and prostaglandin E (PGE) have all been reported to inhibit the acute insulin response to glucose in normal humans. Catecholamines 16-30 insulin Homo sapiens 101-108 2989015-1 1985 In order to evaluate the role of beta-receptor mediated effects of catecholamines in the metabolic deterioration following insulin withdrawal in insulin-dependent diabetic patients we have measured in 5 patients metabolic substrate and hormone concentrations during a 6 hours arrest of insulin infusion, without or with a simultaneous infusion of propranolol. Catecholamines 67-81 insulin Homo sapiens 123-130 6398252-7 1984 This, coupled with the brisk output of catecholamines, may have prevented the heightened sensitivity to insulin anticipated because of their hypoglucagonemia. Catecholamines 39-53 insulin Homo sapiens 104-111 3017797-0 1986 Studies on the insulin-antagonistic effect of catecholamines in normal man. Catecholamines 46-60 insulin Homo sapiens 15-22 2872232-10 1986 When insulin was increased by 752 +/- 115 microU/ml, with no change in glucose uptake, energy expenditure rose by 0.05 +/- 0.02 kcal/min, which correlated with the increase in plasma catecholamines. Catecholamines 183-197 insulin Homo sapiens 5-12 3946504-0 1986 Interrelationship between amniotic fluid C-peptide and catecholamines in the last trimester of diabetic pregnancy. Catecholamines 55-69 insulin Homo sapiens 41-50 3895816-8 1985 These findings indicate that the catecholamines counteracts the inhibitory effect of insulin on lipolysis in IDMs. Catecholamines 33-47 insulin Homo sapiens 85-92 2408480-2 1985 We examined the long-term effects of catecholamines on the insulin-sensitive 2-deoxyglucose (dGlc) uptake in cultured 3T3-L1 adipocytes. Catecholamines 37-51 insulin Homo sapiens 59-66 6389230-7 1984 Thus, early morning increases in plasma glucose concentrations and insulin requirements observed in IDDM and NIDDM may be an exaggeration of a physiologic circadian variation in hepatic insulin sensitivity induced by antecedent changes in catecholamine and/or growth hormone secretion. Catecholamines 239-252 insulin Homo sapiens 67-74 6386840-0 1984 Responses of catecholamines and other counterregulatory hormones to insulin-induced hypoglycemia in totally pancreatectomized patients. Catecholamines 13-27 insulin Homo sapiens 68-75 6391758-7 1984 The alterations in endocrine function, which accompany weight gain, may contribute to an increase in blood pressure and there appears to be a relationship between plasma insulin and catecholamine concentrations, fat cell size and the development of hypertension. Catecholamines 182-195 insulin Homo sapiens 170-177 7036752-8 1982 Cross-correlation analyses indicated that fluctuations in the catecholamines were significantly negatively correlated with oscillations in insulin and were unrelated to fluctuations in glucagon. Catecholamines 62-76 insulin Homo sapiens 139-146 6377920-3 1984 The key additional role of catecholamines in the development of stress hyperglycemia is interference with the normal feedback control of insulin and glucagon secretion by circulating glucose levels. Catecholamines 27-41 insulin Homo sapiens 137-144 6377920-5 1984 Thus, plasma insulin and glucagon levels during stress states will reflect the interaction between the opposing effects of hyperglycemia and catecholamines. Catecholamines 141-155 insulin Homo sapiens 13-20 6146190-6 1984 Insulin, but not MSF, caused a marked increase in plasma catecholamine concentrations in DU patients whereas the acid responses were the same. Catecholamines 57-70 insulin Homo sapiens 0-7 6409465-4 1983 It is likely that other counter-insulin hormones (growth hormone, catecholamines) also contribute to the pathogenesis of DKA, though their role is less well defined. Catecholamines 66-80 insulin Homo sapiens 32-39 6672070-2 1983 Concomitant with a large increase of plasma catecholamines, insulin concentration is reduced and blood