PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 7631779-7 1995 In the presence of insulin, cellular ATP levels were significantly increased by L-Arg, L-Glu, and L-Lys as well. Adenosine Triphosphate 37-40 insulin Homo sapiens 19-26 8058469-0 1994 ATP-induced intracellular Ca2+ signals in isolated human insulin-secreting cells. Adenosine Triphosphate 0-3 insulin Homo sapiens 57-64 7716547-4 1995 The results suggest that the sulfonylurea receptor may sense changes in ATP and ADP concentration, affect KATP channel activity, and thereby modulate insulin release. Adenosine Triphosphate 72-75 insulin Homo sapiens 150-157 11850664-0 1995 Involvement of Elevated Intracellular and Extracellular ATP in the Regulation of Insulin Secretion: Therapeutic Targets in Non-Insulin-Dependent Diabetes Mellitus. Adenosine Triphosphate 56-59 insulin Homo sapiens 81-88 11850664-10 1995 Although a powerful effect of ATP on insulin secretion was demonstrated more than 30 years ago, only recently has it been shown that beta-cells possess P(2)-purinoceptors. Adenosine Triphosphate 30-33 insulin Homo sapiens 37-44 11850664-11 1995 Extracellular ATP and its synthetic agonists are insulin secretagogues by virtue of their activation of membrane purinergic receptors which is coupled to increases in extracellular Ca(2+) influx and mobilization of Ca(2+) from internal stores resulting in insulin release from beta-cell granules. Adenosine Triphosphate 14-17 insulin Homo sapiens 49-56 11850664-11 1995 Extracellular ATP and its synthetic agonists are insulin secretagogues by virtue of their activation of membrane purinergic receptors which is coupled to increases in extracellular Ca(2+) influx and mobilization of Ca(2+) from internal stores resulting in insulin release from beta-cell granules. Adenosine Triphosphate 14-17 insulin Homo sapiens 256-263 11850664-12 1995 The physiological significance of extracellular ATP regulation of insulin secretion as well as the physiological source of these ATP pools have not yet been established. Adenosine Triphosphate 48-51 insulin Homo sapiens 66-73 7816053-6 1994 However, insulin responsiveness was restored in vesicles preloaded with either ATP or Gpp(NH)p, suggesting that insulin may act through a combination of G protein coupling and protein phosphorylation to enhance Na(+)-Ca2+ exchanger activity. Adenosine Triphosphate 79-82 insulin Homo sapiens 9-16 8003509-0 1994 Characterization of an ATP-stimulatable Ca(2+)-independent phospholipase A2 from clonal insulin-secreting HIT cells and rat pancreatic islets: a possible molecular component of the beta-cell fuel sensor. Adenosine Triphosphate 23-26 insulin Homo sapiens 88-95 7833453-5 1994 KCl-and ATP-stimulated insulin release from RINm5F-cells was attenuated by calmidazolium, whereas basal hormone secretion was unaffected. Adenosine Triphosphate 8-11 insulin Homo sapiens 23-30 7534700-2 1995 When studied at the optimal growth stage for each cell line, insulin-stimulated responses measured in cells containing kinase-defective receptors with a Lys1018-Ala1018 substitution in the ATP-binding site of the kinase domain (A/K1018). Adenosine Triphosphate 189-192 insulin Homo sapiens 61-68 1535194-1 1992 Phosphofructokinases from granulocytes isolated from insulin-resistant patients, mainly those from type II diabetics where the degree of insulin resistance was more pronounced, exhibit some changes in their kinetic behavior when assayed under allosteric conditions, characterized by an increased affinity for fructose-6-phosphate, being more resistant to ATP inhibition while it became more sensitive to citrate inhibitory effect. Adenosine Triphosphate 355-358 insulin Homo sapiens 53-60 7912059-0 1994 Roles of ATP in insulin actions. Adenosine Triphosphate 9-12 insulin Homo sapiens 16-23 8257685-1 1993 Pancreatic islets, when stimulated with D-glucose, secrete insulin by processes requiring glycolytic metabolism and generation of ATP. Adenosine Triphosphate 130-133 insulin Homo sapiens 59-66 8303861-0 1993 [The connection between insulin-dependent biosynthesis of cell membrane signal ATP with amiloride-sensitive Na+/H+-metabolism in human erythrocytes]. Adenosine Triphosphate 79-82 insulin Homo sapiens 24-31 8303861-1 1993 Plasma membrane signal ATP (psATP) was synthesized in response to the effect insulin (0.4 microgram/ml) in erythrocyte membranes, washed in 0.25 M sucrose and maintained in the mixture containing all the components required for aerobic phosphorylation. Adenosine Triphosphate 23-26 insulin Homo sapiens 77-84 8303861-3 1993 Monensin (0.3 x 10(-6) M) activated ATP formation 2-fold approximately in erythrocyte membranes both stimulated by insulin and free of the hormone effect. Adenosine Triphosphate 36-39 insulin Homo sapiens 115-122 8392837-3 1993 After incubating with insulin, insulin receptors were incubated with SH2 proteins in the presence of 100 mu ATP at 4 degrees C for 3 hr, and then immunoprecipitated and analyzed by SDS-PAGE. Adenosine Triphosphate 108-111 insulin Homo sapiens 31-38 8504095-10 1993 These observations demonstrate that: (1) both ATP and insulin regulate reaction in each autophosphorylation subdomain, (2) insulin stimulation occurs predominantly in the central and carboxy-terminal regions, and (3) autophosphorylation observed with the cytoplasmic kinase domain was similar to native insulin receptor in the absence of insulin. Adenosine Triphosphate 46-49 insulin Homo sapiens 123-130 8504095-10 1993 These observations demonstrate that: (1) both ATP and insulin regulate reaction in each autophosphorylation subdomain, (2) insulin stimulation occurs predominantly in the central and carboxy-terminal regions, and (3) autophosphorylation observed with the cytoplasmic kinase domain was similar to native insulin receptor in the absence of insulin. Adenosine Triphosphate 46-49 insulin Homo sapiens 123-130 8499439-1 1993 D-Glucose induces insulin secretion from beta-cells of pancreatic islets by processes involving glycolytic metabolism and generation of ATP. Adenosine Triphosphate 136-139 insulin Homo sapiens 18-25 8462446-6 1993 Receptor-mediated insulin internalization in HIR delta 978 cells was markedly decreased due entirely to a decrease in ATP-dependent, coated pit-mediated internalization. Adenosine Triphosphate 118-121 insulin Homo sapiens 18-25 8462446-10 1993 2) Internalization of insulin receptors by the ATP-independent noncoated invagination pathway is not regulated by residues in the insulin receptor beta-subunit distal to 978. Adenosine Triphosphate 47-50 insulin Homo sapiens 22-29 8511877-0 1993 [Synthesis of cell membrane "signal" ATP in human erythrocyte membranes stimulated by insulin as criteria of the efficacy of therapeutic plasmapheresis]. Adenosine Triphosphate 37-40 insulin Homo sapiens 86-93 8511877-1 1993 Insulin-stimulated synthesis of plasma membraneous "signal" ATP (psATP) from ADP and P(i) in oxidation coupled with that of NADH was detected in a preparation of plasma membranes from human erythrocytes; psATP was formed at concentrations of 10(-8)-10(-9) M. Effect of medicinal plasmapheresis on ability of erythrocyte membranes to produce psATP was studied. Adenosine Triphosphate 60-63 insulin Homo sapiens 0-7 1445913-0 1992 Intramolecular subunit interactions between insulin and insulin-like growth factor 1 alpha beta half-receptors induced by ligand and Mn/MgATP binding. Adenosine Triphosphate 136-141 insulin Homo sapiens 44-51 1445913-0 1992 Intramolecular subunit interactions between insulin and insulin-like growth factor 1 alpha beta half-receptors induced by ligand and Mn/MgATP binding. Adenosine Triphosphate 136-141 insulin Homo sapiens 56-63 1445913-5 1992 In the present study, we have examined this assembly process by determining the effect of ligand occupancy and Mn/MgATP binding on the dimerization of mutant and wild-type insulin and IGF-1 alpha beta half-receptors. Adenosine Triphosphate 114-119 insulin Homo sapiens 172-179 1358898-3 1992 ATP acted synergistically with insulin, IGF-1, EGF, PDGF, and various other mitogens. Adenosine Triphosphate 0-3 insulin Homo sapiens 31-38 8365551-7 1993 These results suggest that mitochondrial ATP is required for both the preservation of the basal levels of cytoskeleton-bound glycolytic enzymes and cell structure, as well as for the expression of the stimulatory action of insulin on glycolytic enzymes" binding to muscle cytoskeleton. Adenosine Triphosphate 41-44 insulin Homo sapiens 223-230 8388375-3 1993 When combined with EGF or insulin, ATP restored the greatly reduced mitogenic responsiveness of aged cells nearly to the level noted for young cells. Adenosine Triphosphate 35-38 insulin Homo sapiens 26-33 8511877-3 1993 Distinct values of basal content of ATP (without insulin) and insulin-stimulated biosynthesis of ATP were detected in volunteers. Adenosine Triphosphate 97-100 insulin Homo sapiens 62-69 8511877-4 1993 Elevation of ATP biosynthesis, in response to insulin effect, was equal to 8.029 +/- 0.163 nmol/mg of membrane protein per min. Adenosine Triphosphate 13-16 insulin Homo sapiens 46-53 8518410-9 1993 Also, a very similar insulin stimulated Km value for ATP was showed by the tyrosine kinase of insulin receptors from breast cancer and normal breast tissue (11.1 and 10.8 microM ATP, respectively). Adenosine Triphosphate 53-56 insulin Homo sapiens 21-28 8518410-9 1993 Also, a very similar insulin stimulated Km value for ATP was showed by the tyrosine kinase of insulin receptors from breast cancer and normal breast tissue (11.1 and 10.8 microM ATP, respectively). Adenosine Triphosphate 53-56 insulin Homo sapiens 94-101 8518410-9 1993 Also, a very similar insulin stimulated Km value for ATP was showed by the tyrosine kinase of insulin receptors from breast cancer and normal breast tissue (11.1 and 10.8 microM ATP, respectively). Adenosine Triphosphate 178-181 insulin Homo sapiens 21-28 8518410-9 1993 Also, a very similar insulin stimulated Km value for ATP was showed by the tyrosine kinase of insulin receptors from breast cancer and normal breast tissue (11.1 and 10.8 microM ATP, respectively). Adenosine Triphosphate 178-181 insulin Homo sapiens 94-101 1331080-11 1992 We propose that insulin binding leads to a transient receptor form that may allow ATP binding and, subsequently, autophosphorylation. Adenosine Triphosphate 82-85 insulin Homo sapiens 16-23 1385393-8 1992 The dependence of the degree of phosphorylation of insulin receptor on the ATP:ADP ratio may provide a mechanism for modulating the cellular response to insulin. Adenosine Triphosphate 75-78 insulin Homo sapiens 51-58 1535194-1 1992 Phosphofructokinases from granulocytes isolated from insulin-resistant patients, mainly those from type II diabetics where the degree of insulin resistance was more pronounced, exhibit some changes in their kinetic behavior when assayed under allosteric conditions, characterized by an increased affinity for fructose-6-phosphate, being more resistant to ATP inhibition while it became more sensitive to citrate inhibitory effect. Adenosine Triphosphate 355-358 insulin Homo sapiens 137-144 1627180-0 1992 ATP synthesis in plasma membrane enriched particles by the action of insulin and related growth factors. Adenosine Triphosphate 0-3 insulin Homo sapiens 69-76 1627180-1 1992 Early biosynthesis of short-life ATP was observed in plasma membranes of target cells stimulated by insulin or other polypeptide growth factors in the presence of all components of aerobic phosphorylation and cytochrome c. Adenosine Triphosphate 33-36 insulin Homo sapiens 100-107 1627180-4 1992 Insulin-stimulated synthesis of the plasma membrane "signal" ATP in an amount of 1-10 nM is potentized by ionophores carbonyl cyanide p-trifluorometoxyphenylhydrazone and monensin and inhibited by amiloride and ouabain. Adenosine Triphosphate 61-64 insulin Homo sapiens 0-7 1991577-4 1991 Rat liver insulin receptors were "activated" by incubation with 10 nM insulin in the presence of ATP. Adenosine Triphosphate 97-100 insulin Homo sapiens 10-17 1515169-1 1992 The hexokinase-mitochondrial acceptor theory provides a model of insulin action which unifies the metabolic effects of this hormone and suggests that these result from insulin"s stimulatory effect on mitochondrial ATP synthesis. Adenosine Triphosphate 214-217 insulin Homo sapiens 65-72 1515169-1 1992 The hexokinase-mitochondrial acceptor theory provides a model of insulin action which unifies the metabolic effects of this hormone and suggests that these result from insulin"s stimulatory effect on mitochondrial ATP synthesis. Adenosine Triphosphate 214-217 insulin Homo sapiens 168-175 1449066-4 1992 However, insulin itself inhibited ATP hydrolysis by the (Ca(2+)+Mg2+)-ATPase when it was present in the assay medium containing buffer, ATP, Mg2+ and Ca2+, the hydrolytic activity being initiated by addition of the membranes without prior phosphorylation. Adenosine Triphosphate 34-37 insulin Homo sapiens 9-16 1449066-4 1992 However, insulin itself inhibited ATP hydrolysis by the (Ca(2+)+Mg2+)-ATPase when it was present in the assay medium containing buffer, ATP, Mg2+ and Ca2+, the hydrolytic activity being initiated by addition of the membranes without prior phosphorylation. Adenosine Triphosphate 70-73 insulin Homo sapiens 9-16 1849890-0 1991 Evidence that insulin plus ATP may induce a conformational change in the beta subunit of the insulin receptor without inducing receptor autophosphorylation. Adenosine Triphosphate 27-30 insulin Homo sapiens 93-100 1849890-5 1991 Insulin at concentrations as low as 100 pM potentiated the effect of ATP; at 100 nM where insulin had its maximal effect, insulin lowered the one-half maximal inhibitory concentration of ATP to 16 +/- 6 microM. Adenosine Triphosphate 69-72 insulin Homo sapiens 0-7 1849890-5 1991 Insulin at concentrations as low as 100 pM potentiated the effect of ATP; at 100 nM where insulin had its maximal effect, insulin lowered the one-half maximal inhibitory concentration of ATP to 16 +/- 6 microM. Adenosine Triphosphate 69-72 insulin Homo sapiens 90-97 1849890-5 1991 Insulin at concentrations as low as 100 pM potentiated the effect of ATP; at 100 nM where insulin had its maximal effect, insulin lowered the one-half maximal inhibitory concentration of ATP to 16 +/- 6 microM. Adenosine Triphosphate 69-72 insulin Homo sapiens 122-129 1849890-5 1991 Insulin at concentrations as low as 100 pM potentiated the effect of ATP; at 100 nM where insulin had its maximal effect, insulin lowered the one-half maximal inhibitory concentration of ATP to 16 +/- 6 microM. Adenosine Triphosphate 187-190 insulin Homo sapiens 0-7 1849890-5 1991 Insulin at concentrations as low as 100 pM potentiated the effect of ATP; at 100 nM where insulin had its maximal effect, insulin lowered the one-half maximal inhibitory concentration of ATP to 16 +/- 6 microM. Adenosine Triphosphate 187-190 insulin Homo sapiens 90-97 1849890-5 1991 Insulin at concentrations as low as 100 pM potentiated the effect of ATP; at 100 nM where insulin had its maximal effect, insulin lowered the one-half maximal inhibitory concentration of ATP to 16 +/- 6 microM. Adenosine Triphosphate 187-190 insulin Homo sapiens 122-129 1849890-8 1991 This nonhydrolyzable analog of ATP inhibited 17A3 binding, and the effect of AMP-PNP (like ATP) was potentiated by insulin. Adenosine Triphosphate 31-34 insulin Homo sapiens 115-122 1849890-8 1991 This nonhydrolyzable analog of ATP inhibited 17A3 binding, and the effect of AMP-PNP (like ATP) was potentiated by insulin. Adenosine Triphosphate 91-94 insulin Homo sapiens 115-122 1849890-11 1991 In contrast, mutant receptor M1030, where the lysine in the ATP binding site at residue 1030 was changed to methionine, bound 17A3, but unlike either normal receptors or F3 receptors, the binding of 17A3 was not inhibited by insulin and ATP. Adenosine Triphosphate 60-63 insulin Homo sapiens 225-232 1849890-12 1991 Therefore, these studies raise the possibility that, in vivo, ATP binding in the presence of insulin may induce a conformational change in the insulin receptor beta subunit which in turn signals some of the biological effects of insulin. Adenosine Triphosphate 62-65 insulin Homo sapiens 93-100 1849890-12 1991 Therefore, these studies raise the possibility that, in vivo, ATP binding in the presence of insulin may induce a conformational change in the insulin receptor beta subunit which in turn signals some of the biological effects of insulin. Adenosine Triphosphate 62-65 insulin Homo sapiens 143-150 1849890-12 1991 Therefore, these studies raise the possibility that, in vivo, ATP binding in the presence of insulin may induce a conformational change in the insulin receptor beta subunit which in turn signals some of the biological effects of insulin. Adenosine Triphosphate 62-65 insulin Homo sapiens 143-150 1607382-10 1992 When insulin and GTP gamma S were added together, in the presence of ATP, PM GLUT4 levels were similar to levels observed when either insulin or GTP gamma S was added individually. Adenosine Triphosphate 69-72 insulin Homo sapiens 5-12 1607382-11 1992 Addition of GTP gamma S was able to overcome this ATP dependence of insulin-stimulated GLUT4 movement. Adenosine Triphosphate 50-53 insulin Homo sapiens 68-75 1607382-14 1992 We conclude that the insulin-stimulated movement of GLUT4 to the cell surface in adipocytes may require ATP early in the insulin signaling pathway and a GTP-binding protein(s) at a later step(s). Adenosine Triphosphate 104-107 insulin Homo sapiens 21-28 2026596-2 1991 Insulin stimulated pyruvate dehydrogenase activity in cells that expressed normal insulin receptors (RAT 1 HIRc, and CHO-WT and CHO-T cells), or receptors in which lysine 1018 in the ATP-binding site of the tyrosine kinase domain was exchanged for alanine (RAT 1 A/K1018 and CHO-mut cells). Adenosine Triphosphate 183-186 insulin Homo sapiens 0-7 1985910-6 1991 In contrast, the insulin response was completely absent in cells expressing large numbers of receptors that contained a mutation at the ATP-binding site that destroyed intrinsic protein tyrosine kinase activity (A/K 1018-B cells). Adenosine Triphosphate 136-139 insulin Homo sapiens 17-24 2146119-0 1990 Degradation of insulin in isolated liver endosomes is functionally linked to ATP-dependent endosomal acidification. Adenosine Triphosphate 77-80 insulin Homo sapiens 15-22 2146119-14 1990 It is concluded that ATP-dependent acidification, in part by enhancing the dissociation of the insulin-receptor complex, is required for optimum degradation of insulin within liver endosomes. Adenosine Triphosphate 21-24 insulin Homo sapiens 95-102 2146119-1 1990 The degradation of insulin in isolated liver endosomes and the relationships of this process with ATP-dependent endosomal acidification have been studied. Adenosine Triphosphate 98-101 insulin Homo sapiens 19-26 2185848-11 1990 Insulin stimulated the Vmax of the kinase reaction about 3-fold, decreased the Km for ATP from 35 +/- 5 microM (mean +/- S.E.) Adenosine Triphosphate 86-89 insulin Homo sapiens 0-7 2157363-0 1990 Separate effects of Mg2+, MgATP, and ATP4- on the kinetic mechanism for insulin receptor tyrosine kinase. Adenosine Triphosphate 26-31 insulin Homo sapiens 72-79 2157363-1 1990 The separate effects of the equilibrium species Mg2+, MgATP substrate, and ATP4- on the reaction catalyzed by insulin receptor tyrosine kinase were examined. Adenosine Triphosphate 54-59 insulin Homo sapiens 110-117 2404452-3 1990 Depletion of intracellular Ca2+ with ethylene glycol bis(beta-aminoethyl ether) N,N"-tetraacetic acid reduced the effect of ATP by 50% and completely abolished the stimulatory effect of vasopressin on adipocyte pyruvate dehydrogenase but had no effect on the stimulation induced by insulin or adenosine. Adenosine Triphosphate 124-127 insulin Homo sapiens 282-289 1966976-1 1990 The release of insulin evoked by D-glucose and other nutrient secretagogues in the pancreatic B-cell is causally linked to an increase in ATP generation rate. Adenosine Triphosphate 138-141 insulin Homo sapiens 15-22 2404452-0 1990 Insulin-like effects of ATP on adipocyte pyruvate dehydrogenase and phosphorylase. Adenosine Triphosphate 24-27 insulin Homo sapiens 0-7 2175823-1 1990 Insulin secretion from beta cells of the islets of Langerhans in the endocrine pancreas is regulated by glucose, glucose metabolites, metabolic intermediates such as ATP, acetyl CoA and reduced pyridine nucleotides, and classical second messengers. Adenosine Triphosphate 166-169 insulin Homo sapiens 0-7 33808310-3 2021 The pyruvate is subsequently metabolized to induce mitochondrial ATP and trigger the downstream insulin secretion response. Adenosine Triphosphate 65-68 insulin Homo sapiens 96-103 34987473-10 2021 ATP surplus in the pancreatic beta-cells and alpha-cells causes excess secretion of insulin and glucagon, respectively, leading to peripheral insulin resistance in the early phase of type 2 diabetes. Adenosine Triphosphate 0-3 insulin Homo sapiens 84-91 34987473-10 2021 ATP surplus in the pancreatic beta-cells and alpha-cells causes excess secretion of insulin and glucagon, respectively, leading to peripheral insulin resistance in the early phase of type 2 diabetes. Adenosine Triphosphate 0-3 insulin Homo sapiens 142-149 34987473-11 2021 In the skeletal muscle and liver, the ATP surplus contributes to insulin resistance through suppression of AMPK and activation of mTOR. Adenosine Triphosphate 38-41 insulin Homo sapiens 65-72 34825567-2 2021 Physiological opening and closing of KATPs present in pancreatic beta-cells, in response to changes in the ATP/ADP concentration ratio, are correlated with insulin release into the bloodstream. Adenosine Triphosphate 107-110 insulin Homo sapiens 156-163 35577931-3 2022 In this scenario, we have developed a novel surface plasmon resonance (SPR) method which allows for directly measuring the enzyme cooperativity for the binding of insulin in the presence of different IDE activity modulators: carnosine, ATP, and EDTA. Adenosine Triphosphate 236-239 insulin Homo sapiens 163-170 34655986-7 2021 The novelty of the finding here is that insulin receptors on the acinar cell transduce a glycolytic supply of ATP to fuel the PMCA and, thereby, link diabetes to pancreatitis through Ca2+signaling. Adenosine Triphosphate 110-113 insulin Homo sapiens 40-47 34110637-6 2021 In the present work, we have found that neurons differentiated from human neuroblastoma MSN exposed to high but nontoxic concentrations of PA generate ATP through mitochondrial metabolism, which is associated with an increase in the cytosolic Ca2+ and diminished insulin signaling in neurons. Adenosine Triphosphate 151-154 insulin Homo sapiens 263-270 34392929-3 2021 Mitochondria of the pancreatic beta cell play a central role in the secretion of insulin in response to glucose through their ability to produce ATP. Adenosine Triphosphate 145-148 insulin Homo sapiens 81-88 34180254-1 2022 SIGNIFICANCE: Mitochondria determine glucose-stimulated insulin secretion (GSIS) in pancreatic beta-cells by elevating ATP synthesis. Adenosine Triphosphate 119-122 insulin Homo sapiens 56-63 34405550-2 2021 Under normal conditions cardiac tissue utilizes roughly 70% fatty acids (FA), and 30% glucose for the production of ATP; however, during impaired metabolic conditions like insulin resistance and diabetes glucose metabolism is dysregulated and FA account for 99% of energy production. Adenosine Triphosphate 116-119 insulin Homo sapiens 172-179 35134563-6 2022 ATP and NADH, derivatives of adenosine, inhibit insulin signaling inside cells by downregulation of activities of AMPK and SIRT1, respectively. Adenosine Triphosphate 0-3 insulin Homo sapiens 48-55 35592612-0 2022 Acute bioenergetic insulin sensitivity of skeletal muscle cells: ATP-demand-provoked glycolysis contributes to stimulation of ATP supply. Adenosine Triphosphate 65-68 insulin Homo sapiens 19-26 35592612-2 2022 Insulin resistance during development of type 2 diabetes is associated with decreased ATP synthesis, but the causality of this association is controversial. Adenosine Triphosphate 86-89 insulin Homo sapiens 0-7 35592612-3 2022 In this paper, we report real-time oxygen uptake and medium acidification data that we use to quantify acute insulin effects on intracellular ATP supply and ATP demand in rat and human skeletal muscle cells. Adenosine Triphosphate 142-145 insulin Homo sapiens 109-116 35592612-3 2022 In this paper, we report real-time oxygen uptake and medium acidification data that we use to quantify acute insulin effects on intracellular ATP supply and ATP demand in rat and human skeletal muscle cells. Adenosine Triphosphate 157-160 insulin Homo sapiens 109-116 35592612-4 2022 We demonstrate that insulin increases overall cellular ATP supply by stimulating the rate of glycolytic ATP synthesis. Adenosine Triphosphate 55-58 insulin Homo sapiens 20-27 35592612-4 2022 We demonstrate that insulin increases overall cellular ATP supply by stimulating the rate of glycolytic ATP synthesis. Adenosine Triphosphate 104-107 insulin Homo sapiens 20-27 35592612-8 2022 While nitrite has a similar stimulatory effect on glycolytic ATP supply as insulin, it does not amplify insulin stimulation. Adenosine Triphosphate 61-64 insulin Homo sapiens 75-82 35134563-7 2022 ATP, ADP and AMP, the well-known energy carriers, regulate cellular responses to insulin outside cells through the purinergic receptors in cell surface. Adenosine Triphosphate 0-3 insulin Homo sapiens 81-88 35134563-8 2022 Current evidence suggests that ATP, NADH, cGAMP and uridine are potential biomarkers of insulin resistance. Adenosine Triphosphate 31-34 insulin Homo sapiens 88-95 35148993-5 2022 We show that silencing of DIMT1 in insulin-secreting cells impacted mitochondrial function, leading to lower expression of mitochondrial OXPHOS proteins, reduced oxygen consumption rate, dissipated mitochondrial membrane potential, and a slower rate of ATP production. Adenosine Triphosphate 253-256 insulin Homo sapiens 35-42 2693587-0 1989 ATP mediates both activation and inhibition of K(ATP) channel activity via cAMP-dependent protein kinase in insulin-secreting cell lines. Adenosine Triphosphate 0-3 insulin Homo sapiens 108-115 35001557-0 2022 ATP is an essential autocrine factor for pancreatic beta-cell signaling and insulin secretion. Adenosine Triphosphate 0-3 insulin Homo sapiens 76-83 35001557-1 2022 ATP has been previously identified as an autocrine signaling factor that is co-released with insulin to modulate and propagate beta-cell activity within islets of Langerhans. Adenosine Triphosphate 0-3 insulin Homo sapiens 93-100 35001557-2 2022 Here, we show that beta-cell activity and insulin secretion essentially rely on the presence of extracellular ATP. Adenosine Triphosphate 110-113 insulin Homo sapiens 42-49 2557329-8 1989 Treatment of the mixed alpha beta heterodimeric insulin and IGF-1 receptors with Mn/MgATP also resulted in the formation of cross-immunoreactive (42-46%) alpha 2 beta 2 heterotetrameric receptors. Adenosine Triphosphate 84-89 insulin Homo sapiens 48-55 2557329-9 1989 These data directly demonstrate the formation of insulin/IGF-1 hybrid receptors by both a combination of insulin plus IGF-1 or Mn/MgATP treatment of purified human placenta alpha beta heterodimeric insulin and IGF-1 half-receptors in vitro. Adenosine Triphosphate 130-135 insulin Homo sapiens 49-56 2687278-10 1989 Subsequently, the addition of insulin led to receptor autophosphorylation by virtue of the endogenous ATP pool. Adenosine Triphosphate 102-105 insulin Homo sapiens 30-37 35001557-4 2022 Extensive washing of cells or depletion of extracellular ATP levels by recombinant apyrase reduced (Ca2+ )i oscillations and insulin secretion in pancreatic cell lines and primary beta-cells. Adenosine Triphosphate 57-60 insulin Homo sapiens 125-132 35001557-6 2022 Inhibition of endogenous ecto-ATP nucleotidases increased extracellular ATP levels, along with (Ca2+ )i oscillations and insulin secretion, indicating that there is a constant supply of ATP to the extracellular space. Adenosine Triphosphate 186-189 insulin Homo sapiens 121-128 2557329-1 1989 Insulin and Mn/MgATP treatment of immunoaffinity-purified alpha beta heterodimeric insulin receptors induced the formation of an alpha 2 beta 2 heterotetrameric insulin receptor complex. Adenosine Triphosphate 15-20 insulin Homo sapiens 83-90 2557329-1 1989 Insulin and Mn/MgATP treatment of immunoaffinity-purified alpha beta heterodimeric insulin receptors induced the formation of an alpha 2 beta 2 heterotetrameric insulin receptor complex. Adenosine Triphosphate 15-20 insulin Homo sapiens 161-168 2560739-0 1989 Interaction of MnATP and peptide substrate with insulin receptor tyrosine kinase. Adenosine Triphosphate 15-20 insulin Homo sapiens 48-55 2479642-5 1989 The phosphorylation of several of these could be stimulated in vitro by the addition of insulin to a detergent extract of cells in the presence of Mn2+ and ATP. Adenosine Triphosphate 156-159 insulin Homo sapiens 88-95 2693587-1 1989 The single-channel recording technique was employed to investigate the mechanism conferring ATP sensitivity to a metabolite-sensitive K channel in insulin-secreting cells. Adenosine Triphosphate 92-95 insulin Homo sapiens 147-154 2849108-0 1988 ATP sensitizes the insulin receptor to insulin. Adenosine Triphosphate 0-3 insulin Homo sapiens 19-26 2540806-7 1989 Insulin treatment of the isolated alpha beta heterodimeric complex in the presence of IAN demonstrated that the Mn/MgATP-induce noncovalent association into the alpha 2 beta 2 heterotetrameric state was sufficient for insulin stimulation of beta-subunit autophosphorylation and exogenous substrate protein kinase activity. Adenosine Triphosphate 115-120 insulin Homo sapiens 0-7 2540806-7 1989 Insulin treatment of the isolated alpha beta heterodimeric complex in the presence of IAN demonstrated that the Mn/MgATP-induce noncovalent association into the alpha 2 beta 2 heterotetrameric state was sufficient for insulin stimulation of beta-subunit autophosphorylation and exogenous substrate protein kinase activity. Adenosine Triphosphate 115-120 insulin Homo sapiens 218-225 2691979-2 1989 After standard breakfast preceded by insulin injection such patients show a lower blood content of ATP as compared to children without metabolic signs of insulin overdosage, which may be of importance in the pathogenesis of insulin resistance development. Adenosine Triphosphate 99-102 insulin Homo sapiens 37-44 2465197-3 1989 Lectin-purified insulin receptors were labeled with 125I-labeled NAPA-DP-insulin and autophosphorylated in the presence of 500 microM unlabeled ATP. Adenosine Triphosphate 144-147 insulin Homo sapiens 16-23 2540806-0 1989 Relationship between insulin receptor subunit association and protein kinase activation: insulin-dependent covalent and Mn/MgATP-dependent noncovalent association of alpha beta heterodimeric insulin receptors into an alpha 2 beta 2 heterotetrameric state. Adenosine Triphosphate 123-128 insulin Homo sapiens 21-28 2540806-2 1989 In the presence of Mn/MgATP, insulin binding to the isolated alpha beta heterodimeric insulin receptor was found to induce the formation of a covalent disulfide-linked alpha 2 beta 2 heterotetrameric complex. Adenosine Triphosphate 22-27 insulin Homo sapiens 29-36 2540806-2 1989 In the presence of Mn/MgATP, insulin binding to the isolated alpha beta heterodimeric insulin receptor was found to induce the formation of a covalent disulfide-linked alpha 2 beta 2 heterotetrameric complex. Adenosine Triphosphate 22-27 insulin Homo sapiens 86-93 2540806-3 1989 In the absence of insulin, a noncovalent association of the alpha beta heterodimeric insulin receptor complex into an alpha 2 beta 2 heterotetrameric state required the continuous presence of both a divalent metal ion (Mn or Mg) and an adenine nucleotide (ATP, ADP, or AMPPCP). Adenosine Triphosphate 256-259 insulin Homo sapiens 85-92 3100537-0 1987 Human insulin receptors mutated at the ATP-binding site lack protein tyrosine kinase activity and fail to mediate postreceptor effects of insulin. Adenosine Triphosphate 39-42 insulin Homo sapiens 6-13 2846847-0 1988 Ion permeation and rectification in ATP-sensitive channels from insulin-secreting cells (RINm5F): effects of K+, Na+ and Mg2+. Adenosine Triphosphate 36-39 insulin Homo sapiens 64-71 2847822-4 1988 The insulin-dependent activation of IRTK was minimal in the absence of excess free divalent metal, even when the concentration of MnATP or MgATP substrate present exceeded the apparent Km of the kinase. Adenosine Triphosphate 130-135 insulin Homo sapiens 4-11 2847822-4 1988 The insulin-dependent activation of IRTK was minimal in the absence of excess free divalent metal, even when the concentration of MnATP or MgATP substrate present exceeded the apparent Km of the kinase. Adenosine Triphosphate 139-144 insulin Homo sapiens 4-11 2847822-7 1988 This enhancement of the responsiveness to insulin in the presence of both cations was not due to differing affinities of the kinase for substrate, as evidenced by nearly identical apparent Km values for MnATP and MgATP. Adenosine Triphosphate 203-208 insulin Homo sapiens 42-49 2847822-7 1988 This enhancement of the responsiveness to insulin in the presence of both cations was not due to differing affinities of the kinase for substrate, as evidenced by nearly identical apparent Km values for MnATP and MgATP. Adenosine Triphosphate 213-218 insulin Homo sapiens 42-49 3315010-1 1987 The interaction of monoclonal antibodies of three types with the ATP-labeled insulin dimer was studied by the luminescent immunocofactor method. Adenosine Triphosphate 65-68 insulin Homo sapiens 77-84 2957374-1 1987 We have previously demonstrated that the human insulin receptor, mutated in the ATP-binding domain of the beta-subunit, is kinase-defective and fails to mediate multiple post-receptor actions of insulin in stably transfected Chinese hamster ovary cells (Chou, C.-K., Dull, T. J., Russell, D. S., Gherzi, R., Lebwohl, D., Ullrich, A., and Rosen, O. M. (1987) J. Biol. Adenosine Triphosphate 80-83 insulin Homo sapiens 47-54 2822236-1 1987 In insulin-producing cells of the RINm5F line, the nonmetabolized analogue of L-leucine, 2-aminobicyclo[2,2,1]heptane-2-carboxylic acid decreases O2 consumption, lowers ATP content, and inhibits insulin release despite stimulation of both NH4 production and 14CO2 output from cells prelabeled with L-[U-14C]glutamine. Adenosine Triphosphate 169-172 insulin Homo sapiens 3-10 2822236-4 1987 These findings suggest that, in tumor as in normal islet cells, the regulation of insulin release by exogenous nutrients depends on the availability of endogenous ATP. Adenosine Triphosphate 163-166 insulin Homo sapiens 82-89 2444772-7 1987 Insulin significantly enhanced ATP-dependent Ca2+ binding to SL and SR membranes by approximately 100 and 40%, respectively. Adenosine Triphosphate 31-34 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. Adenosine Triphosphate 241-244 insulin Homo sapiens 40-47 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. Adenosine Triphosphate 241-244 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. Adenosine Triphosphate 241-244 insulin Homo sapiens 160-167 3546303-3 1987 The effect of ATP and divalent cation addition on the production of insulin mediators from liver plasma membranes was investigated. Adenosine Triphosphate 14-17 insulin Homo sapiens 68-75 3546303-4 1987 ATP (1 mM) added to liver plasma membranes in the absence of divalent cations enhanced insulin-stimulated release/generation of mediator slightly (approximately 3-fold). Adenosine Triphosphate 0-3 insulin Homo sapiens 87-94 2447283-1 1987 The single-channel current recording technique has been used to study the effects of diazoxide, tolbutamide and ATP, separately and combined, on the gating of nucleotide-regulated K+ channels in the insulin-secreting cell line RINm5F. Adenosine Triphosphate 112-115 insulin Homo sapiens 199-206 3032719-6 1987 A Lineweaver Burk analysis of the insulin stimulated receptor phosphorylation revealed that the Michaelis constant for adenosine triphosphate of the receptor kinase from phorbolester and isoprenaline treated cells was increased to greater than 100 mumol/l compared with less than 50 mumol/l for receptor from control cells. Adenosine Triphosphate 119-141 insulin Homo sapiens 34-41 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. Adenosine Triphosphate 187-209 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. Adenosine Triphosphate 187-209 insulin Homo sapiens 321-328 3527260-6 1986 That is, the dipeptide substrates inhibit insulin-activated glucose uptake to a greater extent than basal transport, and they do so even when vesicle translocation and fusion have already taken place as in ATP-depleted cells and isolated vesicles. Adenosine Triphosphate 206-209 insulin Homo sapiens 42-49 3542074-0 1986 [ATP generation by the plasma membranes of human placental cells as affected by insulin and epidermal growth factor]. Adenosine Triphosphate 1-4 insulin Homo sapiens 80-87 3542074-1 1986 Transient ATP synthesized by preparations enriched with plasmatic membranes of particles from the human placenta in the presence of insulin (4 micrograms/ml) and epidermal growth factor (1 microgram/ml) within 1 min after the addition of hormones at 30 degrees C, was isolated by means of chromatography on Dowex 1 X 8. Adenosine Triphosphate 10-13 insulin Homo sapiens 132-139 3891384-4 1985 The present work shows that each of the two growth factors, EGF and insulin, when added separately to quiescent cells was able to stimulate the phosphorylation of the organic acid-soluble compounds (Po) pool and ATP turnover. Adenosine Triphosphate 212-215 insulin Homo sapiens 68-75 3518702-3 1986 When autophosphorylation of the beta-subunit of the receptor was initiated by ATP prior to the addition of the exogenous substrate, both basal and insulin-stimulated kinase activity was increased. Adenosine Triphosphate 78-81 insulin Homo sapiens 147-154 3907719-1 1985 Insulin receptors in rat and human central nervous system have been identified by binding of 125I-insulin on purified synaptic plasma membranes; affinity labelling of receptors by chemical cross-linking 125I-insulin; or phosphorylation of receptors with [gamma-32P]ATP. Adenosine Triphosphate 265-268 insulin Homo sapiens 0-7 3896518-4 1985 Depletion of ATP stores prevents movement of proinsulin from the Golgi stacks to the secretory granules; under these conditions, the prohormone in preformed coated granules is converted to insulin, whereas that bound to the Golgi complex is not. Adenosine Triphosphate 13-16 insulin Homo sapiens 45-55 3896518-4 1985 Depletion of ATP stores prevents movement of proinsulin from the Golgi stacks to the secretory granules; under these conditions, the prohormone in preformed coated granules is converted to insulin, whereas that bound to the Golgi complex is not. Adenosine Triphosphate 13-16 insulin Homo sapiens 48-55 3017297-12 1986 The purified insulin receptor phosphorylates its own beta-subunit and exogenous protein and peptide substrates on tyrosine residues, a reaction which is insulin-sensitive, Mn2+-dependent and specific for ATP. Adenosine Triphosphate 204-207 insulin Homo sapiens 13-20 6379307-10 1984 The mean adenosine triphosphate content in the insulin group was 7.43 mumol/gm wet weight and was significantly (p less than 0.01) higher than that of the control group (4.28 mumol/gm). Adenosine Triphosphate 9-31 insulin Homo sapiens 47-54 3884627-8 1985 During the total investigation period ATP- and CP-concentrations in the insulin-group were higher compared to the control-group, whereas ADP and lactate of the control-group were above the insulin-group. Adenosine Triphosphate 38-41 insulin Homo sapiens 72-79 2988200-0 1985 [Coupling of insulin-stimulated ATP formation by preparations of plasma membrane-enriched particles with proton transport across the plasma membranes of target cells]. Adenosine Triphosphate 32-35 insulin Homo sapiens 13-20 2988200-1 1985 In the particles enriched with plasmatic membranes of target cells (human erythrocytes, skeletal muscles and adipocytes of rats) ATP was steadily formed within 1 