glucose levels slowly increase. Catecholamines 44-58 insulin Homo sapiens 60-67 6311185-2 1983 Challenging the cells with insulin alone had no effect on either the basal rate of pyruvate carboxylation or gluconeogenesis, although it did suppress the responses to both glucagon and catecholamines. Catecholamines 186-200 insulin Homo sapiens 27-34 6337875-2 1983 When no hormones were present, N6-phenylisopropyladenosine had little or no effect; however, the nucleoside potentiated insulin inhibition of catecholamine-stimulated events, such as lipolysis, and, conversely, diminished or blocked catecholamine inhibition of insulin-stimulated processes, such as 2-deoxyglucose uptake, glucose oxidation and esterification, even under conditions where N6-phenylisopropyladenosine, alone, was ineffective in reversing catecholamine actions. Catecholamines 142-155 insulin Homo sapiens 120-127 6337875-2 1983 When no hormones were present, N6-phenylisopropyladenosine had little or no effect; however, the nucleoside potentiated insulin inhibition of catecholamine-stimulated events, such as lipolysis, and, conversely, diminished or blocked catecholamine inhibition of insulin-stimulated processes, such as 2-deoxyglucose uptake, glucose oxidation and esterification, even under conditions where N6-phenylisopropyladenosine, alone, was ineffective in reversing catecholamine actions. Catecholamines 233-246 insulin Homo sapiens 120-127 6337875-2 1983 When no hormones were present, N6-phenylisopropyladenosine had little or no effect; however, the nucleoside potentiated insulin inhibition of catecholamine-stimulated events, such as lipolysis, and, conversely, diminished or blocked catecholamine inhibition of insulin-stimulated processes, such as 2-deoxyglucose uptake, glucose oxidation and esterification, even under conditions where N6-phenylisopropyladenosine, alone, was ineffective in reversing catecholamine actions. Catecholamines 233-246 insulin Homo sapiens 120-127 6296187-6 1983 It is concluded that the stimulatory effect of catecholamines on PDE may be one reason for the failure of these agents to produce a sustained increase in the cAMP level and that the effect of insulin on PDE may be one mechanism by which insulin reduces the rate of lipolysis. Catecholamines 47-61 insulin Homo sapiens 237-244 6339003-0 1983 Effect of insulin on central catecholamines. Catecholamines 29-43 insulin Homo sapiens 10-17 6339003-1 1983 The effects of insulin on levels and turnover of catecholamines in the hypothalamus and medulla oblongata were investigated. Catecholamines 49-63 insulin Homo sapiens 15-22 6339003-4 1983 These results indicate that the effects of insulin on central catecholamines are elicited by its action in the brain. Catecholamines 62-76 insulin Homo sapiens 43-50 7040390-13 1982 These results provide evidence that exercise and catecholamines activate sugar transport by a process that requires protein synthesis for its reversal, while the increases in permeability induced by insulin and trypsin involve a different mechanism. Catecholamines 49-63 insulin Homo sapiens 199-206 7043177-0 1982 Variations in plasma glucose, insulin, growth hormone and catecholamines in response to insulin in trained and non-trained subjects. Catecholamines 58-72 insulin Homo sapiens 88-95 6130677-5 1982 It is postulated that the effect of prazosin is mediated by an increase in circulating catecholamines acting on the pancreatic beta-cell alpha 2-adrenoceptors, which are responsible for the well-known inhibitory action of alpha-adrenergic agents upon the release of insulin. Catecholamines 87-101 insulin Homo sapiens 266-273 7036752-9 1982 These fluctuations in plasma catecholamines may be related to mechanisms controlling the periodicity observed in plasma insulin and glucose. Catecholamines 29-43 insulin Homo sapiens 120-127 6122546-2 1982 Insulin is the major anabolic hormone, and its actions are antagonized by rapidly