min of incubation of the particles with insulin (4 microgram/ml) in the medium containing Tris-HCl buffer, pH 7.5, ADP, Mg2+, inorganic phosphate, NaF, during NADH oxidation in presence of cytochrome c and oxygen (30 degrees). Adenosine Triphosphate 129-132 insulin Homo sapiens 202-209 2988200-3 1985 In presence of 10(-4) M pFCCP the insulin-stimulated ATP accumulation was increased 2-fold in the particles from rat adipocytes. Adenosine Triphosphate 53-56 insulin Homo sapiens 34-41 3933479-4 1985 The onset of insulin action is preceded by a lag phase of about 20 s and found to be ATP-dependent. Adenosine Triphosphate 85-88 insulin Homo sapiens 13-20 6379307-14 1984 It is concluded that the preventive application of high doses of insulin leads to an augmented myocardial adenosine triphosphate provision and a maintained cellular energy charge during coronary ischemia. Adenosine Triphosphate 106-128 insulin Homo sapiens 65-72 6374370-0 1984 ATP and other nucleoside triphosphates inhibit the binding of insulin to its receptor. Adenosine Triphosphate 0-3 insulin Homo sapiens 62-69 6374370-1 1984 ATP, in a dose-dependent manner, inhibited the binding of 125I-insulin to its receptor in rat liver and human placental membranes. Adenosine Triphosphate 0-3 insulin Homo sapiens 63-70 6374370-8 1984 In human placental membranes, ATP had a similar effect in inhibiting 125I-insulin binding to its receptor. Adenosine Triphosphate 30-33 insulin Homo sapiens 74-81 6374370-9 1984 Moreover, ATP was active in inhibiting insulin binding to purified human placental insulin receptors at 0.01 mmol/L, a concentration 1/100 of that needed for inhibiting binding to intact membranes. Adenosine Triphosphate 10-13 insulin Homo sapiens 39-46 6374370-9 1984 Moreover, ATP was active in inhibiting insulin binding to purified human placental insulin receptors at 0.01 mmol/L, a concentration 1/100 of that needed for inhibiting binding to intact membranes. Adenosine Triphosphate 10-13 insulin Homo sapiens 83-90 6374370-10 1984 These studies indicate, therefore, that ATP and other nucleoside triphosphates influence the ability of the insulin receptor to bind insulin. Adenosine Triphosphate 40-43 insulin Homo sapiens 108-115 6374370-10 1984 These studies indicate, therefore, that ATP and other nucleoside triphosphates influence the ability of the insulin receptor to bind insulin. Adenosine Triphosphate 40-43 insulin Homo sapiens 133-140 6325418-12 1984 At [ATP] less than 0.5 mM, insulin-stimulated kinase is substantially higher with Mn2+ as the sole divalent cation, as compared to Mg2+. Adenosine Triphosphate 4-7 insulin Homo sapiens 27-34 6370244-5 1984 These results suggest that N alpha-p-tosyl-l-arginine methyl ester inhibits an initial ATP and Mn2+ dependent reaction in insulin-stimulated phosphorylation process. Adenosine Triphosphate 87-90 insulin Homo sapiens 122-129 6367210-0 1983 [Isolation and quantitative analysis of ATP, synthesized by preparations of enriched plasma membrane portions from various tissues in the presence of insulin and somatotropin]. Adenosine Triphosphate 40-43 insulin Homo sapiens 150-157 6367210-6 1983 Conditions of insulin-stimulated formation of the transient ATP in the preparation of human erythrocyte plasmatic membranes were studied. Adenosine Triphosphate 60-63 insulin Homo sapiens 14-21 6327744-0 1984 The effect of phenformin and other adenosine triphosphate (ATP)-lowering agents on insulin binding to IM-9 human cultured lymphocytes. Adenosine Triphosphate 59-62 insulin Homo sapiens 83-90 6327744-5 1984 The phenformin-induced increase in insulin binding to IM-9 cells was related to a time- and dose-dependent decrease in ATP levels. Adenosine Triphosphate 119-122 insulin Homo sapiens 35-42 6327744-6 1984 Other agents that lowered ATP levels, including antimycin, dinitrophenol, and 2-deoxyglucose, also raised insulin binding. Adenosine Triphosphate 26-29 insulin Homo sapiens 106-113 6327744-7 1984 These studies indicated, therefore, that phenformin enhances insulin binding to receptors on IM-9 cells and that this effect on insulin receptors may be related to alterations in metabolic functions that are reflected by a lowering of ATP levels. Adenosine Triphosphate 235-238 insulin Homo sapiens 128-135 6367210-1 1983 A transiently existent ATP, synthesized by the preparation enriched with plasmatic membranes of particles from rat skeletal muscles in presence of insulin 4 micrograms/ml and somatotropin 10-22 micrograms/ml within 1 min after addition of the hormones at 30 degrees, was isolated by means of chromatography on Dowex 1X8. Adenosine Triphosphate 23-26 insulin Homo sapiens 147-154 6367210-3 1983 This form of ATP was isolated from particles enriched with plasmatic membranes and from plasmatic membranes of rat adipocytes, lymphocytes and liver tissue as well as of human erythrocytes within 1 min after addition of insulin into the mixture. Adenosine Triphosphate 13-16 insulin Homo sapiens 220-227 6367210-4 1983 The highest insulin-stimulated ATP-producing activity was found in plasmatic membranes of rat adipocytes--7.45 nmole/mg/min. Adenosine Triphosphate 31-34 insulin Homo sapiens 12-19 6367210-5 1983 Radiolabelled ATP, in presence of insulin transiently synthesized from ADP and 32P, was isolated from the preparation of human erythrocyte plasmatic membranes. Adenosine Triphosphate 14-17 insulin Homo sapiens 34-41 6299798-1 1983 The insulin-stimulated cyclic AMP phosphodiesterase from liver plasma membranes is shown to be activated upon incubation with guanine nucleotides in the presence of ATP. Adenosine Triphosphate 165-168 insulin Homo sapiens 4-11 6574482-3 1983 Activation is dependent upon ATP, divalent cations (Mg2+ and Mn2+), and insulin (half-maximal activation occurs at 6-8 nM insulin). Adenosine Triphosphate 29-32 insulin Homo sapiens 122-129 6757253-7 1982 In the presence of Mn2+, insulin-stimulated phosphorylation is not detected at less than 50 microM ATP, whereas EGF-stimulated phosphorylation is well expressed at 5 microM ATP. Adenosine Triphosphate 99-102 insulin Homo sapiens 25-32 6340724-7 1983 However, when photolabeling was performed in the presence of excess adenosine 5"-(beta, gamma-imidotriphosphate), a nonhydrolyzable ATP derivative, the beta subunit of the insulin receptor was the only species protected from label incorporation. Adenosine Triphosphate 132-135 insulin Homo sapiens 172-179 6336757-2 1983 A solubilized lectin-purified preparation of insulin receptors from rat liver membranes was preincubated with or without insulin at 4 degrees C and labeled for 10 min with Mn[gamma- 32P]ATP; the receptor subunits were isolated by specific immunoprecipitation with anti-receptor antibodies, followed by gel electrophoresis in sodium dodecyl sulfate. Adenosine Triphosphate 186-189 insulin Homo sapiens 45-52 6178581-7 1982 Insulin-treated cells had approximately a 1.5-fold increased specific activity of [3H]uridine or 32Pi into the total nucleotide pool and in ATP, GTP, and UTP pools. Adenosine Triphosphate 140-143 insulin Homo sapiens 0-7 6754726-8 1982 By lowering the ATP level with 2,4-dinitrophenol, one could separately determine the insulin-like stimulatory effect of low temperature and its inhibitory effect on the transport process itself. Adenosine Triphosphate 16-19 insulin Homo sapiens 85-92 6178891-0 1982 [Determination of insulin-generated ATP in plasma membranes as an approach to the diagnosis of disturbances in postreceptor signal transmission]. Adenosine Triphosphate 36-39 insulin Homo sapiens 18-25 6918294-7 1982 Preperfusion with insulin enhanced the lactate production but resulted in the maintenance of ATP for a longer period during ischaemia, even though acidosis was enhanced. Adenosine Triphosphate 93-96 insulin Homo sapiens 18-25 6263106-6 1981 Reduction of ATP at different time points after addition of insulin blocks further activation; however, the actual state of activity is preserved. Adenosine Triphosphate 13-16 insulin Homo sapiens 60-67 6263106-8 1981 Internalization of insulin as determined in chloroquine-treated cells begins later than transport activation and is in contrast to transport activation not observable at 15 degrees C. In conclusion, the coupling is not related to internalization; it is ATP-dependent, whereas the initial binding and the activated transport system are ATP-independent. Adenosine Triphosphate 253-256 insulin Homo sapiens 19-26 6263106-8 1981 Internalization of insulin as determined in chloroquine-treated cells begins later than transport activation and is in contrast to transport activation not observable at 15 degrees C. In conclusion, the coupling is not related to internalization; it is ATP-dependent, whereas the initial binding and the activated transport system are ATP-independent. Adenosine Triphosphate 335-338 insulin Homo sapiens 19-26 7012140-14 1981 We now report that the direct addition of insulin to particulate preparations containing high affinity insulin receptors and ribosomes derived from insulin-sensitive cells (not previously exposed to insulin) stimulates incorporation of 32P from [gamma-32P]ATP into ribosomal protein S6 1.5- to 3.0-fold. Adenosine Triphosphate 256-259 insulin Homo sapiens 42-49 7012140-14 1981 We now report that the direct addition of insulin to particulate preparations containing high affinity insulin receptors and ribosomes derived from insulin-sensitive cells (not previously exposed to insulin) stimulates incorporation of 32P from [gamma-32P]ATP into ribosomal protein S6 1.5- to 3.0-fold. Adenosine Triphosphate 256-259 insulin Homo sapiens 103-110 7012140-14 1981 We now report that the direct addition of insulin to particulate preparations containing high affinity insulin receptors and ribosomes derived from insulin-sensitive cells (not previously exposed to insulin) stimulates incorporation of 32P from [gamma-32P]ATP into ribosomal protein S6 1.5- to 3.0-fold. Adenosine Triphosphate 256-259 insulin Homo sapiens 103-110 7012140-14 1981 We now report that the direct addition of insulin to particulate preparations containing high affinity insulin receptors and ribosomes derived from insulin-sensitive cells (not previously exposed to insulin) stimulates incorporation of 32P from [gamma-32P]ATP into ribosomal protein S6 1.5- to 3.0-fold. Adenosine Triphosphate 256-259 insulin Homo sapiens 103-110 702524-11 1978 On the contrary, with ATP and Mn++ this spontaneous reduction of activity was less evident; however, in the presence of insulin there was a clear and marked reduction of the transient reaction rate measured after 1.5 min of incubation. Adenosine Triphosphate 22-25 insulin Homo sapiens 120-127 7008850-1 1981 The hexose transport of insulin-pretreated (80 pM) adipocytes remained elevated for at least 45 min when the cells were depleted of ATP by treatment with dinitrophenol. Adenosine Triphosphate 132-135 insulin Homo sapiens 24-31 7008850-3 1981 Thus, a high ATP-level, but not ongoing glucose metabolism appears to be important for termination of the insulin effect shortly after dissociation of insulin from its receptor. Adenosine Triphosphate 13-16 insulin Homo sapiens 106-113 7008850-3 1981 Thus, a high ATP-level, but not ongoing glucose metabolism appears to be important for termination of the insulin effect shortly after dissociation of insulin from its receptor. Adenosine Triphosphate 13-16 insulin Homo sapiens 151-158 702526-14 1978 43:000), the following differences were found: (i) in the presence of insulin and Mn++, cyclase inactivation was higher with AMP-P(NH)P than with ATP; (ii) fluoride stimulation of the final component was more marked with ATP than with AMP-P(NH)P; (iii) cyclase stimulation by isoproterenol was slightly higher with the nucleotide analog; and (iv) GMP-P(NH)P stimulation of the final component resulted in higher activity with ATP than with AMP-P(NH)P. Adenosine Triphosphate 146-149 insulin Homo sapiens 70-77 702526-14 1978 43:000), the following differences were found: (i) in the presence of insulin and Mn++, cyclase inactivation was higher with AMP-P(NH)P than with ATP; (ii) fluoride stimulation of the final component was more marked with ATP than with AMP-P(NH)P; (iii) cyclase stimulation by isoproterenol was slightly higher with the nucleotide analog; and (iv) GMP-P(NH)P stimulation of the final component resulted in higher activity with ATP than with AMP-P(NH)P. Adenosine Triphosphate 221-224 insulin Homo sapiens 70-77 702526-14 1978 43:000), the following differences were found: (i) in the presence of insulin and Mn++, cyclase inactivation was higher with AMP-P(NH)P than with ATP; (ii) fluoride stimulation of the final component was more marked with ATP than with AMP-P(NH)P; (iii) cyclase stimulation by isoproterenol was slightly higher with the nucleotide analog; and (iv) GMP-P(NH)P stimulation of the final component resulted in higher activity with ATP than with AMP-P(NH)P. Adenosine Triphosphate 221-224 insulin Homo sapiens 70-77 1181275-4 1975 The homoarginyl and arginyl derivatives counteracted the effect of adrenalin by re-elevating the ATP level, and thus they exerted an insulin-like activity. Adenosine Triphosphate 97-100 insulin Homo sapiens 133-140 750762-0 1978 Increase in the affinity of the uridine phosphorylation system for ATP after serum or insulin activation of 3T3 fibroblasts. Adenosine Triphosphate 67-70 insulin Homo sapiens 86-93 750762-1 1978 The stimulation of uridine uptake, brought about by the addition of serum or insulin to quiescent 3T3 fibroblasts, is associated in the half-saturation concentration of the uridine phosphorylating system for the substrate ATP, with relatively little change in the maximum uptake or in the affinity for uridine. Adenosine Triphosphate 222-225 insulin Homo sapiens 77-84 179808-3 1976 The activities of the ATP-metabolising enzymes, adenylate kinase and Mg2+-adenosine triphosphatase are significantly increased by insulin within 1 h and after 4 h. Activity of succinate dehydrogenase and lactic dehydrogenase showed no change at either time interval. Adenosine Triphosphate 22-25 insulin Homo sapiens 130-137 178856-10 1976 When glucose, ATP and Ca2+ are added together a positive cooperative effect is produced with over 85% of the total insulin, added in the form of beta-granules, being released into the medium in 10 min. Adenosine Triphosphate 14-17 insulin Homo sapiens 115-122 178856-12 1976 The system responds to tolbutamide, in the presence of Ca2+ and ATP, by releasing insulin. Adenosine Triphosphate 64-67 insulin Homo sapiens 82-89 165982-7 1975 The role of membrane phosphorylation in the action of insulin is discussed in the context of experiments demonstrating a specific inhibition by ATP of insulin-mediated glucose transport, in association with the phosphorylation of two specific membrane proteins. Adenosine Triphosphate 144-147 insulin Homo sapiens 54-61 165982-7 1975 The role of membrane phosphorylation in the action of insulin is discussed in the context of experiments demonstrating a specific inhibition by ATP of insulin-mediated glucose transport, in association with the phosphorylation of two specific membrane proteins. Adenosine Triphosphate 144-147 insulin Homo sapiens 151-158 697867-0 1978 Direct effect of insulin on the labeling of isolated plasma membranes by [gamma32P] ATP. Adenosine Triphosphate 84-87 insulin Homo sapiens 17-24 66233-7 1977 The reduction in the ATP level coincided with a disappearance of the stimulatory effects of insulin on sugar transport and the hormone-sensitive phosphodiesterase. Adenosine Triphosphate 21-24 insulin Homo sapiens 92-99 66233-13 1977 These results suggest that ATP, or some other compound metabolically related to ATP, may be necessary for the actions of insulin on sugar transport and phosphodiesterase. Adenosine Triphosphate 27-30 insulin Homo sapiens 121-128 66233-13 1977 These results suggest that ATP, or some other compound metabolically related to ATP, may be necessary for the actions of insulin on sugar transport and phosphodiesterase. Adenosine Triphosphate 80-83 insulin Homo sapiens 121-128 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. Adenosine Triphosphate 0-3 insulin Homo sapiens 114-121 13974649-0 1963 Stimulation of insulin secretion in vitro by adenosine triphosphate. Adenosine Triphosphate 45-67 insulin Homo sapiens 15-22 13990873-0 1963 Stimulation of secretion of insulin by adenosine-triphosphate. Adenosine Triphosphate 39-61 insulin Homo sapiens 28-35 34021189-3 2021 The consensus model, as well as a class of currently prescribed anti-diabetic drugs, are based around the observation that glucose-evoked ATP production in beta-cells leads to closure of cell membrane ATP-gated potassium (KATP) channels, plasma membrane depolarisation, Ca2+ influx, and finally the exocytosis of insulin granules. Adenosine Triphosphate 138-141 insulin Homo sapiens 313-320 33939443-3 2021 Red blood cell (RBC)-derived ATP is a recognized stimulus of blood flow, and multiple studies suggest that C-peptide, a hormone secreted in equimolar amounts with insulin from the pancreatic beta-cells, can stimulate that release when delivered by albumin and in combination with Zn2+. Adenosine Triphosphate 29-32 insulin Homo sapiens 107-116 33939443-8 2021 The RBC-derived ATP increased in the presence of a leptin/C-peptide/Zn2+ addition, in a concentration-dependent manner. Adenosine Triphosphate 16-19 insulin Homo sapiens 58-67 33939443-9 2021 Control RBCs ATP release increased (71 +- 5.6%) in the presence of C-peptide and Zn2+, which increased further to (94 +- 5.6%) in the presence of Zn2+, C-peptide, and leptin. Adenosine Triphosphate 13-16 insulin Homo sapiens 67-76 1216187-0 1975 Reversal of insulin resistance by in vivo infusion of ATP in experimental shock. Adenosine Triphosphate 54-57 insulin Homo sapiens 12-19 13552752-0 1958 [Effects of insulin and reserpine on the adrenalin and ATP content of the chromatic granules of the adrenal medulla]. Adenosine Triphosphate 55-58 insulin Homo sapiens 12-19 14945390-0 1952 [The action of insulin and diphosphothiamine on ATP of the liver]. Adenosine Triphosphate 48-51 insulin Homo sapiens 15-22 34047935-5 2021 In this review, multidisciplinary literature is integrated to evaluate ATP as a primary signal for insulin resistance. Adenosine Triphosphate 71-74 insulin Homo sapiens 99-106 34047935-6 2021 The ATP production is elevated in insulin-sensitive cells under obese conditions independent of energy demand, which we have named "mitochondrial overheating." Adenosine Triphosphate 4-7 insulin Homo sapiens 34-41 34047935-8 2021 The ATP overproduction contributes to the systemic insulin resistance through several mechanisms, such as inhibition of AMPK, induction of mTOR, hyperinsulinemia, hyperglucagonemia, and mitochondrial dysfunction. Adenosine Triphosphate 4-7 insulin Homo sapiens 51-58 34047935-12 2021 Therefore, ATP may represent the primary signal of insulin resistance in the cellular protective response to the substrate oversupply. Adenosine Triphosphate 11-14 insulin Homo sapiens 51-58 33725905-3 2021 An impairment of ATP production in pancreatic beta cells is regarded as the main cause of the insulin secretory disorder in patients with MDM, and these patients require insulin replacement therapy early after the diagnosis. Adenosine Triphosphate 17-20 insulin Homo sapiens 94-101 33143630-6 2021 A permanent increase of ATP/ADP ratio leads to a constant inhibition of K+ ATP-channel and therefore a continuous insulin secretion accompanied by an increase in ROS. Adenosine Triphosphate 24-27 insulin Homo sapiens 114-121 33199991-2 2020 Mitochondria uses pyruvate to produce ATP as an intermediate link between glucose intake and insulin secretion in beta-cells, in a process known as glucose-stimulated insulin secretion (GSIS). Adenosine Triphosphate 38-41 insulin Homo sapiens 93-100 33327428-5 2020 We demonstrate that reduced mitochondrial ATP production is linked with the observed defects in insulin and glucagon secretion by utilizing computational modeling approach. Adenosine Triphosphate 42-45 insulin Homo sapiens 96-103 33199991-2 2020 Mitochondria uses pyruvate to produce ATP as an intermediate link between glucose intake and insulin secretion in beta-cells, in a process known as glucose-stimulated insulin secretion (GSIS). Adenosine Triphosphate 38-41 insulin Homo sapiens 167-174 33147479-1 2020 The consensus model of glucose-stimulated insulin secretion (GSIS) holds that ATP generation by oxidative phosphorylation directly regulates KATP channel activity and thus insulin granule release, a concept inconsistent with bioenergetic principles. Adenosine Triphosphate 78-81 insulin Homo sapiens 42-49 33259010-10 2020 The treatment also restored the mitochondrial biogenesis in the insulin-resistant macrophages by improving ATP production, oxygen consumption, mitochondrial content and potential, while it promoted the expression of mitochondrial biogenesis regulator genes such as TFAM, PGC-1alpha and PPAR-gamma. Adenosine Triphosphate 107-110 insulin Homo sapiens 64-71 33147479-1 2020 The consensus model of glucose-stimulated insulin secretion (GSIS) holds that ATP generation by oxidative phosphorylation directly regulates KATP channel activity and thus insulin granule release, a concept inconsistent with bioenergetic principles. Adenosine Triphosphate 78-81 insulin Homo sapiens 172-179 33147484-6 2020 Our findings support a compartmentalized model of beta cell metabolism in which PK locally generates the ATP/ADP required for insulin secretion. Adenosine Triphosphate 105-108 insulin Homo sapiens 126-133 33101053-2 2020 We hypothesized that palmitate-induced ATP release from skeletal muscle cells may increase inflammatory cytokine production and contribute to insulin/anabolic resistance in an autocrine/paracrine manner. Adenosine Triphosphate 39-42 insulin Homo sapiens 142-149 32894309-4 2020 Genetic evidence flowing from both monogenic forms of diabetes and genome-wide association studies for the more common type 2 diabetes, supports the importance for normal glucose-stimulated insulin secretion of metabolic signalling via altered ATP generation, while also highlighting unsuspected roles for Zn2+ storage, intracellular lipid transfer and other processes. Adenosine Triphosphate 244-247 insulin Homo sapiens 190-197 32245801-6 2020 We propose that in those states, exacerbated beta-cell activity due to increased insulin demand and increased cell death produce high levels of ATP that downregulate purinergic receptor expression. Adenosine Triphosphate 144-147 insulin Homo sapiens 81-88 32904391-5 2020 Mitochondrial dysfunction and mtDNA variations during insulin resistance may be connected with a change in ATP levels, generation of ROS, mitochondrial division/fusion and mitophagy. Adenosine Triphosphate 107-110 insulin Homo sapiens 54-61 33552476-5 2020 In the present opinion article, we highlight evidence that IR activity and free intracellular Ca 2+ concentration [Ca 2+] i form a double-negative regulatory feedback loop controlling insulin sensitivity, in which mitochondria play a key role, being involved in adenosine triphosphate (ATP) synthesis and IR activation. Adenosine Triphosphate 286-289 insulin Homo sapiens 184-191 32663099-8 2020 Further analysis suggested an involvement of decreased AMP-to-ATP ratios in the insulin-induced inhibition of AMPK activity, whereas a possible contribution of phosphodiesterases was excluded. Adenosine Triphosphate 62-65 insulin Homo sapiens 80-87 32820316-7 2020 With a focus on the energy surplus in obesity, we explore the mechanism of insulin resistance induced by ATP elevation and provide an answer to the contradiction between the new experimental results and the traditional viewpoint of intracellular ATP. Adenosine Triphosphate 105-108 insulin Homo sapiens 75-82 32820316-7 2020 With a focus on the energy surplus in obesity, we explore the mechanism of insulin resistance induced by ATP elevation and provide an answer to the contradiction between the new experimental results and the traditional viewpoint of intracellular ATP. Adenosine Triphosphate 246-249 insulin Homo sapiens 75-82 32824903-13 2020 On the one part, an increased reliance of cardiomyocytes on the oxidation of free fatty acids, typical for insulin-resistant states, is associated with both a lower yield of ATP per oxygen molecule and lesser availability of ATP for contraction, which might decrease energetic efficiency of the first and second step of energy transfer from MVO2 to EW. Adenosine Triphosphate 174-177 insulin Homo sapiens 107-114 32824903-13 2020 On the one part, an increased reliance of cardiomyocytes on the oxidation of free fatty acids, typical for insulin-resistant states, is associated with both a lower yield of ATP per oxygen molecule and lesser availability of ATP for contraction, which might decrease energetic efficiency of the first and second step of energy transfer from MVO2 to EW. Adenosine Triphosphate 225-228 insulin Homo sapiens 107-114 32302669-3 2020 In this study, by using live cell imaging and biochemical approaches, we demonstrate that IFN-gamma plus high glucose augment endothelial connexin43 hemichannel activity, resulting in the increase of ATP release, ATP-mediated Ca2+ dynamics and production of nitric oxide and superoxide anion, as well as impaired insulin-mediated uptake and intercellular diffusion of glucose and cell survival. Adenosine Triphosphate 213-216 insulin Homo sapiens 313-320 31912945-2 2020 Insulin secretion from islet beta-cells is primarily controlled by mitochondrial ATP generation in response to elevations in extracellular glucose. Adenosine Triphosphate 81-84 insulin Homo sapiens 0-7 32301059-5 2020 We found that ticagrelor treatment significantly prevented depolarization of mitochondrial membrane potential and increases in reactive oxygen species with a marked increase in the ATP level in insulin-resistant H9c2 cells. Adenosine Triphosphate 181-184 insulin Homo sapiens 194-201 32434996-5 2020 Upon OIL intervention, preclamp hepatic and whole-body insulin sensitivity markedly decreased by 28% and 27%, respectively, along with 61% higher rates of hepatic gluconeogenesis and 32% lower rates of net glycogenolysis, while hepatic triglyceride and ATP concentrations did not differ from VCL. Adenosine Triphosphate 253-256 insulin Homo sapiens 55-62 32027066-2 2020 These genes encode the subunits of the beta-cell ATP sensitive potassium channel, a key component of the glucose-stimulated insulin secretion pathway. Adenosine Triphosphate 49-52 insulin Homo sapiens 124-131 31591827-3 2019 Since DAG activates protein kinase D1 (PKD1) to potentiate glucose-stimulated insulin release, we hypothesized that autocrine ATP signaling activates downstream PKD1 to regulate insulin secretion. Adenosine Triphosphate 126-129 insulin Homo sapiens 78-85 31644972-5 2020 However, the reduction of glucose transport into the muscle cells due to insulin resistance / insufficiency, leads to reduction in the ATP producing capacity of the mitochondria. Adenosine Triphosphate 135-138 insulin Homo sapiens 73-80 31591827-1 2019 Along with insulin, beta-cells co-secrete the neurotransmitter ATP which acts as a positive autocrine signal via P2Y1 receptors to activate phospholipase C and increase the production of diacylglycerol (DAG). Adenosine Triphosphate 63-66 insulin Homo sapiens 11-18 31591827-3 2019 Since DAG activates protein kinase D1 (PKD1) to potentiate glucose-stimulated insulin release, we hypothesized that autocrine ATP signaling activates downstream PKD1 to regulate insulin secretion. Adenosine Triphosphate 126-129 insulin Homo sapiens 178-185 31039435-6 2019 Finally, insulin is co-secreting with other components that are present in the secretory granules, including C-peptide, ATP, gamma-aminobutyric acid (GABA), ghrelin and amylin. Adenosine Triphosphate 120-123 insulin Homo sapiens 9-16 31551756-11 2019 In this situation, the insulin receptor pathway would be able to fine tune the mitochondrial biogenesis in neuronal cells, regulation the adenosine triphosphate/adenosine diphosphate intracellular balance, and becoming a key factor involved in the preservation of the synaptic connexions and neuronal plasticity. Adenosine Triphosphate 138-160 insulin Homo sapiens 23-30 31527268-5 2019 We found that the G protein-coupled receptor agonists adenosine triphosphate (ATP) and histamine promoted rapid increases in eNOS phosphorylation, as did the receptor tyrosine kinase agonists insulin and Vascular Endothelial Growth Factor (VEGF). Adenosine Triphosphate 78-81 insulin Homo sapiens 192-199 30912960-0 2019 Chronic fructose renders pancreatic beta-cells hyper-responsive to glucose-stimulated insulin secretion through extracellular ATP signaling. Adenosine Triphosphate 126-129 insulin Homo sapiens 86-93 30763000-0 2019 [Exposure of beta-cells to chronic fructose potentiates glucose-stimulated insulin secretion through ATP signaling]. Adenosine Triphosphate 101-104 insulin Homo sapiens 75-82 31092879-4 2019 Simvastatin (10 microM) reduced membrane integrity and ATP content in myotubes treated for 24 hours, which could be prevented and partially reversed concentration- and time-dependently by insulin. Adenosine Triphosphate 55-58 insulin Homo sapiens 188-195 30926624-1 2019 Mitochondria play an essential role in regulating insulin secretion from beta cells by providing the ATP needed for the membrane depolarization that results in voltage-dependent Ca2+ influx and subsequent insulin granule exocytosis. Adenosine Triphosphate 101-104 insulin Homo sapiens 50-57 30763000-3 2019 Our results reveal that chronic fructose induces extracellular ATP signaling in the beta-cell, resulting in the potentiation of glucose-stimulated insulin secretion. Adenosine Triphosphate 63-66 insulin Homo sapiens 147-154 30528280-8 2019 Importantly, glucose and insulin suppress mitochondrial activity (i.e. ATP-linked respiration) significantly only in preadipocytes of female donors, reflecting their trends towards higher insulin sensitivity. Adenosine Triphosphate 71-74 insulin Homo sapiens 25-32 31827016-3 2019 Furthermore, a Japanese boy with insulin resistance and acanthosis nigricans was found to be heterozygous for a mutation of the insulin receptor gene that resulted in the replacement of glycine-996 with valine in the ATP binding site of the receptor. Adenosine Triphosphate 217-220 insulin Homo sapiens 33-40 30535784-5 2019 Several recent studies indicate that reduced insulin-stimulated ATP synthesis and reduced expression of mitochondrial enzymes and PPAR-gamma coactivator, in high fat feeding (lipid overload) are associated with insulin resistance. Adenosine Triphosphate 64-67 insulin Homo sapiens 45-52 30535784-5 2019 Several recent studies indicate that reduced insulin-stimulated ATP synthesis and reduced expression of mitochondrial enzymes and PPAR-gamma coactivator, in high fat feeding (lipid overload) are associated with insulin resistance. Adenosine Triphosphate 64-67 insulin Homo sapiens 211-218 29218453-10 2018 Since GLTx markedly diminished the mitochondrial membrane potential and cellular ATP content, lack of ATP is assumed to decrease insulin biosynthesis. Adenosine Triphosphate 102-105 insulin Homo sapiens 129-136 29369529-16 2018 Another hypothesis involves the mammalian target of rapamycin complex 1 (mTORC1), which is activated by BCAA, as well as by insulin and glucose via cellular ATP availability. Adenosine Triphosphate 157-160 insulin Homo sapiens 124-131 30025187-9 2018 Additionally, insulin resistance in LECs impaired mitochondrial function by decreasing basal-, maximal-, and ATP-linked OCRs and activated NF-kappaB nuclear translocation coupled with increased pro-inflammatory signaling. Adenosine Triphosphate 109-112 insulin Homo sapiens 14-21 28938426-10 2017 Furthermore, a sustained stimulation of NMDARs impairs beta-cell insulin secretion through decrease of pancreatic duodenal homeobox-1 (Pdx-1) and adenosine triphosphate synthesis. Adenosine Triphosphate 146-168 insulin Homo sapiens 65-72 29261667-5 2017 RESULTS: Increased plasma FFA (440+-93 mumol/Lto 997+-242 muM, p<0.001) decreased insulin-stimulated total glucose disposal (TGD) by 25% (p = 0.008), impaired suppression of endogenous glucose production (p = 0.01), and reduced mitochondrial ATP synthesis with complex 1 (34%, p<0.05) and complex 2 (30%, p<0.05) substrates. Adenosine Triphosphate 245-248 insulin Homo sapiens 85-92 28165182-2 2017 GDH is an allosterically regulated enzyme responsible for amino acid-mediated insulin secretion via the oxidative deamination of glutamate to 2-oxoglutarate, leading to ATP production and insulin release. Adenosine Triphosphate 169-172 insulin Homo sapiens 78-85 30673191-7 2018 Biological role of insulin consists in the formation of the biological function of locomotion, i.e., movement arising from contraction of striated myocytes provided with substrates (FA and glucose) for energy production as macroergic ATP. Adenosine Triphosphate 234-237 insulin Homo sapiens 19-26 28185435-7 2017 I suggest that this increasing ATP deficit is communicated by progressive increases in mitochondrial ROS generation, which signals inhibition of mitophagy via ROS-dependent activation of insulin signaling. Adenosine Triphosphate 31-34 insulin Homo sapiens 187-194 28655753-8 2017 ATP and Pi are 10-100 times greater than ADP, so the increase in energy state is primarily through decrease in ADP The decrease in ADP is considered responsible for altering ion channel conductance and releasing insulin. Adenosine Triphosphate 0-3 insulin Homo sapiens 212-219 30620519-8 2017 This pool, potentially unlimited in number of insulin-dependent subcutaneous adipocytes, is destined to provide with energy substrates produced by adenosine triphosphate only one biological function - a function of locomotion, motion at the expense of contraction of cross-striated skeletal myocytes. Adenosine Triphosphate 147-169 insulin Homo sapiens 46-53 27955719-5 2017 In the presence of 5.5 mM of glucose (Low), a comparison of 10 versus 20 mug/ml insulin showed that high insulin enhanced GC proliferation but exhausted glucose from the medium, which resulted in low energy status including lipid and adenosine triphosphate of the oocyte. Adenosine Triphosphate 234-256 insulin Homo sapiens 105-112 27796771-14 2016 Chromatography of IMS demonstrated an ATP-dependent protease that degraded insulin, similar to described by Sitte et al. Adenosine Triphosphate 38-41 insulin Homo sapiens 75-82 28855921-3 2017 Insulin release from pancreatic beta-cells is mainly regulated by intracellular ATP-generating metabolic pathways. Adenosine Triphosphate 80-83 insulin Homo sapiens 0-7 27473535-7 2016 This market-economic control of myocellular bioenergetics offers a mechanism by which insulin-signalling deficiency can cause apparent mitochondrial dysfunction, as insulin resistance lowers skeletal muscle anabolism and thus dampens ATP demand and, consequently, oxidative ATP synthesis. Adenosine Triphosphate 234-237 insulin Homo sapiens 86-93 27473535-7 2016 This market-economic control of myocellular bioenergetics offers a mechanism by which insulin-signalling deficiency can cause apparent mitochondrial dysfunction, as insulin resistance lowers skeletal muscle anabolism and thus dampens ATP demand and, consequently, oxidative ATP synthesis. Adenosine Triphosphate 274-277 insulin Homo sapiens 86-93 27561923-1 2016 OBJECTIVE: Insulin resistance is associated with mitochondrial dysfunction and decreased ATP synthesis. Adenosine Triphosphate 89-92 insulin Homo sapiens 11-18 27561923-4 2016 The current study examined the effect of improved insulin sensitivity with dapagliflozin on 1) mitochondrial ATP synthesis and 2) substrate oxidation rates and ketone production. Adenosine Triphosphate 109-112 insulin Homo sapiens 50-57 27020404-3 2016 The contribution of mitochondrial dysfunction to impairments in insulin metabolic signaling is also suggested by gene array analysis showing that reductions in gene expression, that regulates mitochondrial ATP production, are associated with insulin resistance and type 2 diabetes mellitus. Adenosine Triphosphate 206-209 insulin Homo sapiens 64-71 27589991-3 2016 Glucose triggers insulin secretion through the well-described pathway of ATP-driven closure of ATP-sensitive potassium channels (KATP), depolarization of the plasma membrane, and opening of the voltage-dependent Ca2+ channels (VDCC). Adenosine Triphosphate 73-76 insulin Homo sapiens 17-24 27107769-5 2016 Upon insulin stimulation, increases in network formation, mitochondrial DNA (mtDNA) content, and ATP production were observed only in cybrid D4. Adenosine Triphosphate 97-100 insulin Homo sapiens 5-12 31529916-10 2016 Under effect of insulin, mitochondria form acetyl-KoA and synthesize ATP from oleic mono-saturated fatty acids but not from palmitic saturated fatty acids. Adenosine Triphosphate 69-72 insulin Homo sapiens 16-53 27195491-11 2016 This lack of beta-cell ATP had functional consequences by negatively affecting both glucose-stimulated membrane depolarisation and ATP-dependent insulin granule exocytosis. Adenosine Triphosphate 23-26 insulin Homo sapiens 145-152 27195491-11 2016 This lack of beta-cell ATP had functional consequences by negatively affecting both glucose-stimulated membrane depolarisation and ATP-dependent insulin granule exocytosis. Adenosine Triphosphate 131-134 insulin Homo sapiens 145-152 31536689-2 2016 The counter-insulin effect of surplus of palmitic fatty acid in food is implemented under: a) formation in vivo of palmitic type of fatty acids metabolism with deficiency of substrate for ATP synthesis and permanent shortage of energy for accomplishment of biologic functions; b) compensatory activation of biologic function of adaptation, biologic reaction of compensation. Adenosine Triphosphate 188-191 insulin Homo sapiens 12-19 26356530-7 2015 Our study uncovers a previously unknown mechanism for the insulin and mTOR pathway in regulation of glycolytic ATP production and cellular redox potential via HDAC3-mediated PGK1 deacetylation. Adenosine Triphosphate 111-114 insulin Homo sapiens 58-65 26236179-3 2015 One of these detectors is AMPK (5" AMP-activated protein kinase), a protein kinase activated by ATP deficiency but also by several natural substances such as polyphenols or synthetic molecules like metformin, used in the treatment of insulin resistance. Adenosine Triphosphate 96-99 insulin Homo sapiens 234-241 25078605-7 2015 CONCLUSION: Our results suggest that mapping the kinetics and unidirectional fluxes from Pi-to-ATP in both the anterior and posterior muscles of the lower leg is feasible at ultra-high field and may provide useful insights for the study of insulin resistance, diabetes and aging. Adenosine Triphosphate 95-98 insulin Homo sapiens 240-247 24641631-2 2014 Insulin regulates glucose metabolism by phosphorylation-dependent signaling and has been shown to stimulate ATP synthesis in human skeletal muscle. Adenosine Triphosphate 108-111 insulin Homo sapiens 0-7 25866366-3 2015 Furthermore, hepatic ATP content may be related to insulin resistance and IHL. Adenosine Triphosphate 21-24 insulin Homo sapiens 51-58 25552662-0 2015 Mechanisms of C-peptide-mediated rescue of low O2-induced ATP release from erythrocytes of humans with type 2 diabetes. Adenosine Triphosphate 58-61 insulin Homo sapiens 14-23 25552662-4 2015 To begin to investigate the mechanisms by which C-peptide influences low O2-induced ATP release, erythrocytes from healthy humans and humans with DM2 were exposed to reduced O2 in a thin-film tonometer, and ATP release under these conditions was compared with release during normoxia. Adenosine Triphosphate 84-87 insulin Homo sapiens 48-57 25552662-5 2015 We determined that 1) low O2-induced ATP release from DM2 erythrocytes is rescued by C-peptide in the presence and absence of insulin, 2) the signaling pathway activated by C-peptide in human erythrocytes involves PKC, as well as soluble guanylyl cyclase (sGC) and 3) inhibitors of cGMP degradation rescue low O2-induced ATP release from DM2 erythrocytes. Adenosine Triphosphate 37-40 insulin Homo sapiens 173-182 25552662-5 2015 We determined that 1) low O2-induced ATP release from DM2 erythrocytes is rescued by