acting catabolic hormones, such as glucagon and the catecholamines, and by others such as cortisol, growth hormone and the thyroid hormones, which generally have more delayed effects. Catecholamines 134-148 insulin Homo sapiens 0-7 7020485-3 1981 2) Absolute or relative insulin lack in connection with increased catecholamine release which is know to inhibit insulin secretion. Catecholamines 66-79 insulin Homo sapiens 24-31 7018642-1 1981 We employed a delayed feeding paradigm to assess regional brain catecholamine changes associated with insulin-elicited glucoprivic feeding. Catecholamines 64-77 insulin Homo sapiens 102-109 7018642-8 1981 Turnover of catecholamines in the telencephalon was also enhanced after insulin, but the increased activity did not persist into the postglucoprivic period and, in addition, was not altered in any consistent manner by food intake. Catecholamines 12-26 insulin Homo sapiens 72-79 7014136-9 1981 There is a negative correlation between plasma catecholamine levels and reduced insulin secretion following the administration of glucose in the postoperative phase. Catecholamines 47-60 insulin Homo sapiens 80-87 7020485-4 1981 3) Decreased sensitivity and responsiveness to insulin in connection with increased levels of counter regulatory hormones (catecholamines, glucagon, growth hormone). Catecholamines 123-137 insulin Homo sapiens 47-54 6996898-7 1980 We conclude that CLON inhibits the catecholamine (but not the glucagon) rise during insulin-induced hypoglycemia. Catecholamines 35-48 insulin Homo sapiens 84-91 744568-6 1978 A modulation of catecholamine release appears to be of importance in the mode of action of alrestatin with respect to the insulin secretion and plasma glucose levels. Catecholamines 16-29 insulin Homo sapiens 122-129 6998757-0 1980 [Counterregulatory action of catecholamines on insulin-induced hypoglycemia in normal subjects and diabetics (author"s transl)]. Catecholamines 29-43 insulin Homo sapiens 47-54 7003689-1 1980 Relationships between changes in plasma water, electrolytes, insulin and catecholamines during attacks. Catecholamines 73-87 insulin Homo sapiens 61-68 478387-1 1979 The effect of insulin on blood phenylalanine, tyrosine and catecholamine levels was investigated in six phenylketonuric patients and eight normal controls. Catecholamines 59-72 insulin Homo sapiens 14-21 478387-6 1979 It appeared that insulin treatment produced some therapeutic effects in patients with smaller phenylalanine-tyrosine ratios or elevated catecholamine levels. Catecholamines 136-149 insulin Homo sapiens 17-24 7012405-0 1980 [Alteration in plasma catecholamines during insulin-induced hypoglycemia and cold pressure test in normal subjects and essential hypertension (author"s transl)]. Catecholamines 22-36 insulin Homo sapiens 44-51 7001835-3 1980 Regarding metabolic functions we found normal responses to graded exercise and insulin-induced hypoglycemia in patients with autonomic neuropathy in spite of blunted catecholamine responses, suggesting increased sensitivity of glycogen stores and adipose tissue towards the action of catecholamine in patients with autonomic neuropathy. Catecholamines 284-297 insulin Homo sapiens 79-86 28664-6 1978 Of these, an increase in insulin antagonistic hormones; among them growth hormone, catecholamines, and glucagon, seems to be of most significance. Catecholamines 83-97 insulin Homo sapiens 25-32 724670-0 1978 [Dynamics of levels of growth hormone and free fatty acids in the blood, and catecholamines in the urine of insulin-resistant and insulin-sensitive diabetes mellitus patients during insulin hypoglycemia]. Catecholamines 77-91 insulin Homo sapiens 108-115 724670-1 1978 The changes in the content of STH and FFA in the blood and of catecholamines in the urine under the effect of insulin hypoglycemia were studied in 28 insulin-sensitive and 40 insulin-resistant patients suffering from diabetes mellitus. Catecholamines 62-76 insulin Homo sapiens 110-117 724670-5 1978 It is suggested that in the insulin-resistant patients, due to reduction of the STH and catecholamine stimuli, FFA is incapable of providing the necessary energy balance at the cellular level in insulin insufficiency. Catecholamines 88-101 insulin Homo sapiens 28-35 724670-7 1978 Reduction of the FFA and catecholamine reserves in the insulin-resistant patients suffering from diabetes mellitus is postulated to be one of the main factors in the resistance pathogenesis. Catecholamines 25-38 insulin Homo sapiens 55-62 324754-5 1977 The VMH medium retained these activities even after oxidation with K3Fe (CN)6, whereas the ability of the catecholamines to inhibit insulin release and stimulate glucagon release was eliminated by this treatment. Catecholamines 106-120 insulin Homo sapiens 132-139 749914-23 1978 Catecholamines, in contrast, have their most potent effects on adipose tissue, stimulating lipolysis and fatty acid release even in the presence of insulin. Catecholamines 0-14 insulin Homo sapiens 148-155 337754-5 1977 There was no proliferation of B cells, but a retention of B cell granules, a manifestation of suppressed secretion of insulin attributed to the overproduction of catecholamines was evident. Catecholamines 162-176 insulin Homo sapiens 118-125 9301-2 1976 Effect on the response of plasma catecholamines and plasma renin activity to insulin-induced hypoglycemia. Catecholamines 33-47 insulin Homo sapiens 77-84 839844-5 1977 Suppression of insulin secretion during perfusion may be the result of increased catecholamine secretion, induced hypothermia, or heparin administration. Catecholamines 81-94 insulin Homo sapiens 15-22 826919-3 1976 When 2-deoxy-D-glucose (2-DG) was added to the perfusate, 3H-NE release was also enhanced, whereas insulin perfused at the same rate caused a delated increase in catecholamine levels as reflected by increased radioactivity. Catecholamines 162-175 insulin Homo sapiens 99-106 178982-4 1976 These findings suggest that the mechanism for enhanced plasma cAMP release during insulin-induced hypoglycemia is catecholamine dependent. Catecholamines 114-127 insulin Homo sapiens 82-89 933798-0 1976 [Insulin secretion in catecholamine-producing tumors]. Catecholamines 22-35 insulin Homo sapiens 1-8 9301-3 1976 The effect of insulin-induced hypoglycemia on the blood levels of catecholamines and renin activity has been studied in five patients with moderate hypertension before and after treatment for 3 - 8 months with penbutolol (PEN) 20 - 30 mg twice daily. Catecholamines 66-80 insulin Homo sapiens 14-21 4749029-0 1973 [Possibility of insulin inhibition during the process of mobilization of catecholamines in stress]. Catecholamines 73-87 insulin Homo sapiens 16-23 992195-8 1976 The results obtained emphasize the influence of catecholamines on insulin responsiveness, possibly constituting a major contribution to the diabetic state. Catecholamines 48-62 insulin Homo sapiens 66-73 1124146-7 1975 The data indicate that these insulin-induced changes are significantly, though variably, attributable to beta-adrenergic activity on the part of endogenous catecholamines released during insulin-induced hypoglycaemia. Catecholamines 156-170 insulin Homo sapiens 29-36 1124146-7 1975 The data indicate that these insulin-induced changes are significantly, though variably, attributable to beta-adrenergic activity on the part of endogenous catecholamines released during insulin-induced hypoglycaemia. Catecholamines 156-170 insulin Homo sapiens 187-194 124057-4 1975 A more pronounced increase in catecholamine excretion was seen in insulin therapy apparently in connection with greater variations in glycemia level. Catecholamines 30-43 insulin Homo sapiens 66-73 1229805-4 1975 These findings suggest that changes in plasma pyruvate, lactate and inorganic phosphates induced by insulin, and regarded as espressions