C-peptide in the presence and absence of insulin, 2) the signaling pathway activated by C-peptide in human erythrocytes involves PKC, as well as soluble guanylyl cyclase (sGC) and 3) inhibitors of cGMP degradation rescue low O2-induced ATP release from DM2 erythrocytes. Adenosine Triphosphate 321-324 insulin Homo sapiens 173-182 25552662-7 2015 In addition, since both C-peptide and phosphodiesterase 5 inhibitors rescue low O2-induced ATP release from erythrocytes of humans with DM2, their administration to humans with DM2 could aid in the treatment and/or prevention of the vascular disease associated with this condition. Adenosine Triphosphate 91-94 insulin Homo sapiens 24-33 24841383-6 2015 IGF-1 and insulin also rescued energy levels in HD peripheral cells, as evaluated by increased ATP and phosphocreatine, and decreased lactate levels. Adenosine Triphosphate 95-98 insulin Homo sapiens 10-17 25080497-0 2014 Low O2-induced ATP release from erythrocytes of humans with type 2 diabetes is restored by physiological ratios of C-peptide and insulin. Adenosine Triphosphate 15-18 insulin Homo sapiens 129-136 25080497-3 2014 Both C-peptide and insulin individually inhibit low O2-induced ATP release from healthy human erythrocytes, yet when coadministered at physiological concentrations and ratios, no inhibition is seen. Adenosine Triphosphate 63-66 insulin Homo sapiens 19-26 24867955-5 2014 Like insulin-dependent activation, IR-TM requires that IR have a competent ATP-binding site and kinase activation loop. Adenosine Triphosphate 75-78 insulin Homo sapiens 5-12 25832429-9 2015 Moreover, ZJ001 increased the ADP/ATP ratio in insulin-treated hepatocytes. Adenosine Triphosphate 34-37 insulin Homo sapiens 47-54 25200303-8 2014 Excitatory ATP may synchronize beta-cells with delta-cells to generate coinciding pulses of insulin and somatostatin. Adenosine Triphosphate 11-14 insulin Homo sapiens 92-99 24353180-2 2014 Impaired muscle mitochondrial function (reduced ATP synthesis) also has been described in insulin-resistant T2DM and obese subjects. Adenosine Triphosphate 48-51 insulin Homo sapiens 90-97 24353180-10 2014 Reduction in plasma FFA in obese NGT and T2DM individuals improves mitochondrial ATP synthesis rate, indicating that the mitochondrial defect in insulin-resistant individuals is, at least in part, reversible. Adenosine Triphosphate 81-84 insulin Homo sapiens 145-152 24781254-5 2014 This review describes the miRNAs that control insulin release and production by regulating cellular membrane electrical excitability (ATP:ADP ratio), insulin granule exocytosis, insulin synthesis in beta-cells, and beta-cell fate and islet mass formation. Adenosine Triphosphate 134-137 insulin Homo sapiens 46-53 24134160-0 2014 Intracellular and extracellular adenosine triphosphate in regulation of insulin secretion from pancreatic beta cells (beta). Adenosine Triphosphate 32-54 insulin Homo sapiens 72-79 24601882-6 2014 Inhibition of mitochondrial AKT attenuated insulin response, indicating that insulin regulation of ATP production required mitochondrial AKT1 signaling. Adenosine Triphosphate 99-102 insulin Homo sapiens 43-50 24601882-6 2014 Inhibition of mitochondrial AKT attenuated insulin response, indicating that insulin regulation of ATP production required mitochondrial AKT1 signaling. Adenosine Triphosphate 99-102 insulin Homo sapiens 77-84 24462282-4 2014 RESULTS: Compared to control islets, human islets cultured with high glucose showed a reduced glucose-stimulated insulin secretion that was associated with lower ATP levels and a lower ATP/ADP ratio. Adenosine Triphosphate 162-165 insulin Homo sapiens 113-120 24462282-4 2014 RESULTS: Compared to control islets, human islets cultured with high glucose showed a reduced glucose-stimulated insulin secretion that was associated with lower ATP levels and a lower ATP/ADP ratio. Adenosine Triphosphate 185-188 insulin Homo sapiens 113-120 24134160-4 2014 In this review, the recent findings regarding the role and mechanism of ATP synthesis and release in regulation of insulin secretion from pancreatic beta cells will be summarized and discussed. Adenosine Triphosphate 72-75 insulin Homo sapiens 115-122 25070829-6 2014 Glucose metabolism dependent GSIS is linked with the production of ATP that is needed for K+ATP channel inhibition and influx of calcium, necessary for insulin granule exocytosis. Adenosine Triphosphate 67-70 insulin Homo sapiens 152-159 24212054-2 2014 The imported glucose is either stored or broken down, as insulin stimulates glycogenesis and ATP synthesis. Adenosine Triphosphate 93-96 insulin Homo sapiens 57-64 24212054-8 2014 Our data improve the mechanistic understanding of insulin-stimulated ATP synthesis, and reveal a hitherto undisclosed insulin sensitivity of cellular bioenergetics that suggests a novel way of detecting insulin responsiveness of cells. Adenosine Triphosphate 69-72 insulin Homo sapiens 50-57 23452341-4 2014 Type 2 diabetes in obese subjects is linked to excess liver fat, whilst there is a negative correlation between hepatic ATP content and insulin resistance. Adenosine Triphosphate 120-123 insulin Homo sapiens 136-143 24009260-7 2014 Three hours of insulin treatment increased Opa-1 protein levels, promoted mitochondrial fusion, increased mitochondrial membrane potential, and elevated both intracellular ATP levels and oxygen consumption in cardiomyocytes in vitro and in vivo. Adenosine Triphosphate 172-175 insulin Homo sapiens 15-22 24559912-6 2014 Glucose metabolism is central to generation of MCFs that lead to insulin release, most notably ATP. Adenosine Triphosphate 95-98 insulin Homo sapiens 65-72 23983178-8 2013 To tackle this intriguing problem, a South Korean group recently combined ATP-affinity chromatography and gel-assisted digestion to identify proteins, differentially expressed upon treatment of 3T3-L1 adipocytes with PUGNAc, involved in protein turnover and insulin signaling. Adenosine Triphosphate 74-77 insulin Homo sapiens 258-265 24089376-0 2013 Synergistic effects of C-peptide and insulin on low O2-induced ATP release from human erythrocytes. Adenosine Triphosphate 63-66 insulin Homo sapiens 23-32 24089376-0 2013 Synergistic effects of C-peptide and insulin on low O2-induced ATP release from human erythrocytes. Adenosine Triphosphate 63-66 insulin Homo sapiens 37-44 24089376-2 2013 It was reported that a concentration of insulin found in humans with insulin resistance inhibits low O2-induced ATP release. Adenosine Triphosphate 112-115 insulin Homo sapiens 40-47 24089376-2 2013 It was reported that a concentration of insulin found in humans with insulin resistance inhibits low O2-induced ATP release. Adenosine Triphosphate 112-115 insulin Homo sapiens 69-76 24089376-4 2013 Here, we investigate the hypothesis that C-peptide and insulin work synergistically to maintain low O2-induced ATP release from human erythrocytes. Adenosine Triphosphate 111-114 insulin Homo sapiens 41-50 24089376-4 2013 Here, we investigate the hypothesis that C-peptide and insulin work synergistically to maintain low O2-induced ATP release from human erythrocytes. Adenosine Triphosphate 111-114 insulin Homo sapiens 55-62 24089376-5 2013 Using a thin-film tonometer to alter O2 tension, we determined that either C-peptide or insulin alone inhibits low O2-induced ATP release in a concentration-dependent manner; however, coadministration of the peptides at a 1:1 ratio does not (n = 5; P < 0.05). Adenosine Triphosphate 126-129 insulin Homo sapiens 75-84 24089376-5 2013 Using a thin-film tonometer to alter O2 tension, we determined that either C-peptide or insulin alone inhibits low O2-induced ATP release in a concentration-dependent manner; however, coadministration of the peptides at a 1:1 ratio does not (n = 5; P < 0.05). Adenosine Triphosphate 126-129 insulin Homo sapiens 88-95 24089376-8 2013 However, at a concentration of insulin found in the peripheral circulation of humans under postprandial conditions (0.5 nM), a ratio of C-peptide to insulin of 6:1 inhibited low O2-induced ATP release (n = 5). Adenosine Triphosphate 189-192 insulin Homo sapiens 136-145 24089376-8 2013 However, at a concentration of insulin found in the peripheral circulation of humans under postprandial conditions (0.5 nM), a ratio of C-peptide to insulin of 6:1 inhibited low O2-induced ATP release (n = 5). Adenosine Triphosphate 189-192 insulin Homo sapiens 149-156 23274898-8 2013 ATP stimulated 2-NBDG uptake in normal and insulin-resistant adult muscle fibers, resembling the reported effect of exercise. Adenosine Triphosphate 0-3 insulin Homo sapiens 43-50 23875676-13 2013 The addition of ATP significantly increased the toxicity of the insulin fibril-chaperonin reaction products toward mammalian cells. Adenosine Triphosphate 16-19 insulin Homo sapiens 64-71 23274898-9 2013 Hence, the ATP-induced pathway may be tapped to bypass insulin resistance. Adenosine Triphosphate 11-14 insulin Homo sapiens 55-62 23314177-3 2013 Furthermore, Ahsg inhibits InsR autophosphorylation of highly-purified insulin holoreceptors in a cell-free, ATP-dependent system, with an IC50 within the range of single-chain Ahsg concentrations in human serum. Adenosine Triphosphate 109-112 insulin Homo sapiens 71-78 23093656-4 2012 Observations from our group and others suggest that the inorganic phosphate (P(i)) ATP flux in skeletal muscle may be modulated by certain conditions, including aging, insulin resistance, and diabetes, and may reflect inherent alterations in mitochondrial metabolism. Adenosine Triphosphate 85-88 insulin Homo sapiens 170-177 23471659-9 2013 Decreasing ATP level by suppression of production or stimulation of utilization is a promising approach in the treatment of insulin resistance. Adenosine Triphosphate 11-14 insulin Homo sapiens 124-131 23471659-10 2013 In support, many of existing insulin sensitizing medicines inhibit ATP production in mitochondria. Adenosine Triphosphate 67-70 insulin Homo sapiens 29-36 23471659-11 2013 The effective therapies such as weight loss, exercise, and caloric restriction all reduce ATP in insulin sensitive cells. Adenosine Triphosphate 90-93 insulin Homo sapiens 97-104 22967500-2 2012 Insulin enhances muscle mitochondrial PS and ATP production when hypoaminoacidemia is prevented by exogenous amino acid (AA) replacement. Adenosine Triphosphate 45-48 insulin Homo sapiens 0-7 22967500-3 2012 We determined whether insulin would stimulate mitochondrial PS and ATP production in the absence of AA replacement. Adenosine Triphosphate 67-70 insulin Homo sapiens 22-29 22352808-4 2012 In the presence of ATP, the simultaneous presence of DnaK, DnaJ, and ClpB allows good protection of insulin against aggregation. Adenosine Triphosphate 19-22 insulin Homo sapiens 100-107 22914748-8 2012 Insulin effects were eliminated in the presence of a ATP-dependent K+ (K(ATP)) channel antagonist tolbutamide (200 muM), or the phosphatidylinositol 3-kinase (PI3K) inhibitor wortmannin (100 nM), suggesting that insulin inhibition of excitatory input to gastric-related DMV neurons was mediated by K(ATP) channels and depended on PI3K activity. Adenosine Triphosphate 53-56 insulin Homo sapiens 0-7 22814106-6 2012 It was also found that TGF-beta1 but not BMP2 induced ATP oscillations and inhibition of TGF-beta but not BMP signaling prevented insulin-induced ATP oscillations. Adenosine Triphosphate 146-149 insulin Homo sapiens 130-137 22934004-8 2012 The model further predicts how insulin, at concentrations found in pre-diabetes, enhances the activity of PDE3 and reduces intracellular cAMP levels leading to decreased low O(2)-induced ATP release from erythrocytes. Adenosine Triphosphate 187-190 insulin Homo sapiens 31-38 22934004-10 2012 This model also predicts network-level effects of decreased ATP release resulting from elevated insulin levels. Adenosine Triphosphate 60-63 insulin Homo sapiens 96-103 22082043-1 2012 Potassium inwardly rectifying channel, subfamily-J, member 11 (KCNJ11) gene encodes Kir6.2 subunits of the adenosine triphosphate (ATP)-sensitive potassium channel involved in glucose-mediated metabolic signaling pathway and has attracted considerable attention as a candidate gene for type 2 diabetes (T2D) based on its function in glucose-stimulated insulin secretion. Adenosine Triphosphate 107-129 insulin Homo sapiens 352-359 22082043-1 2012 Potassium inwardly rectifying channel, subfamily-J, member 11 (KCNJ11) gene encodes Kir6.2 subunits of the adenosine triphosphate (ATP)-sensitive potassium channel involved in glucose-mediated metabolic signaling pathway and has attracted considerable attention as a candidate gene for type 2 diabetes (T2D) based on its function in glucose-stimulated insulin secretion. Adenosine Triphosphate 131-134 insulin Homo sapiens 352-359 22826313-2 2012 Measurement of flux between inorganic phosphate (Pi) and ATP using (31)P MRS magnetization transfer has been used in resting muscle to assess what is claimed to be mitochondrial ATP synthesis and has been particularly popular in the study of insulin effects and insulin resistance. Adenosine Triphosphate 57-60 insulin Homo sapiens 242-249 22826313-2 2012 Measurement of flux between inorganic phosphate (Pi) and ATP using (31)P MRS magnetization transfer has been used in resting muscle to assess what is claimed to be mitochondrial ATP synthesis and has been particularly popular in the study of insulin effects and insulin resistance. Adenosine Triphosphate 57-60 insulin Homo sapiens 262-269 22207502-2 2012 During severe hypoglycaemia energy production is blocked, and an increase of AMP:ATP activates the energy sensor and putative insulin-sensitiser AMP-activated protein kinase (AMPK). Adenosine Triphosphate 81-84 insulin Homo sapiens 126-133 22414059-5 2012 In addition, ROS activate UCP2 via peroxidation of the mitochondrial membrane phospholipids, which results in proton leak leading to reduced ATP synthesis and content in beta-cells - critical parameters in the regulation of glucose-stimulated insulin secretion. Adenosine Triphosphate 141-144 insulin Homo sapiens 243-250 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. Adenosine Triphosphate 268-271 insulin Homo sapiens 9-16 21388348-2 2011 The mechanism has been assumed to be an enhancement of glucose storage as glycogen, but no direct measurement has tested this concept or its possible relationship to the reported impairment in insulin-stimulated muscle ATP production. Adenosine Triphosphate 219-222 insulin Homo sapiens 193-200 22110477-5 2012 ROS activate UCP2, which results in proton leak across the mitochondrial inner membrane, and this leads to reduced beta-cell ATP synthesis and content, which is a critical parameter in regulating glucose-stimulated insulin secretion. Adenosine Triphosphate 125-128 insulin Homo sapiens 215-222 21897708-7 2011 In patients who had IRS with ATP criteria, 80% and 86.6% were found to have McA and FI in the insulin resistant range. Adenosine Triphosphate 29-32 insulin Homo sapiens 94-101 20731624-8 2011 DM2 erythrocytes and erythrocytes incubated with insulin at levels similar to those seen in pre-diabetes fail to release ATP in response to reduced O(2) tension. Adenosine Triphosphate 121-124 insulin Homo sapiens 49-56 21325017-1 2011 CONTEXT: Mitochondrial ATP production is important in the regulation of glucose-stimulated insulin secretion. Adenosine Triphosphate 23-26 insulin Homo sapiens 91-98 21050717-9 2011 RESULTS: Insulin-stimulated glucose transport, muscle glycogen, and adenosine triphosphate content were decreased in patients with PDAC compared with controls, and insulin stimulation did not significantly increase glucose incorporation into glycogen in vitro in patients with PDAC. Adenosine Triphosphate 68-90 insulin Homo sapiens 9-16 21216854-0 2011 Liver ATP synthesis is lower and relates to insulin sensitivity in patients with type 2 diabetes. Adenosine Triphosphate 6-9 insulin Homo sapiens 44-51 21453644-10 2011 CONCLUSIONS: The m.3243A>G mutation not only underlies a dysfunction of the insulin-producing beta cell of the pancreas but also results in a reduction in adenosine triphosphate production of the strial marginal cells of the inner ear, thus diminishing the energy (in the form of potassium ion gradient) needed for the outer hair cells of the organ of Corti to amplify the soundwaves, particularly at high frequencies. Adenosine Triphosphate 158-180 insulin Homo sapiens 79-86 21114984-3 2011 Since both insulin and physical training is known to activate K(ATP) and K(Ca2+) channels and increase nitric oxide (NO) synthesis, we hypothesized that insulin and exercise might use a common mechanism in mediating their vascular effect. Adenosine Triphosphate 64-67 insulin Homo sapiens 11-18 21114984-3 2011 Since both insulin and physical training is known to activate K(ATP) and K(Ca2+) channels and increase nitric oxide (NO) synthesis, we hypothesized that insulin and exercise might use a common mechanism in mediating their vascular effect. Adenosine Triphosphate 64-67 insulin Homo sapiens 153-160 21114984-4 2011 The present study was carried out to investigate the role of NO, K(ATP) and K(Ca2+) channels in enhancement of insulin-induced cutaneous vasorelaxation by exercise in rats. Adenosine Triphosphate 67-70 insulin Homo sapiens 111-118 21216854-2 2011 Because muscular insulin resistance relates to myocellular fat deposition and disturbed energy metabolism, we hypothesized that reduced hepatic ATP turnover (fATP) underlies insulin resistance and elevated hepatocellular lipid (HCL) contents. Adenosine Triphosphate 144-147 insulin Homo sapiens 17-24 21216854-2 2011 Because muscular insulin resistance relates to myocellular fat deposition and disturbed energy metabolism, we hypothesized that reduced hepatic ATP turnover (fATP) underlies insulin resistance and elevated hepatocellular lipid (HCL) contents. Adenosine Triphosphate 144-147 insulin Homo sapiens 174-181 20623795-0 2010 Measuring the acute effect of insulin infusion on ATP turnover rate in human skeletal muscle using phosphorus-31 magnetic resonance saturation transfer spectroscopy. Adenosine Triphosphate 50-53 insulin Homo sapiens 30-37 21205021-0 2011 Impaired insulin stimulation of muscular ATP production in patients with type 1 diabetes. Adenosine Triphosphate 41-44 insulin Homo sapiens 9-16 20623795-2 2010 However, the relative time course of insulin action in stimulating ATP turnover rate and glucose uptake in skeletal muscle has not been examined. Adenosine Triphosphate 67-70 insulin Homo sapiens 37-44 20623795-7 2010 The in vivo time course of insulin stimulation of skeletal muscle ATP turnover rate is not consistent with a rate limiting effect upon the initiation of insulin-stimulated glycogen synthesis. Adenosine Triphosphate 66-69 insulin Homo sapiens 27-34 20806839-3 2010 Here we discuss the concept that insulin, at levels found in pre-diabetes, contributes to microvascular disease in skeletal muscle by inhibiting the release of the vasodilator, adenosine triphosphate (ATP), from erythrocytes. Adenosine Triphosphate 177-199 insulin Homo sapiens 33-40 20609596-5 2010 For instance, ATP and gamma-amino butyric acid (GABA) modulate insulin and glucagon secretion, respectively; C-peptide protects beta-cells and kidney cells; and amylin reduces gastric emptying and food intake via the brain. Adenosine Triphosphate 14-17 insulin Homo sapiens 63-70 20806839-3 2010 Here we discuss the concept that insulin, at levels found in pre-diabetes, contributes to microvascular disease in skeletal muscle by inhibiting the release of the vasodilator, adenosine triphosphate (ATP), from erythrocytes. Adenosine Triphosphate 201-204 insulin Homo sapiens 33-40 19656320-5 2010 A K(ATP) mutation (R201H; KCNJ11) was detected in the infant, the mother, and 6-yr-old sister with PNDM; both were also subsequently transitioned off insulin onto glyburide. Adenosine Triphosphate 4-7 insulin Homo sapiens 150-157 20225132-3 2010 Beta cell mitochondria play a key role in this process, not only by providing energy in the form of ATP to support insulin secretion, but also by synthesising metabolites (anaplerosis) that can act, both