of its peripheral metabolism, are greatly dependent on the beta-adrenergic effect of the endogenous catecholamines released during the time when blood glucose values are low. Catecholamines 237-251 insulin Homo sapiens 100-107 4679299-2 1972 Effect of catecholamines on insulin secretion in response to tolbutamide]. Catecholamines 10-24 insulin Homo sapiens 28-35 4916534-0 1970 Effect of catecholamines precursors on insulin secretion. Catecholamines 10-24 insulin Homo sapiens 39-46 5036567-0 1972 Antagonism of catecholamine inhibition of insulin secretion by methysergide. Catecholamines 14-27 insulin Homo sapiens 42-49 5152027-6 1971 Hypoglycaemia induced by insulin increased catecholamine secretion, with the adrenaline to noradrenaline ratio significantly higher than in the adrenal gland itself.6. Catecholamines 43-56 insulin Homo sapiens 25-32 14125818-0 1963 [THE BLOOD CATECHOLAMINE LEVEL OF MENTAL PATIENTS AND ITS CHANGES UNDER THE INFLUENCE OF AMINAZIN AND INSULIN]. Catecholamines 11-24 insulin Homo sapiens 102-110 5474394-0 1970 [Changes in urinary catecholamines and vanilmandelic acid under the influence of insulin in patients with hyperestrogenism]. Catecholamines 20-34 insulin Homo sapiens 81-88 5420607-5 1970 This suppression of insulin secretion is probably due to the reduced blood flow to the pancreas together with a high level of circulating catecholamines. Catecholamines 138-152 insulin Homo sapiens 20-27 5800291-0 1969 Inhibition of insulin secretion by catecholamines in pheochromocytoma. Catecholamines 35-49 insulin Homo sapiens 14-21 4299220-0 1968 Inhibition of insulin release by diazoxide and its relation to catecholamine effects in man. Catecholamines 63-76 insulin Homo sapiens 14-21 14480963-0 1962 [The relation of the hyperglycemic effect of BAL and BAL with insulin on the liberation of catecholamine from the adrenal medulla]. Catecholamines 91-104 insulin Homo sapiens 62-69 33851554-6 2021 Notably, we found that such insulin-suppressing effects on catecholamine-induced constriction are diminished following beta-adrenergic receptor blockade. Catecholamines 59-72 insulin Homo sapiens 28-35 13783908-0 1960 The effect of insulin on the catecholamines and adenine nucleotides of adrenal glands. Catecholamines 29-43 insulin Homo sapiens 14-21 13662376-0 1959 [Insulin- and reserpine-induced changes of the content of catecholamine, ascorbic acid and cholesterol of the adrenal with or without iproniazid pretreatment]. Catecholamines 58-71 insulin Homo sapiens 1-8 33522899-9 2021 As the NR4A3 could regulate the catecholamine catabolism, which could affect insulin sensitivity, we inferred that IRLnc influence IMF decomposition by regulating the expression of NR4A3. Catecholamines 32-45 insulin Homo sapiens 77-84 33463901-5 2021 The release of major stress and steroid hormones, catecholamine overload, and glucagon all participate in generating a state of insulin resistance with increased hepatic glucose output and glycogen breakdown. Catecholamines 50-63 insulin Homo sapiens 128-135 30506451-4 2019 RESULTS: Insulin withdrawal increased levels of glucose (6.1 +- 0.5 vs 18.6 +- 0.5 mmol/l), NEFA, 3-OHB (127 +- 18 vs 1837 +- 298 mumol/l), glucagon, cortisol and growth hormone and decreased HCO3- and pH, without affecting catecholamine or cytokine levels. Catecholamines 224-237 insulin Homo sapiens 9-16 31019023-10 2019 Thus, propionate may activate a catecholamine-mediated increase in insulin counter-regulatory signals, leading to insulin resistance and hyperinsulinemia, which, over time, may promote adiposity and metabolic abnormalities. Catecholamines 32-45 insulin Homo sapiens 67-74 31019023-10 2019 Thus, propionate may activate a catecholamine-mediated increase in insulin counter-regulatory signals, leading to insulin resistance and hyperinsulinemia, which, over time, may promote adiposity and metabolic abnormalities. Catecholamines 32-45 insulin Homo sapiens 114-121 