intra- and extramitochondrially, as factors that couple glucose sensing to insulin granule exocytosis. Adenosine Triphosphate 100-103 insulin Homo sapiens 115-122 20207810-5 2010 In addition, we determined that insulin, at concentrations measured in humans and Zucker diabetic fatty rats with prediabetes, inhibited the O(2)-dependent release of ATP from rat red blood cells (RBCs). Adenosine Triphosphate 167-170 insulin Homo sapiens 32-39 20207810-8 2010 The finding that insulin attenuates the O(2)-dependent release of ATP from RBCs suggests that this defect in RBC physiology could contribute to a failure in the regulation of O(2) supply to meet the demand in skeletal muscle in prediabetes. Adenosine Triphosphate 66-69 insulin Homo sapiens 17-24 20382691-14 2010 These adaptations mainly result in reduced mitochondrial ATP production rate in response to insulin resistance. Adenosine Triphosphate 57-60 insulin Homo sapiens 92-99 19656320-8 2010 Pancreatic insulin disappears in an animal model of K(ATP)-induced NDM, unless glycemia is well controlled, thus, a dramatically lower glyburide requirement in the infant may reflect preserved insulin content because of early sulfonylurea intervention. Adenosine Triphosphate 54-57 insulin Homo sapiens 11-18 20546268-1 2010 BACKGROUND: Closure of the adenosine triphosphate (ATP)-sensitive potassium (K(ATP)) channel plays a key role in insulin secretion from the pancreatic beta-cells. Adenosine Triphosphate 27-49 insulin Homo sapiens 113-120 24843406-1 2010 Sulfonylureas (SU), commonly used in the treatment of type 2 diabetes mellitus (T2DM), stimulate insulin secretion by inhibiting adenosine triphosphate (ATP)-sensitive K(+) (KATP) channels in pancreatic beta-cells. Adenosine Triphosphate 129-151 insulin Homo sapiens 97-104 24843406-1 2010 Sulfonylureas (SU), commonly used in the treatment of type 2 diabetes mellitus (T2DM), stimulate insulin secretion by inhibiting adenosine triphosphate (ATP)-sensitive K(+) (KATP) channels in pancreatic beta-cells. Adenosine Triphosphate 153-156 insulin Homo sapiens 97-104 19948081-2 2010 Several pyruvate-dependent and -independent shuttles enhance tricarboxylic acid cycle intermediate (TACI) anaplerosis and increase beta-cell ATP:ADP ratio, triggering insulin exocytotic mechanisms. Adenosine Triphosphate 141-144 insulin Homo sapiens 167-174 19948081-9 2010 Furthermore, insulin release is tightly coupled to ATP:ADP rise which in turn is related to TACI anaplerosis. Adenosine Triphosphate 51-54 insulin Homo sapiens 13-20 20546268-1 2010 BACKGROUND: Closure of the adenosine triphosphate (ATP)-sensitive potassium (K(ATP)) channel plays a key role in insulin secretion from the pancreatic beta-cells. Adenosine Triphosphate 51-54 insulin Homo sapiens 113-120 19637187-11 2009 Even after adjustment for HLVF, hepatic ATP and Pi related negatively to hepatic insulin sensitivity (iEGP) (r =-0.665, P = 0.010, r =-0.680, P = 0.007) but not to whole-body insulin sensitivity. Adenosine Triphosphate 40-43 insulin Homo sapiens 81-88 20404042-0 2010 Insulin inhibits human erythrocyte cAMP accumulation and ATP release: role of phosphodiesterase 3 and phosphoinositide 3-kinase. Adenosine Triphosphate 57-60 insulin Homo sapiens 0-7 20404042-4 2010 Although insulin inhibits ATP release from human erythrocytes in response to Gi activation by mastoparan 7 (Mas 7), no effect on cAMP was described. Adenosine Triphosphate 26-29 insulin Homo sapiens 9-16 20404042-5 2010 Here, we investigated the hypothesis that insulin activates PDE3 in human erythrocytes via a PI3K-mediated mechanism resulting in cAMP hydrolysis and inhibition of ATP release. Adenosine Triphosphate 164-167 insulin Homo sapiens 42-49 20404042-10 2010 This effect of insulin leads, ultimately, to decreased ATP release in response to Mas 7. Adenosine Triphosphate 55-58 insulin Homo sapiens 15-22 20404042-12 2010 Thus, pathological increases in circulating insulin could, via activation of PDE3 in erythrocytes, inhibit ATP release from these cells, depriving the peripheral circulation of one mechanism that could aid in the regulation of the delivery of O(2) to meet tissue metabolic need. Adenosine Triphosphate 107-110 insulin Homo sapiens 44-51 21099295-2 2010 Under hyperglycemic conditions, glucose enters the cell, generates ATP, leading to a subsequent closure of voltage-dependent ATP channels, membrane depolarization, Ca2(+) entry and exocytosis of insulin vesicles. Adenosine Triphosphate 67-70 insulin Homo sapiens 195-202 19770186-5 2009 Importantly, ATP-dependent potassium (K(ATP)) channels are regulated both by ATP (from glucose metabolism) and by leptin and insulin, and directly control electrical excitability of both POMC and AgRP neurons. Adenosine Triphosphate 13-16 insulin Homo sapiens 125-132 19817800-1 2009 Insulin secretion is regulated by a series of complex events generated by various intracellular signals including Ca(2+), ATP, cAMP and phospholipid-derived signals. Adenosine Triphosphate 122-125 insulin Homo sapiens 0-7 19426882-3 2009 The corresponding increased synthesis rates of both ATP and of anaplerotic metabolites have been shown to be mediators for nutrient-stimulated insulin secretion. Adenosine Triphosphate 52-55 insulin Homo sapiens 143-150 19412833-0 2009 Insulin inhibits low oxygen-induced ATP release from human erythrocytes: implication for vascular control. Adenosine Triphosphate 36-39 insulin Homo sapiens 0-7 19412833-5 2009 RESULTS: Insulin significantly attenuated mastoparan 7- and reduced pO(2)-induced ATP release. Adenosine Triphosphate 82-85 insulin Homo sapiens 9-16 19412833-8 2009 CONCLUSIONS: These studies demonstrate that insulin inhibits ATP release from erythrocytes in response to reduced pO(2) and impairs their ability to stimulate dilation of skeletal muscle arterioles. Adenosine Triphosphate 61-64 insulin Homo sapiens 44-51 19265027-7 2009 Relatives responding to exercise training with increased ATP synthesis (+19%, P = 0.009) showed improved insulin sensitivity (P = 0.009) compared with those whose insulin sensitivity did not improve. Adenosine Triphosphate 57-60 insulin Homo sapiens 105-112 19265027-10 2009 CONCLUSIONS: The ability of short-term exercise to stimulate ATP production distinguished individuals with improved insulin sensitivity from those whose insulin sensitivity did not improve. Adenosine Triphosphate 61-64 insulin Homo sapiens 116-123 19402213-5 2009 Nitration of heat shock protein 60 in vitro was found to decrease its ATP hydrolysis and interaction with proinsulin, suggesting a mechanism by which protein nitration could diminish insulin secretion. Adenosine Triphosphate 70-73 insulin Homo sapiens 106-116 19183935-7 2009 The ROS/ATP ratio in obese insulin-resistant participants was similar to that in lean insulin-sensitive participants, while the ratio was significantly elevated in type 2 diabetes participants. Adenosine Triphosphate 8-11 insulin Homo sapiens 27-34 20039004-3 2009 To date, the key metrics that have been measured involving C-peptide and RBCs include an increase in glucose uptake by these cells and a subsequent increase in adenosine triphosphate (ATP) release. Adenosine Triphosphate 160-182 insulin Homo sapiens 59-68 20039004-3 2009 To date, the key metrics that have been measured involving C-peptide and RBCs include an increase in glucose uptake by these cells and a subsequent increase in adenosine triphosphate (ATP) release. Adenosine Triphosphate 184-187 insulin Homo sapiens 59-68 20039004-5 2009 The C-peptide-induced release of ATP is of interest when considering that ATP is a purinergic signaling molecule known to stimulate the production of nitric oxide (NO) in the endothelium and in platelets. Adenosine Triphosphate 33-36 insulin Homo sapiens 4-13 20039004-5 2009 The C-peptide-induced release of ATP is of interest when considering that ATP is a purinergic signaling molecule known to stimulate the production of nitric oxide (NO) in the endothelium and in platelets. Adenosine Triphosphate 74-77 insulin Homo sapiens 4-13 20039004-10 2009 Finally, a mechanism is proposed that explains how C-peptide is exerting its effects on other cells in the bloodstream, particularly on endothelial cells and platelets, via its ability to stimulate the release of ATP from RBCs. Adenosine Triphosphate 213-216 insulin Homo sapiens 51-60 19429412-3 2009 ATP also triggers a positive feedback signal amplifying glucose-induced insulin release, which argues for a potential pharmacological application. Adenosine Triphosphate 0-3 insulin Homo sapiens 72-79 19127548-5 2009 The roles that IDE/insulin concentration ratio, reaction time, adenosine 5"-triphosphate (ATP) and metal ions (Zn and Cu) have on the insulin cleavage pattern produced by IDE are investigated and a plausible interpretation involving the proteolytic action of the different IDE oligomeric forms is proposed. Adenosine Triphosphate 63-88 insulin Homo sapiens 134-141 19127548-5 2009 The roles that IDE/insulin concentration ratio, reaction time, adenosine 5"-triphosphate (ATP) and metal ions (Zn and Cu) have on the insulin cleavage pattern produced by IDE are investigated and a plausible interpretation involving the proteolytic action of the different IDE oligomeric forms is proposed. Adenosine Triphosphate 90-93 insulin Homo sapiens 134-141 19108584-0 2009 Homology modeling of GLUT4, an insulin regulated facilitated glucose transporter and docking studies with ATP and its inhibitors. Adenosine Triphosphate 106-109 insulin Homo sapiens 31-38 19961265-2 2009 The insulin-secreting beta-cells are oscillators with intrinsic variations of cytoplasmic ATP and Ca(2+). Adenosine Triphosphate 90-93 insulin Homo sapiens 4-11 18802678-2 2008 Myocellular ATP production (flux through ATP synthase [fATP]) increases by up to 90% during 8 h of insulin stimulation. Adenosine Triphosphate 12-15 insulin Homo sapiens 99-106 19251047-10 2009 The initial trigger for insulin granule fusion with the plasma membrane is a rise in intracellular calcium and in the case of glucose stimulation results from increased production of ATP, closure of the ATP-sensitive potassium channel and cellular depolarization. Adenosine Triphosphate 183-186 insulin Homo sapiens 24-31 18728221-2 2008 Glucose exerts its effects on insulin secretion via its metabolism in beta-cells to generate stimulus/secretion coupling factors, including a rise in the ATP/ADP ratio, which serves to suppress ATP-sensitive K(+) (K(ATP)) channels and activate voltage-gated Ca(2+) channels, leading to stimulation of insulin granule exocytosis. Adenosine Triphosphate 154-157 insulin Homo sapiens 30-37 18959471-2 2008 In humans, reduced or absent beta-cell K ATP channel activity resulting from loss-of-function K ATP mutations induces insulin hypersecretion. Adenosine Triphosphate 41-44 insulin Homo sapiens 118-125 18716044-2 2008 RESEARCH DESIGN AND METHODS: Insulin sensitivity was measured by hyperinsulinemic-euglycemic clamp and ATP production in mitochondria isolated from vastus lateralis biopsies of 42 healthy sedentary and endurance-trained young (18-30 years old) and older (59-76 years old) subjects. Adenosine Triphosphate 103-106 insulin Homo sapiens 29-36 18940398-0 2008 Insulin-stimulated mitochondrial adenosine triphosphate synthesis is blunted in skeletal muscles of high-fat-fed rats. Adenosine Triphosphate 33-55 insulin Homo sapiens 0-7 18940398-1 2008 Physiologic elevation of insulin levels induces a significant increase in muscle adenosine triphosphate (ATP) synthesis rate in normal individuals, indicative of an appropriate acceleration in mitochondrial activity. Adenosine Triphosphate 81-103 insulin Homo sapiens 25-32 18940398-1 2008 Physiologic elevation of insulin levels induces a significant increase in muscle adenosine triphosphate (ATP) synthesis rate in normal individuals, indicative of an appropriate acceleration in mitochondrial activity. Adenosine Triphosphate 105-108 insulin Homo sapiens 25-32 18940398-3 2008 In the absence of similar data from preclinical models, the present study investigated the inhibitory effects of increased dietary fat intake on insulin-stimulated ATP synthesis rates in rats. Adenosine Triphosphate 164-167 insulin Homo sapiens 145-152 18940398-8 2008 Moreover, chow-fed animals showed a significant increase (25%, P < .05 vs basal) in muscle ATP synthesis activity upon insulin stimulation, whereas high-fat-fed animals displayed no substantial change. Adenosine Triphosphate 94-97 insulin Homo sapiens 122-129 18940398-9 2008 These data demonstrated for the first time in a preclinical model that the insulin challenge not only facilitates an improvement in the dynamic range of ATP turnover measurement by (31)P saturation transfer between normal and insulin-resistant rats, but also mimics challenge that is relevant for pharmacologic studies on antidiabetic drugs aimed at improving mitochondrial function. Adenosine Triphosphate 153-156 insulin Homo sapiens 75-82 18940398-9 2008 These data demonstrated for the first time in a preclinical model that the insulin challenge not only facilitates an improvement in the dynamic range of ATP turnover measurement by (31)P saturation transfer between normal and insulin-resistant rats, but also mimics challenge that is relevant for pharmacologic studies on antidiabetic drugs aimed at improving mitochondrial function. Adenosine Triphosphate 153-156 insulin Homo sapiens 226-233 19069677-8 2008 On the contrary, the members of families with familial combined hyperlipidemia with the presence of metabolic syndrome (NCEP-ATP III) had significantly higher fasting insulin [FCH with MS 12.74 +/- 1.42 vs HL without MS 9.21 +/- 0.92 (p = 0.030); and vs NL without MS 6.75 +/- 0.80 (p = 0.001)], and proinsulin levels [FCH with MS 25.28 vs HL without MS 15.69 +/- 1.75 (p = 0.002); and vs NL without MS 11.20 +/- 1.51 (p = 0.0001)], and HOMA index [FCH with MS 3.03 +/- 0.39 vs HL without MS 2.13 +/- 0.25 (p = 0.042); and vs. NL without MS 1.56 +/- 0.22 (p = 0.003)] in comparison with their relatives without metabolic syndrome and controls. Adenosine Triphosphate 125-128 insulin Homo sapiens 167-174 19069677-8 2008 On the contrary, the members of families with familial combined hyperlipidemia with the presence of metabolic syndrome (NCEP-ATP III) had significantly higher fasting insulin [FCH with MS 12.74 +/- 1.42 vs HL without MS 9.21 +/- 0.92 (p = 0.030); and vs NL without MS 6.75 +/- 0.80 (p = 0.001)], and proinsulin levels [FCH with MS 25.28 vs HL without MS 15.69 +/- 1.75 (p = 0.002); and vs NL without MS 11.20 +/- 1.51 (p = 0.0001)], and HOMA index [FCH with MS 3.03 +/- 0.39 vs HL without MS 2.13 +/- 0.25 (p = 0.042); and vs. NL without MS 1.56 +/- 0.22 (p = 0.003)] in comparison with their relatives without metabolic syndrome and controls. Adenosine Triphosphate 125-128 insulin Homo sapiens 300-310 18281290-1 2008 ATP/ADP-sensing (sulfonylurea receptor (SUR)/K(IR)6)(4) K(ATP) channels regulate the excitability of our insulin secreting and other vital cells via the differential MgATP/ADP-dependent stimulatory actions of their tissue-specific ATP-binding cassette regulatory subunits (sulfonylurea receptors), which counterbalance the nearly constant inhibitory action of ATP on the K(+) inwardly rectifying pore. Adenosine Triphosphate 0-3 insulin Homo sapiens 105-112 18593850-0 2008 Deleterious action of FA metabolites on ATP synthesis: possible link between lipotoxicity, mitochondrial dysfunction, and insulin resistance. Adenosine Triphosphate 40-43 insulin Homo sapiens 122-129 18511483-7 2008 However, small molecules like ATP and GABA, which are stored together with insulin in the granules, are small enough to be released via the narrow fusion pore, which accordingly functions as a molecular sieve. Adenosine Triphosphate 30-33 insulin Homo sapiens 75-82 18285554-0 2008 Asian Indians have enhanced skeletal muscle mitochondrial capacity to produce ATP in association with severe insulin resistance. Adenosine Triphosphate 78-81 insulin Homo sapiens 109-116 18433713-3 2008 Mitochondria play a central role in GSIS by coupling glucose oxidation to production of ATP, a signal that triggers a series of events that ultimately leads to insulin release. Adenosine Triphosphate 88-91 insulin Homo sapiens 160-167 17956307-4 2007 Mitochondria generate ATP (the main coupling messenger in insulin secretion) and other factors that serve as sensors for the control of the exocytotic process. Adenosine Triphosphate 22-25 insulin Homo sapiens 58-65 17965850-2 2008 We hypothesised that incubation of erythrocytes with C-peptide would improve the ability of these cells to release ATP, a stimulus for nitric oxide production. Adenosine Triphosphate 115-118 insulin Homo sapiens 53-62 17965850-6 2008 RESULTS: The release of ATP from the erythrocytes of patients with diabetes increased from 64 +/- 13 to 260 +/- 39 nmol/l upon incubation of the cells in C-peptide. Adenosine Triphosphate 24-27 insulin Homo sapiens 154-163 17965850-8 2008 The increase in ATP release from the erythrocytes is due to metal-activated C-peptide stimulation of glucose transfer into the erythrocytes via the GLUT1 transporter. Adenosine Triphosphate 16-19 insulin Homo sapiens 76-85 17965850-10 2008 CONCLUSIONS/INTERPRETATION: When complexed to Fe2+ or Cr3+, C-peptide has the ability to promote ATP release from erythrocytes. Adenosine Triphosphate 97-100 insulin Homo sapiens 60-69 18270681-1 2008 AIMS/HYPOTHESIS: Insulin secretion in pancreatic islets is dependent upon mitochondrial function and production of ATP. Adenosine Triphosphate 115-118 insulin Homo sapiens 17-24 17980145-4 2008 We show that low concentration of atorvastatin, a drug inhibiting HMG-CoA reductase and cholesterol metabolism, or the natural agonist extracellular ATP rapidly decreased the level of insulin-induced phosphorylated Akt in the nucleus. Adenosine Triphosphate 149-152 insulin Homo sapiens 184-191 17980145-7 2008 These data indicate that extracellular ATP and statins via the P2X7 receptor modulate insulin-induced Akt signaling in epithelial cells. Adenosine Triphosphate 39-42 insulin Homo sapiens 86-93 17956307-5 2007 The main factors that mediate the key amplifying pathway over the Ca(2+) signal in nutrient-stimulated insulin secretion are nucleotides (ATP, GTP, cAMP and NADPH), although metabolites have also been proposed, such as long-chain acyl-CoA derivatives and glutamate. Adenosine Triphosphate 138-141 insulin Homo sapiens 103-110 17660267-2 2007 We determined the impact of insulin deficiency on muscle mitochondrial ATP production by temporarily depriving type 1 diabetic patients of insulin treatment. Adenosine Triphosphate 71-74 insulin Homo sapiens 28-35 17660267-6 2007 Insulin deprivation decreased muscle mitochondrial ATP production rate (MAPR) despite an increase in whole-body oxygen consumption and altered expression of many muscle mitochondrial gene transcripts. Adenosine Triphosphate 51-54 insulin Homo sapiens 0-7 17449130-2 2007 In pancreatic beta-cells, intracellular glucose metabolism regulates exocytosis of insulin granules, according to metabolism-secretion coupling in which glucose-induced mitochondrial ATP production plays an essential role. Adenosine Triphosphate 183-186 insulin Homo sapiens 83-90 18064068-1 2007 The ATP-sensitive potassium (K(ATP)) channels which extensively distribute in diverse tissues (e.g. vascular smooth muscle, cardiac cells, and pancreas) are well-established for characteristics like vasodilatation, myocardial protection against ischemia, and insulin secretion. Adenosine Triphosphate 4-7 insulin Homo sapiens 259-266 18064068-1 2007 The ATP-sensitive potassium (K(ATP)) channels which extensively distribute in diverse tissues (e.g. vascular smooth muscle, cardiac cells, and pancreas) are well-established for characteristics like vasodilatation, myocardial protection against ischemia, and insulin secretion. Adenosine Triphosphate 31-34 insulin Homo sapiens 259-266 17978456-2 2007 It has been recently discovered that mutation in KCNJ11 gene encoding Kir6.2, the pore forming subunit of ATP sensitive potassium channel (K ATP) is the most common cause and such patients may respond better to oral sulphonylurea drugs than insulin. Adenosine Triphosphate 106-109 insulin Homo sapiens 241-248 17668386-6 2007 Functional studies of selected mutations showed a reduced response to ATP consistent with an activating mutation that results in reduced insulin secretion. Adenosine Triphosphate 70-73 insulin Homo sapiens 137-144 17125872-2 2007 Mutations in mitochondrial DNA (mtDNA) are associated with type 2 diabetes mellitus (T2DM) because ATP plays a critical role in the production and the release of insulin. Adenosine Triphosphate 99-102 insulin Homo sapiens 162-169 17496364-5 2007 Moreover, insulin infusion while maintaining glucose and amino acid levels results in increase in muscle mitochondrial gene transcript levels and ATP production indicating that insulin is a key regulator of muscle mitochondrial biogenesis. Adenosine Triphosphate 146-149 insulin Homo sapiens 10-17 17373958-7 2007 Recent studies showed that reduced mitochondrial ATP synthesis in skeletal muscle is a feature of certain hereditary and acquired forms of insulin resistance and diabetes mellitus. Adenosine Triphosphate 49-52 insulin Homo sapiens 139-146 17496364-5 2007 Moreover, insulin infusion while maintaining glucose and amino acid levels results in increase in muscle mitochondrial gene transcript levels and ATP production indicating that insulin is a key regulator of muscle mitochondrial biogenesis. Adenosine Triphosphate 146-149 insulin Homo sapiens 177-184 17496364-6 2007 At a similar post-absorptive insulin levels both type 2 diabetic patients and non diabetic controls have similar muscle mitochondrial ATP production but increasing insulin from low to high levels stimulate ATP production only in non diabetic people but not in the diabetic people. Adenosine Triphosphate 206-209 insulin Homo sapiens 164-171 17139575-3 2006 Changes in the ATP/ADP ratio within the beta cells will then trigger the release of insulin granules from them. Adenosine Triphosphate 15-18 insulin Homo sapiens 84-91 17300718-0 2007 Utility of the modified ATP III defined metabolic syndrome and severe obesity as predictors of insulin resistance in overweight children and adolescents: a cross-sectional study. Adenosine Triphosphate 24-27 insulin Homo sapiens 95-102 16843639-5 2007 ATP stimulated phospholipase C activity, and also suppressed uptake of insulin, but not beta2gpI. Adenosine Triphosphate 0-3 insulin Homo sapiens 71-78 17296510-4 2006 The K(ATP) channels play multiple physiological roles in the glucose metabolism regulation, especially in beta-cells where it regulates insulin secretion, in response to an increase in ATP concentration. Adenosine Triphosphate 6-9 insulin Homo sapiens 136-143 17296510-12 2006 Sulfonylureas close K(ATP) channels by binding with high affinity to SUR suggesting they could replace insulin in these patients. Adenosine Triphosphate 22-25 insulin Homo sapiens 103-110 17451083-2 2007 Severe congenital hyperinsulinism is most often due to inactivating mutations in either the ABCC8 or KCNJ11 genes, which encode the SUR1 and Kir6.2 proteins, respectively--the two components of the ATP-sensitive K+ (KATP) channel; neonatal hypoglycemia due to macroscopic insulin-producing pancreatic lesions or adenomas are extremely rare. Adenosine Triphosphate 198-201 insulin Homo sapiens 23-30 16849626-3 2007 One route is an increased ATP production that, via ATP-sensitive K(+) (K(ATP)) channels, modulates the cell membrane potential to allow calcium influx, which triggers insulin secretion. Adenosine Triphosphate 26-29 insulin Homo sapiens 167-174 16849626-3 2007 One route is an increased ATP production that, via ATP-sensitive K(+) (K(ATP)) channels, modulates the cell membrane potential to allow calcium influx, which triggers insulin secretion. Adenosine Triphosphate 51-54 insulin Homo sapiens 167-174 16636122-2 2006 Activating mutations in Kir6.2 are the major cause of neonatal diabetes and reduce insulin secretion by altering the closure of the beta-cell ATP-sensitive potassium channel in the presence of ATP. Adenosine Triphosphate 142-145 insulin Homo sapiens 83-90 17075779-3 2006 Basal secretion of insulin occurs in an oscillating manner presumably triggered by ATP-dependent feedback inhibition of glycolytic flux. Adenosine Triphosphate 83-86 insulin Homo sapiens 19-26 16380486-0 2006 Increased lipid availability impairs insulin-stimulated ATP synthesis in human skeletal muscle. Adenosine Triphosphate 56-59 insulin Homo sapiens 37-44 16644693-8 2006 These results show that insulin secretory response to glucose deteriorates with increasing age and that it may be related to changes in ATP generation in beta-cells. Adenosine Triphosphate 136-139 insulin Homo sapiens 24-31 16505524-12 2006 CONCLUSIONS: Application of the ATP-III metabolic syndrome criteria provides good specificity but low sensitivity to screen asymptomatic white adults for insulin resistance. Adenosine Triphosphate 32-35 insulin Homo sapiens 154-161 16735096-5 2006 These causative factors bring about increasing amounts of toxins and radicals which impair the ATP generation in the CNS so that through the announcement of a non-existing hypoglycaemia the release of the insulin antagonists hGH, cortisol and adrenaline is induced. Adenosine Triphosphate 95-98 insulin Homo sapiens 205-212 16300674-7 2005 With insulin + glucose, both glycogen and ATP rates were strongly related to the glucose concentration; the magnitude of net glycogen flux was linearly correlated to the magnitude of net ATP flux: flux(glycogen) = 72.543(fluxATP) + 172.08, R2 = 0.98. Adenosine Triphosphate 42-45 insulin Homo sapiens 5-12 16300674-7 2005 With insulin + glucose, both glycogen and ATP rates were strongly related to the glucose concentration; the magnitude of net glycogen flux was linearly correlated to the magnitude of net ATP flux: flux(glycogen) = 72.543(fluxATP) + 172.08, R2 = 0.98. Adenosine Triphosphate 187-190 insulin Homo sapiens 5-12 16300674-8 2005 CONCLUSION: Only the co-infusion of 30 mM glucose and insulin led to (i) a net glycogen synthesis, (ii) the maintenance of the hepatic ATP content, and a strong positive correlation between their net fluxes. Adenosine Triphosphate 135-138 insulin Homo sapiens 54-61 16300674-0 2005 Insulin induces a positive relationship between the rates of ATP and glycogen changes in isolated rat liver in presence of glucose; a 31P and 13C NMR study. Adenosine Triphosphate 61-64 insulin Homo sapiens 0-7 16300674-10 2005 The specific effect of insulin on ATP change is likely related to a rapid stimulation of the hepatic mitochondrial oxidative phosphorylation. Adenosine Triphosphate 34-37 insulin Homo sapiens 23-30 16300674-11 2005 We propose that variations in the correlation between rates of ATP and glycogen changes could be a probe for insulin resistance due to the action of substrates, drugs or pathologic situations. Adenosine Triphosphate 63-66 insulin Homo sapiens 109-116 15955806-1 2005 The mechanisms involved in glucose regulation of insulin secretion by ATP-sensitive (K(ATP)) and calcium-activated (K(CA)) potassium channels have been extensively studied, but less is known about the role of voltage-gated (K(V)) potassium channels in pancreatic beta-cells. Adenosine Triphosphate 70-73 insulin Homo sapiens 49-56 16383643-3 2005 These two are coupled to interact with each other in the combined model, and two basic assumptions are made on the basis of biological observations: The conductance gK(ATP) for the ATP-dependent potassium current is a decreasing function of the glucose concentration whereas the insulin secretion rate is given by a function of the intracellular calcium concentration. Adenosine Triphosphate 168-171 insulin Homo sapiens 279-286 16383643-3 2005 These two are coupled to interact with each other in the combined model, and two basic assumptions are made on the basis of biological observations: The conductance gK(ATP) for the ATP-dependent potassium current is a decreasing function of the glucose concentration whereas the insulin secretion rate is given by a function of the intracellular calcium concentration. Adenosine Triphosphate 181-184 insulin Homo sapiens 279-286 16123337-1 2005 Closure of ATP-sensitive K(+) channels (K(ATP) channels) in response to metabolically generated ATP or binding of sulfonylurea drugs stimulates insulin release from pancreatic beta-cells. Adenosine Triphosphate 11-14 insulin Homo sapiens 144-151 16123337-1 2005 Closure of ATP-sensitive K(+) channels (K(ATP) channels) in response to metabolically generated ATP or binding of sulfonylurea drugs stimulates insulin release from pancreatic beta-cells. Adenosine Triphosphate 42-45 insulin Homo sapiens 144-151 16123337-4 2005 All mutations appear to cause neonatal diabetes by reducing K(ATP) channel ATP sensitivity and increasing the K(ATP) current, which inhibits beta-cell electrical activity and insulin secretion. Adenosine Triphosphate 62-65 insulin Homo sapiens 175-182 16089501-0 2005 Decreased insulin-stimulated ATP synthesis and phosphate transport in muscle of insulin-resistant offspring of type 2 diabetic parents. Adenosine Triphosphate 29-32 insulin Homo sapiens 10-17 16089501-0 2005 Decreased insulin-stimulated ATP synthesis and phosphate transport in muscle of insulin-resistant offspring of type 2 diabetic parents. Adenosine Triphosphate 29-32 insulin Homo sapiens 80-87 16089501-3 2005 In order to further characterize mitochondrial activity in these individuals, we examined insulin-stimulated rates of adenosine triphosphate (ATP) synthesis and phosphate transport in skeletal muscle in a similar cohort of participants. Adenosine Triphosphate 118-140 insulin Homo sapiens 90-97 16089501-3 2005 In order to further characterize mitochondrial activity in these individuals, we examined insulin-stimulated rates of adenosine triphosphate (ATP) synthesis and phosphate transport in skeletal muscle in a similar cohort of participants. Adenosine Triphosphate 142-145 insulin Homo sapiens 90-97 16089501-7 2005 In contrast, insulin-stimulated rates of muscle mitochondrial ATP synthesis increased by only 5% in the IR offspring (p = 0.001 versus controls) and was associated with a severe reduction of insulin-stimulated increases in the intramyocellular Pi concentrations (IR offspring: 4.7% +/- 1.9% versus controls: 19.3% +/- 5.7%; p = 0.03). Adenosine Triphosphate 62-65 insulin Homo sapiens 13-20 16089501-8 2005 Insulin-induced increases in intramyocellular Pi concentrations correlated well with insulin-stimulated increases in rates of ATP synthesis (r = 0.67; p = 0.008). Adenosine Triphosphate 126-129 insulin Homo sapiens 0-7 16089501-8 2005 Insulin-induced increases in intramyocellular Pi concentrations correlated well with insulin-stimulated increases in rates of ATP synthesis (r = 0.67; p = 0.008). Adenosine Triphosphate 126-129 insulin Homo sapiens 85-92 16089501-9 2005 CONCLUSIONS: These data demonstrate that insulin-stimulated rates of mitochondrial ATP synthesis are reduced in IR offspring of parents with type 2 diabetes. Adenosine Triphosphate 83-86 insulin Homo sapiens 41-48 16089501-10 2005 Furthermore, these IR offspring also have impaired insulin-stimulated phosphate transport in muscle, which may contribute to their defects in insulin-stimulated rates of mitochondrial ATP synthesis. Adenosine Triphosphate 184-187 insulin Homo sapiens 51-58 16089501-10 2005 Furthermore, these IR offspring also have impaired insulin-stimulated phosphate transport in muscle, which may contribute to their defects in insulin-stimulated rates of mitochondrial ATP synthesis. Adenosine Triphosphate 184-187 insulin Homo sapiens 142-149 15955806-1 2005 The mechanisms involved in glucose regulation of insulin secretion by ATP-sensitive (K(ATP)) and calcium-activated (K(CA)) potassium channels have been extensively studied, but less is known about the role of voltage-gated (K(V)) potassium channels in pancreatic beta-cells. Adenosine Triphosphate 87-90 insulin Homo sapiens 49-56 15883415-9 2005 However, the insulin-induced increase in muscle mitochondrial ATP production is defective in type 2 diabetic patients with insulin resistance. Adenosine Triphosphate 62-65 insulin Homo sapiens 13-20 15930967-2 2005 Recent findings show that other hormones (steroids, leptin, insulin) regulate the efficiency of mitochondrial adenosine triphosphate production. Adenosine Triphosphate 110-132 insulin Homo sapiens 60-67 15930967-9 2005 Finally, recent data and opinions suggest that mitochondria and adenosine triphosphate production could be central in the pathogenesis of both insulin resistance and beta cell deficiency. Adenosine Triphosphate 64-86 insulin Homo sapiens 143-150 15883415-9 2005 However, the insulin-induced increase in muscle mitochondrial ATP production is defective in type 2 diabetic patients with insulin resistance. Adenosine Triphosphate 62-65 insulin Homo sapiens 123-130 16128165-1 2005 The recent ATP III classification defines metabolic syndrome as including > or = 3 of the following characteristics: abdominal adiposity, atherogenic dyslipidemia, high blood pressure, and insulin resistance. Adenosine Triphosphate 11-14 insulin Homo sapiens 192-199 15585595-2 2005 In glucose-induced insulin secretion, the rate of pyruvate carboxylation is very high and correlates more strongly with the glucose concentration the beta-cell is exposed to (and thus with insulin release) than does pyruvate decarboxylation, which produces acetyl-CoA for metabolism in the citric acid cycle to produce ATP. Adenosine Triphosphate 319-322 insulin Homo sapiens 19-26 15479952-9 2005 These results indicate that glucose-stimulated insulin release is decreased by chronic exposure to tacrolimus due to reduced ATP production and glycolysis derived from reduced glucokinase activity. Adenosine Triphosphate 125-128 insulin Homo sapiens 47-54 15797443-8 2005 It is proposed that mTOR, the central control point for protein synthesis of the PI 3-K kinase cascade stimulated by insulin, is regulated by MgATP(2-) which varies directly with cytosolic Mg(2+). Adenosine Triphosphate 142-147 insulin Homo sapiens 117-124 15607940-0 2005 Insulin enhances mitochondrial inner membrane potential and increases ATP levels through phosphoinositide 3-kinase in adult sensory neurons. Adenosine Triphosphate 70-73 insulin Homo sapiens 0-7 15607940-7 2005 Additionally, insulin elevated the redox state of the mitochondrial NAD(P)H pool, increased hexokinase activity (first committed step of glycolysis), and raised ATP levels. Adenosine Triphosphate 161-164 insulin Homo sapiens 14-21 15607940-8 2005 This study demonstrates that insulin utilizes the PI 3-K/Akt pathway to augment ATP synthesis that we propose contributes to the energy requirement for neurotrophic factor-driven axon regeneration. Adenosine Triphosphate 80-83 insulin Homo sapiens 29-36 15180566-9 2004 The energy status of the beta cell controls insulin release via regulation of open probability of the ATP sensitive potassium (K(ATP)) channels to affect membrane potential and the intracellular calcium concentration [Ca(2+)](i). Adenosine Triphosphate 102-105 insulin Homo sapiens 44-51 15336815-3 2004 We observed the association between CRP, insulin resistance and metabolic syndrome as defined by the ATP III report, and thus identified the role of CRP in the relation to insulin resistance. Adenosine Triphosphate 101-104 insulin Homo sapiens 172-179 15356080-7 2004 However, in vitro studies showed that when adjusted for IR concentration, maximal insulin-stimulated (100 nm) IR tyrosine phosphorylation (0.75 +/- 0.06 vs. 0.92 +/- 0.08 U) and IR tyrosine kinase activity (183.8 +/- 27.0 vs. 204.3 +/- 23.7 fmol ATP/ng IR) were unchanged. Adenosine Triphosphate 246-249 insulin Homo sapiens 82-89 15350011-4 2004 Insulin could significantly decrease adenosine triphosphate (ATP) level after 3 hours of preservation, as well as total adenine nucleotides (TANs) and energy charge (EC) levels. Adenosine Triphosphate 37-59 insulin Homo sapiens 0-7 15350011-4 2004 Insulin could significantly decrease adenosine triphosphate (ATP) level after 3 hours of preservation, as well as total adenine nucleotides (TANs) and energy charge (EC) levels. Adenosine Triphosphate 61-64 insulin Homo sapiens 0-7 15350011-5 2004 Energy regeneration deteriorated in the grafts preserved by insulin in terms of ATP and EC levels at 24 hours after transplantation. Adenosine Triphosphate 80-83 insulin Homo sapiens 60-67 15501029-1 2004 2-(4-Methoxyphenoxy)-5-nitro-N-(4-sulfamoylphenyl)benzamide and close analogues inhibit glucose stimulated insulin release through activation of Kir6.2/SUR1 K(ATP) channels of beta cells. Adenosine Triphosphate 159-162 insulin Homo sapiens 107-114 15148320-10 2004 This inability likely results in its failure to produce the ATP necessary for stimulated secretion of insulin. Adenosine Triphosphate 60-63 insulin Homo sapiens 102-109 14749274-7 2004 The molecular mechanism by which the A3243G mutation affects insulin secretion may involve an attenuation of cytosolic ADP/ATP levels leading to a resetting of the glucose sensor in the pancreatic beta-cell, such as in maturity-onset diabetes of the young (MODY)-2 patients with mutations in glucokinase. Adenosine Triphosphate 123-126 insulin Homo sapiens 61-68 15111486-1 2004 The Adult Treatment Panel III (ATP III) has published criteria for diagnosing the metabolic syndrome, a cluster of closely related abnormalities related to insulin resistance that increase cardiovascular disease risk. Adenosine Triphosphate 31-34 insulin Homo sapiens 156-163 15503794-3 2004 Major messengers which mediate glucose action for insulin release are Ca2+, adenosine triphosphate (ATP) and diacylglycerol (DAG). Adenosine Triphosphate 76-98 insulin Homo sapiens 50-57 15503794-3 2004 Major messengers which mediate glucose action for insulin release are Ca2+, adenosine triphosphate (ATP) and diacylglycerol (DAG). Adenosine Triphosphate 100-103 insulin Homo sapiens 50-57 14744991-6 2004 Insulin induced the release of adenosine trisphosphate (ATP), adenosine, and serotonin from platelet-dense granules in a NO-dependent manner. Adenosine Triphosphate 56-59 insulin Homo sapiens 0-7 14744991-8 2004 Insulin-induced ATP release from human platelets correlated with the association of syntaxin 2 with the vesicle-associated membrane protein 3 but was not associated with the activation of alphaIIbbeta3 integrin. Adenosine Triphosphate 16-19 insulin Homo sapiens 0-7 14744991-9 2004 Thus, insulin elicits the release of vasoactive concentrations of ATP and adenosine from human platelets via a NO-G kinase-dependent signaling cascade. Adenosine Triphosphate 66-69 insulin Homo sapiens 6-13 15090909-5 2004 RECENT FINDINGS: Insulin acutely stimulates skeletal muscle mitochondrial protein synthesis and adenosine triphosphate production. Adenosine Triphosphate 96-118 insulin Homo sapiens 17-24 14728986-2 2004 Insulin secretion is coupled to glucose metabolism by effects of the intracellular ATP/ADP ratio on the multimeric beta-cell potassium channel. Adenosine Triphosphate 83-86 insulin Homo sapiens 0-7 14679173-3 2003 A new study demonstrates that hyperglycemia-induced mitochondrial superoxide production activates uncoupling protein 2, which decreases the ATP/ADP ratio and thus reduces the insulin-secretory response. Adenosine Triphosphate 140-143 insulin Homo sapiens 175-182 14679178-3 2003 Uncoupling protein 2 (UCP2), by virtue of its mitochondrial proton leak activity and consequent negative effect on ATP production, impairs glucose-stimulated insulin secretion. Adenosine Triphosphate 115-118 insulin Homo sapiens 158-165 12640462-3 2003 The mechanism by which nutrients stimulate insulin secretion has been studied extensively: ATP has been identified as the main messenger and the ATP-sensitive potassium channel as an essential transducer in this process. Adenosine Triphosphate 91-94 insulin Homo sapiens 43-50 14641647-11 2003 Our results show that in adult sensory neurons, treatment with insulin can elevate the input of reducing equivalents into the mitochondrial electron transport chain, which leads to greater mitochondrial membrane polarization and