29999126-2 2018 In response to an acute injury, high levels of counterregulatory hormones such as glucocorticoids and catecholamines are released causing increased hepatic gluconeogenesis and insulin resistance. Catecholamines 102-116 insulin Homo sapiens 176-183 28596236-7 2017 Insulin-stimulated glycogen synthase activity was completely ablated during hyperinsulinemic hypoglycemia, and catecholamine signaling via cAMP-dependent protein kinase and phosphorylation of inhibiting sites on glycogen synthase all increased. Catecholamines 111-124 insulin Homo sapiens 0-7 28613940-4 2017 RESULTS: Glucose intolerance and diabetes mellitus, resulting from high circulating levels of catecholamines, are mainly the product of compromised insulin secretion from the beta-cells in the pancreas, decreased glucose uptake in the peripheral tissues, and increased insulin resistance. Catecholamines 94-108 insulin Homo sapiens 148-155 28613940-4 2017 RESULTS: Glucose intolerance and diabetes mellitus, resulting from high circulating levels of catecholamines, are mainly the product of compromised insulin secretion from the beta-cells in the pancreas, decreased glucose uptake in the peripheral tissues, and increased insulin resistance. Catecholamines 94-108 insulin Homo sapiens 269-276 28028077-1 2017 In pancreatic beta-cells, pharmacological concentrations of catecholamines, including adrenaline, have been used to inhibit insulin release and explore the multiple mechanisms involved. Catecholamines 60-74 insulin Homo sapiens 124-131 26488603-7 2016 Therefore, catecholamine resistance in childhood obesity may promote insulin signaling in adipose tissue, thereby increasing lipogenesis. Catecholamines 11-24 insulin Homo sapiens 69-76 26499437-2 2016 Although catecholamine-induced lipolysis is well known to be impaired in obesity and insulin resistance, it is not known whether the effect of NPs is also altered. Catecholamines 9-22 insulin Homo sapiens 85-92 25790708-3 2014 The authors review modern concepts of AH development in patients with insulin resistance associated with enhanced blood insulin level and increased production of catecholamines playing an important role in AH pathogenesis mediated through sympathetic stimulation of heart, vessels while kidneys. Catecholamines 162-176 insulin Homo sapiens 70-77 24075245-11 2014 CONCLUSION: In SAH patients, appetite loss may be induced by lower serum ghrelin and higher serum leptin concentrations resulting from high plasma glucose and insulin levels due to a catecholamine surge following SAH. Catecholamines 183-196 insulin Homo sapiens 159-166 25904189-16 2015 As an explanation, it was hypothesized that catecholamines, which reduce insulin levels and stimulate melatonin synthesis, control insulin-melatonin interactions. Catecholamines 44-58 insulin Homo sapiens 73-80 25904189-16 2015 As an explanation, it was hypothesized that catecholamines, which reduce insulin levels and stimulate melatonin synthesis, control insulin-melatonin interactions. Catecholamines 44-58 insulin Homo sapiens 131-138 24899891-1 2014 Hyperglycemia (HG) and insulin resistance are the hallmarks of a profoundly altered metabolism in critical illness resulting from the release of cortisol, catecholamines, and cytokines, as well as glucagon and growth hormone. Catecholamines 155-169 insulin Homo sapiens 23-30 22093677-1 2012 In the present study, we explored the association of catecholamines with insulin sensitivity in "metabolically healthy but obese" (MHO) individuals, by examining the metabolic characteristics and plasma catecholamine levels in 100 obese, sedentary postmenopausal women. Catecholamines 53-67 insulin Homo sapiens 73-80 24067174-2 2013 Numerous effects of exercise, both degree and duration, dietary change, illness, stress, mountain sickness, counter-regulatory hormones, and altitude increased sympathetic output, and catecholamines have led to conflicting accounts of