enhanced ATP synthesis. Adenosine Triphosphate 238-241 insulin Homo sapiens 63-70 14511357-3 2003 The aim of this study was to test the hypothesis that insulin regulates the ATP-dependent ubiquitin proteolytic pathway in human muscle. Adenosine Triphosphate 76-79 insulin Homo sapiens 54-61 14511357-5 2003 The effect of insulin on the activity of the ATP-dependent ubiquitin pathway was assessed from the mRNA expression of ubiquitin and the ubiquitin-conjugating enzyme E214k in human myocytes. Adenosine Triphosphate 45-48 insulin Homo sapiens 14-21 14511357-9 2003 CONCLUSIONS: In human muscle we have demonstrated regulation by insulin of the ATP-dependent ubiquitin pathway at the level of ubiquitin conjugation. Adenosine Triphosphate 79-82 insulin Homo sapiens 64-71 12808136-2 2003 Although insulin is a major regulator of fuel metabolism, its effect on mitochondrial ATP production is not known. Adenosine Triphosphate 86-89 insulin Homo sapiens 9-16 12771873-13 2003 The protective effect of continuous insulin infusion may stem from the effective metabolic use of excess glucose to favorably alter pathways of myocardial adenosine triphosphate production. Adenosine Triphosphate 155-177 insulin Homo sapiens 36-43 14561494-1 2003 The modulation of ATP-sensitive K+ channel (K(ATP)) by insulin plays a role in neuromuscular disorders associated to altered K+ homeostasis. Adenosine Triphosphate 18-21 insulin Homo sapiens 55-62 14580754-4 2003 investigated the stimulatory action of insulin on mitochondrial activities in key cellular events, such as ATP production, enzyme activity, mitochondrial protein synthesis, and mRNA expression of transcripts encoding mitochondrial proteins. Adenosine Triphosphate 107-110 insulin Homo sapiens 39-46 12702923-1 2003 BACKGROUND AND OBJECTIVES: Several studies suggested that the insulin resistance-associated metabolic syndrome (MS) is a major risk factor for coronary artery disease (CAD), but the criteria to identify MS were only recently standardized by the National Cholesterol Education Program (NCEP) Adult Treatment Panel (ATP) III. Adenosine Triphosphate 314-317 insulin Homo sapiens 62-69 12419479-6 2002 The metabolic syndrome, as defined by ATP III, incorporates a number of the components of these syndromes, including insulin resistance and intra-abdominal fat. Adenosine Triphosphate 38-41 insulin Homo sapiens 117-124 12213059-1 2002 6-Chloro-3-alkylamino-4H-thieno[3,2-e]-1,2,4-thiadiazine 1,1-dioxide derivatives were synthesized and characterized as activators of adenosine 5"-triphosphate (ATP) sensitive potassium (K(ATP)) channels in the beta-cells by measuring effects on membrane potential and insulin release in vitro. Adenosine Triphosphate 133-158 insulin Homo sapiens 268-275 12351459-0 2002 Variations in insulin secretion in carriers of the E23K variant in the KIR6.2 subunit of the ATP-sensitive K(+) channel in the beta-cell. Adenosine Triphosphate 93-96 insulin Homo sapiens 14-21 12044525-7 2002 Conversely, addition of S-nitroso-N-acetylpenicillamine, a NO donor, inhibited the insulin-stimulated ATP increase synthesis in iNOS(-/-) hepatocytes, but not the insulin-stimulated glycogen synthesis. Adenosine Triphosphate 102-105 insulin Homo sapiens 83-90 12213059-4 2002 6-Chloro-3-(1-methylcyclobutyl)amino-4H-thieno[3,2-e]-1,2,4-thiadiazine 1,1-dioxide (54) was found to bind and activate the SUR1/Kir6.2 K(ATP) channels in the low nanomolar range and to be at least 1000 times more potent than the reference compound diazoxide with respect to inhibition of insulin release from rat islets. Adenosine Triphosphate 138-141 insulin Homo sapiens 289-296 12045211-1 2002 Variants in mitochondrial DNA (mtDNA) could be associated with type 2 diabetes because ATP plays a critical role in the production and release of insulin. Adenosine Triphosphate 87-90 insulin Homo sapiens 146-153 12031957-8 2002 The enhanced rate of entry of glucose-derived pyruvate into the tricarboxylic acid (TCA) cycle in the presence of alanine may have stimulated rates of generation of key metabolites, including ATP, which affect the insulin secretory process. Adenosine Triphosphate 192-195 insulin Homo sapiens 214-221 11171597-7 2001 These data suggest that cellular ATP depletion by glucosamine, NaN3, and DNP exerts differential effects on basal and insulin-stimulated glucose transport and that ATP depletion per se does not induce insulin resistance in 3T3-L1 adipocytes. Adenosine Triphosphate 33-36 insulin Homo sapiens 118-125 11956956-5 2002 This abnormality along with a reduction in brain insulin concentration is assumed to induce a cascade-like process of disturbances including cellular glucose, acetylcholine, cholesterol, and ATP associated with abnormalities in membrane pathology and the formation of both amyloidogenic derivatives and hyperphosphorylated tau protein. Adenosine Triphosphate 191-194 insulin Homo sapiens 49-56 11886082-5 2001 Insulin receptor tyrosine kinase was isolated from monocytes by immunoprecipitation and the activity was determined using exogenous substrate poly glu-tyr (4:1) and radioactive ATP. Adenosine Triphosphate 177-180 insulin Homo sapiens 0-7 11994906-2 2002 Recently, a role for calcium-dependent and ATP-dependent potassium (K(Ca) and K(ATP)) channels in insulin-induced vasodilation has been demonstrated in in vitro studies. Adenosine Triphosphate 43-46 insulin Homo sapiens 98-105 11815456-3 2002 ATP also exerts a permissive action on insulin exocytosis. Adenosine Triphosphate 0-3 insulin Homo sapiens 39-46 11595666-0 2001 Chronic exposure to high leucine impairs glucose-induced insulin release by lowering the ATP-to-ADP ratio. Adenosine Triphosphate 89-92 insulin Homo sapiens 57-64 11798951-8 2001 It might interfere with the energy metabolism and the production of ATP, thus causing insulin resistance in peripheral tissues. Adenosine Triphosphate 68-71 insulin Homo sapiens 86-93 11158979-6 2001 However, the combination of ATP and insulin stimulated only an additive activation of Raf (ATP, 5-fold; insulin, <2-fold; and ATP + insulin, 8-fold over basal) and Ras (ATP, 5-fold; insulin, 2-fold; and ATP + insulin, 8-fold over basal). Adenosine Triphosphate 28-31 insulin Homo sapiens 104-111 11158979-6 2001 However, the combination of ATP and insulin stimulated only an additive activation of Raf (ATP, 5-fold; insulin, <2-fold; and ATP + insulin, 8-fold over basal) and Ras (ATP, 5-fold; insulin, 2-fold; and ATP + insulin, 8-fold over basal). Adenosine Triphosphate 28-31 insulin Homo sapiens 104-111 11158979-5 2001 A similar synergistic stimulation of extracellular signal-regulated kinase (ERK) and mitogen-activated protein or ERK kinase activities was observed (ATP, 7-fold; insulin, 2-fold; and ATP + insulin, 16-fold over basal). Adenosine Triphosphate 184-189 insulin Homo sapiens 190-197 11158979-6 2001 However, the combination of ATP and insulin stimulated only an additive activation of Raf (ATP, 5-fold; insulin, <2-fold; and ATP + insulin, 8-fold over basal) and Ras (ATP, 5-fold; insulin, 2-fold; and ATP + insulin, 8-fold over basal). Adenosine Triphosphate 28-31 insulin Homo sapiens 104-111 11158979-6 2001 However, the combination of ATP and insulin stimulated only an additive activation of Raf (ATP, 5-fold; insulin, <2-fold; and ATP + insulin, 8-fold over basal) and Ras (ATP, 5-fold; insulin, 2-fold; and ATP + insulin, 8-fold over basal). Adenosine Triphosphate 91-94 insulin Homo sapiens 36-43 11158979-6 2001 However, the combination of ATP and insulin stimulated only an additive activation of Raf (ATP, 5-fold; insulin, <2-fold; and ATP + insulin, 8-fold over basal) and Ras (ATP, 5-fold; insulin, 2-fold; and ATP + insulin, 8-fold over basal). Adenosine Triphosphate 28-31 insulin Homo sapiens 104-111 11158979-6 2001 However, the combination of ATP and insulin stimulated only an additive activation of Raf (ATP, 5-fold; insulin, <2-fold; and ATP + insulin, 8-fold over basal) and Ras (ATP, 5-fold; insulin, 2-fold; and ATP + insulin, 8-fold over basal). Adenosine Triphosphate 129-134 insulin Homo sapiens 36-43 11158979-6 2001 However, the combination of ATP and insulin stimulated only an additive activation of Raf (ATP, 5-fold; insulin, <2-fold; and ATP + insulin, 8-fold over basal) and Ras (ATP, 5-fold; insulin, 2-fold; and ATP + insulin, 8-fold over basal). Adenosine Triphosphate 91-94 insulin Homo sapiens 36-43 11158979-6 2001 However, the combination of ATP and insulin stimulated only an additive activation of Raf (ATP, 5-fold; insulin, <2-fold; and ATP + insulin, 8-fold over basal) and Ras (ATP, 5-fold; insulin, 2-fold; and ATP + insulin, 8-fold over basal). Adenosine Triphosphate 206-211 insulin Homo sapiens 36-43 11158979-9 2001 However, when ATP and insulin were added in combination, ATP dramatically reduced the insulin-stimulated Akt activation (2-fold above basal). Adenosine Triphosphate 14-17 insulin Homo sapiens 86-93 11158979-9 2001 However, when ATP and insulin were added in combination, ATP dramatically reduced the insulin-stimulated Akt activation (2-fold above basal). Adenosine Triphosphate 57-60 insulin Homo sapiens 22-29 11158979-9 2001 However, when ATP and insulin were added in combination, ATP dramatically reduced the insulin-stimulated Akt activation (2-fold above basal). Adenosine Triphosphate 57-60 insulin Homo sapiens 86-93 11158979-10 2001 Thus these results are consistent with ATP relieving an insulin-induced Akt-dependent inhibitory effect on the ERK signaling pathway, leading to synergistic stimulation of CASMC proliferation. Adenosine Triphosphate 39-42 insulin Homo sapiens 56-63 10993895-10 2000 We suggest that the lower expression of the mutant channel and the reduced affinity of NBF2 for MgADP may lead to a smaller K(ATP)(+) current in R1420C-PHHI beta-cells and thereby to the enhanced insulin secretion. Adenosine Triphosphate 126-129 insulin Homo sapiens 196-203 10823244-2 2000 The normal regulation of insulin secretion is coupled to glucose metabolism in the pancreatic B cell, a major but not exclusive signal for secretion being closure of K+ ATP (adenosine" triphosphate)-dependent channels in the cell membrane through an increase in cytosolic ATP/adenosine diphosphate. Adenosine Triphosphate 169-172 insulin Homo sapiens 25-32 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. Adenosine Triphosphate 198-201 insulin Homo sapiens 43-50 11016448-7 2000 We propose that in contrast to skeletal muscle, in which AMPK stimulation promotes glucose transport to provide ATP as a fuel, AMPK stimulation inhibits insulin-stimulated glucose transport in adipocytes, inhibiting triacylglycerol synthesis, to conserve ATP under conditions of cellular stress. Adenosine Triphosphate 255-258 insulin Homo sapiens 153-160 10896818-0 2000 The use of insulin and glucose during resuscitation from hemorrhagic shock increases hepatic ATP. Adenosine Triphosphate 93-96 insulin Homo sapiens 11-18 10896818-12 2000 RESULTS: The insulin-treated group had significantly increased hepatic ATP and energy charge following resuscitation compared with the other two groups. Adenosine Triphosphate 71-74 insulin Homo sapiens 13-20 10896818-14 2000 Total adenine nucleotides (ATP, ADP, and AMP) were significantly elevated 90 min postresuscitation in the insulin group. Adenosine Triphosphate 27-30 insulin Homo sapiens 106-113 10896818-17 2000 CONCLUSIONS: Resuscitation with insulin and dextrose significantly increased hepatic ATP and adenylate energy charge after hemorrhagic shock in rats. Adenosine Triphosphate 85-88 insulin Homo sapiens 32-39 10896818-18 2000 Total nucleotide pool levels were not different between groups, indicating that there was a shift of the equilibrium away from the metabolites toward ATP and ADP in the insulin-treated group. Adenosine Triphosphate 150-153 insulin Homo sapiens 169-176 10966860-2 2000 Glucose metabolism generates oscillations in the ATP/ADP ratio which lead to opening and closing of ATP-sensitive K(+)-channels producing subsequent oscillations in membrane potential, cytoplasmic calcium and insulin release. Adenosine Triphosphate 49-52 insulin Homo sapiens 209-216 10891367-5 2000 273, 20658-20668) suggests a trivial explanation of glucosamine-induced insulin resistance whereby intracellular ATP pools are depleted presumably due to the phosphorylation of glucosamine to glucosamine 6-phosphate, a hexosamine pathway intermediate. Adenosine Triphosphate 113-116 insulin Homo sapiens 72-79 10875252-4 2000 Insulin inhibited ATP- and ubiquitin-dependent lysozyme degradation more than 90% by reticulocyte extract, in a dose-dependent manner (IC50 approximately 50 nM). Adenosine Triphosphate 18-21 insulin Homo sapiens 0-7 11107928-2 2000 The normal regulation of insulin secretion is linked to glucose metabolism in the pancreatic beta-cell, a major but not exclusive signal for secretion being closure of K+ ATP-dependent channels in the cell membrane through an increase in the cytosolic ATP/ADP. Adenosine Triphosphate 171-174 insulin Homo sapiens 25-32 10909997-7 2000 Ex vivo by microcalorimetry, the heat produced after 1 hour by the enzyme-induced hydrolysis of adenosine triphosphate (ATP), was measured in a thermostated microcalorimeter at 37 degrees C. The results showed that Na/K ATPase activity was significantly increased by insulin (12.4 +/- 0.5 v 15.4 +/- 0.9 mW/L RBCs, P < .05, n = 23) but not by C-peptide (11.9 +/- 0.7 v 12.9 +/- 0.9 mW/L RBCs, NS, P = .26, n = 12). Adenosine Triphosphate 96-118 insulin Homo sapiens 267-274 10909997-7 2000 Ex vivo by microcalorimetry, the heat produced after 1 hour by the enzyme-induced hydrolysis of adenosine triphosphate (ATP), was measured in a thermostated microcalorimeter at 37 degrees C. The results showed that Na/K ATPase activity was significantly increased by insulin (12.4 +/- 0.5 v 15.4 +/- 0.9 mW/L RBCs, P < .05, n = 23) but not by C-peptide (11.9 +/- 0.7 v 12.9 +/- 0.9 mW/L RBCs, NS, P = .26, n = 12). Adenosine Triphosphate 96-118 insulin Homo sapiens 346-355 10909997-7 2000 Ex vivo by microcalorimetry, the heat produced after 1 hour by the enzyme-induced hydrolysis of adenosine triphosphate (ATP), was measured in a thermostated microcalorimeter at 37 degrees C. The results showed that Na/K ATPase activity was significantly increased by insulin (12.4 +/- 0.5 v 15.4 +/- 0.9 mW/L RBCs, P < .05, n = 23) but not by C-peptide (11.9 +/- 0.7 v 12.9 +/- 0.9 mW/L RBCs, NS, P = .26, n = 12). Adenosine Triphosphate 120-123 insulin Homo sapiens 267-274 10909997-7 2000 Ex vivo by microcalorimetry, the heat produced after 1 hour by the enzyme-induced hydrolysis of adenosine triphosphate (ATP), was measured in a thermostated microcalorimeter at 37 degrees C. The results showed that Na/K ATPase activity was significantly increased by insulin (12.4 +/- 0.5 v 15.4 +/- 0.9 mW/L RBCs, P < .05, n = 23) but not by C-peptide (11.9 +/- 0.7 v 12.9 +/- 0.9 mW/L RBCs, NS, P = .26, n = 12). Adenosine Triphosphate 120-123 insulin Homo sapiens 346-355 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). Adenosine Triphosphate 116-119 insulin Homo sapiens 75-82 10965681-11 2000 Defect in insulin release attributable to reduced ATP content in the pancreatic islets induced partially by high intracellular calcium, secondary to augmented PTH-induced calcium entry into cells. Adenosine Triphosphate 50-53 insulin Homo sapiens 10-17 9705342-0 1998 ATP-dependent desensitization of insulin binding and tyrosine kinase activity of the insulin receptor kinase. Adenosine Triphosphate 0-3 insulin Homo sapiens 33-40 10604477-2 1999 In the consensus model of glucose-stimulated insulin secretion, ATP is generated by mitochondrial metabolism, promoting closure of ATP-sensitive potassium (KATP) channels, which depolarizes the plasma membrane. Adenosine Triphosphate 64-67 insulin Homo sapiens 45-52 9731791-13 1998 Intracellular adenosine triphosphate was improved by 75% in cells exposed to high glucose concentrations in the presence of insulin. Adenosine Triphosphate 14-36 insulin Homo sapiens 124-131 9705342-0 1998 ATP-dependent desensitization of insulin binding and tyrosine kinase activity of the insulin receptor kinase. Adenosine Triphosphate 0-3 insulin Homo sapiens 85-92 9705342-2 1998 Incubating endosomes with ATP decreased binding of 125I-insulin but not 125I-labeled human growth hormone. Adenosine Triphosphate 26-29 insulin Homo sapiens 56-63 9705342-3 1998 Increasing ATP concentrations from 0.1 to 1 mM increased beta-subunit tyrosine phosphorylation and insulin receptor kinase (IRK) activity assayed after partial purification. Adenosine Triphosphate 11-14 insulin Homo sapiens 99-106 9595270-10 1998 ATP acts synergistically with polypeptide growth factors (PDGF, bFGF, IGF-1, EGF, insulin) and growth factors acting via G-protein-coupled receptors (noradrenaline, neuropeptide Y, 5-hydroxytryptamine, angiotensin II, endothelin-1). Adenosine Triphosphate 0-3 insulin Homo sapiens 82-89 9881813-3 1998 According to this hypothesis, insulin resistance leads to inadequate intracellular glucose, which in turn leads to insufficient amounts of adenosine triphosphate needed for ion transfer, and to drive energy-requiring reactions. Adenosine Triphosphate 139-161 insulin Homo sapiens 30-37 9685425-0 1998 Glucosamine-induced insulin resistance in 3T3-L1 adipocytes is caused by depletion of intracellular ATP. Adenosine Triphosphate 100-103 insulin Homo sapiens 20-27 9534008-6 1998 These results support the notion that variations in the ATP/ADP ratio are sufficient to induce pulsatile insulin release. Adenosine Triphosphate 56-59 insulin Homo sapiens 105-112 9228006-2 1997 Injection of human C-peptide prevented or attenuated vascular and neural (electrophysiological) dysfunction and impaired Na+- and K+-dependent adenosine triphosphate activity in tissues of diabetic rats. Adenosine Triphosphate 143-165 insulin Homo sapiens 19-28 9493129-11 1998 The insulin-induced increases in single channel conductance and open probability were reversibly decreased by application of PTK catalytic subunit in the presence of ATP through a decrease in the sensitivity to cytosolic Ca2+, but not by protein kinase A. Adenosine Triphosphate 166-169 insulin Homo sapiens 4-11 9032110-0 1997 Amino acid polymorphisms in the ATP-regulatable inward rectifier Kir6.2 and their relationships to glucose- and tolbutamide-induced insulin secretion, the insulin sensitivity index, and NIDDM. Adenosine Triphosphate 32-35 insulin Homo sapiens 132-139 9233793-7 1997 Thus, mitochondrially driven insulin secretion at permissive [Ca2+]c requires both a substrate for the TCA cycle and a rise in [Ca2+]m. Therefore, mitochondrial metabolism generates factors distinct from Ca2+ and ATP capable of inducing insulin exocytosis. Adenosine Triphosphate 213-216 insulin Homo sapiens 29-36 9201908-8 1997 These findings demonstrate basal state binding of ATP to the CKD leading to cis-autophosphorylation and novel basal state regulatory interactions among the subdomains of the insulin receptor kinase. Adenosine Triphosphate 50-53 insulin Homo sapiens 174-181 9054578-8 1997 Our observation that ATP binds to the insulin receptor in the presence and absence of insulin supports the idea that the conformational change produced by insulin binding increases the rate of autophosphorylation rather than increases ATP affinity. Adenosine Triphosphate 21-24 insulin Homo sapiens 38-45 9054578-8 1997 Our observation that ATP binds to the insulin receptor in the presence and absence of insulin supports the idea that the conformational change produced by insulin binding increases the rate of autophosphorylation rather than increases ATP affinity. Adenosine Triphosphate 235-238 insulin Homo sapiens 38-45 9006957-3 1997 Here we report that ATP also greatly enhanced the mitogenic effects of ChoP (0.1-1 mM) both in the absence and presence of insulin; maximal potentiating effects required 50-100 microM ATP. Adenosine Triphosphate 20-23 insulin Homo sapiens 123-130 8769317-5 1996 Responses elicited by 10 micrograms/ml insulin are slower, smaller and more transient than responses to ATP, and are inhibited by preincubation with 100 nM wortmannin. Adenosine Triphosphate 104-107 insulin Homo sapiens 39-46