insulin requirement increasing or decreasing at altitude. Catecholamines 184-198 insulin Homo sapiens 235-242 24106479-2 2013 Increased circulating catecholamine and activation of the different adrenergic receptors deployed in the various organs produce important metabolic responses which include: (1) increased lipolysis and elevated levels of fatty acids in plasma, (2) increased gluconeogenesis by the liver to provide substrate for the brain, and (3) moderate inhibition of insulin release by the pancreas to conserve glucose and to shift fuel metabolism of muscle in the direction of fatty acid oxidation. Catecholamines 22-35 insulin Homo sapiens 353-360 21984048-1 2013 In the setting of acute myocardial infarction, hyperglycemia and acute insulin resistance may represent a stress response to myocardial injury mainly related to acute catecholamine release. Catecholamines 167-180 insulin Homo sapiens 71-78 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. Catecholamines 5-18 insulin Homo sapiens 151-158 22093677-1 2012 In the present study, we explored the association of catecholamines with insulin sensitivity in "metabolically healthy but obese" (MHO) individuals, by examining the metabolic characteristics and plasma catecholamine levels in 100 obese, sedentary postmenopausal women. Catecholamines 53-66 insulin Homo sapiens 73-80 22009377-7 2011 Moreover, subjects in the highest quartile of catecholamine-induced visceral lipolysis had higher levels of systolic blood pressure, estimated liver fat, plasma levels of glucose, insulin, cholesterol, LDL-cholesterol, triglycerides and apolipoprotein B and lower whole-body insulin sensitivity than those in the lowest quartile (p=0.0004-0.048). Catecholamines 46-59 insulin Homo sapiens 180-187 22009377-7 2011 Moreover, subjects in the highest quartile of catecholamine-induced visceral lipolysis had higher levels of systolic blood pressure, estimated liver fat, plasma levels of glucose, insulin, cholesterol, LDL-cholesterol, triglycerides and apolipoprotein B and lower whole-body insulin sensitivity than those in the lowest quartile (p=0.0004-0.048). Catecholamines 46-59 insulin Homo sapiens 275-282 21905812-8 2011 In addition to specific behaviours, dysregulation of the stress system through increased secretion of cortisol and catecholamines, especially in the evening hours, and in concert with concurrently elevated insulin concentrations, leads to development of central obesity, insulin resistance and the metabolic syndrome. Catecholamines 115-129 insulin Homo sapiens 271-278 21255940-4 2011 Patients with CIAP usually suffer from chronic pain and associated depression, both of which have been proposed to cause insulin resistance (IR) by such mechanisms as a sustained increase in the corticosteroids and catecholamines, and chronic low grade inflammation. Catecholamines 215-229 insulin Homo sapiens 121-128 21864755-21 2011 In very high intensity exercise (about 80% of VO(2 max)) or when high intensity exercise follows a low intensity one, there is a tendency of the BG to increase due to excessive circulating catecholamines necessitating postexercise short acting insulin. Catecholamines 189-203 insulin Homo sapiens 244-251 20801543-9 2011 This reduced suppression of insulin sensitivity in critically ill patients could be a result of saturation due to already increased levels of catecholamines and cortisol common in critically illness. Catecholamines 142-156 insulin Homo sapiens 28-35 21164481-3 2010 Although the mechanism is unclear, catecholamine signalling is thought to be disrupted in obesity, leading to the development of insulin resistance. Catecholamines 35-48 insulin Homo sapiens 129-136 20934461-10 2010 Increased pancreastatin plasma levels, correlating with catecholamines levels, have been found in insulin resistance states, such as gestational diabetes or essential hypertension. Catecholamines 56-70 insulin Homo sapiens 98-105