PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 21031461-8 2011 Further, the phosphorylation of insulin receptor was attenuated in response to insulin stimulation under high glucose conditions, and PJ34 could reverse this effect. Glucose 110-117 insulin receptor Homo sapiens 32-48 20938636-2 2011 Phosphorylation of TBC1 domain family, member 4 (TBC1D4) is at present the most distal insulin receptor signalling event linked to glucose transport. Glucose 131-138 insulin receptor Homo sapiens 87-103 21931226-0 2011 Recurrent hypoglycemia during pregnancies in a woman with multiple autoantibodies including anti-insulin receptor antibody and anti-platelet antibody, whose serum lowered murine blood glucose levels and phosphorylated insulin receptor of CHO-IR cells. Glucose 184-191 insulin receptor Homo sapiens 97-113 20352052-8 2010 Incubation of adult worms in vitro, both with a specific insulin receptor inhibitor and anti-SjIRs antibodies, resulted in a significant decrease in worm glucose levels, suggesting again the same function for SjIRs in regulating glucose uptake as described for mammalian cells. Glucose 154-161 insulin receptor Homo sapiens 57-73 21036152-8 2010 In CHO cells constitutively expressing human insulin receptor (CHO-IR), there was a concentration dependent increase of promoter activity by insulin in the presence of glucose. Glucose 168-175 insulin receptor Homo sapiens 45-61 20352052-8 2010 Incubation of adult worms in vitro, both with a specific insulin receptor inhibitor and anti-SjIRs antibodies, resulted in a significant decrease in worm glucose levels, suggesting again the same function for SjIRs in regulating glucose uptake as described for mammalian cells. Glucose 229-236 insulin receptor Homo sapiens 57-73 19862665-10 2010 Long-term (48 h) stimulation of HUVECs with high glucose augmented expression of the insulin receptor and E-selectin, but downregulated COUP-TFII protein expression. Glucose 49-56 insulin receptor Homo sapiens 85-101 19384726-6 2009 For example, in a model of metabolic disease with type II diabetes, proteolytic cleavage of the insulin receptor causes the inability of insulin to signal glucose transport across membranes. Glucose 155-162 insulin receptor Homo sapiens 96-112 19690174-6 2009 This is associated with a decrease in glucose-stimulated phosphorylation of key proteins in the insulin signaling pathway including Akt, AS160, and other Akt substrates, ERK as well as the insulin receptor. Glucose 38-45 insulin receptor Homo sapiens 189-205 19662499-0 2009 Sphingosine 1-phosphate increases glucose uptake through trans-activation of insulin receptor. Glucose 34-41 insulin receptor Homo sapiens 77-93 19800084-10 2010 Our results confirmed the activity of BBR on InsR in humans and its relationship with the glucose-lowering effect. Glucose 90-97 insulin receptor Homo sapiens 45-49 19221977-10 2009 Activation of the muscle insulin receptor was increased by 140% with glucose ingestion (Pre 0.62+/-0.12; Post 1.49+/-0.35), but pinitol did not influence this response. Glucose 69-76 insulin receptor Homo sapiens 25-41 18768589-7 2008 A small inhibiting RNA against insulin receptor significantly blocked visfatin-mediated glucose uptake. Glucose 88-95 insulin receptor Homo sapiens 31-47 18984735-6 2009 In 3T3-L1 adipocytes, this inhibition of insulin receptor phosphorylation is followed by a decrease in the phosphorylation state of protein kinase B and AS160, as well as an inhibition of glucose transport in response to insulin. Glucose 188-195 insulin receptor Homo sapiens 41-57 19251034-1 2009 Binding of insulin to the insulin receptor (IR) leads to a cascade of intracellular signaling events, which regulate multiple biological processes such as glucose and lipid metabolism, gene expression, protein synthesis, and cell growth, division, and survival. Glucose 155-162 insulin receptor Homo sapiens 26-42 19251034-1 2009 Binding of insulin to the insulin receptor (IR) leads to a cascade of intracellular signaling events, which regulate multiple biological processes such as glucose and lipid metabolism, gene expression, protein synthesis, and cell growth, division, and survival. Glucose 155-162 insulin receptor Homo sapiens 44-46 18691010-4 2008 Recent studies have revealed that DGK isozymes play pivotal roles in a wide variety of mammalian signal transduction pathways conducting growth factor/cytokine-dependent cell proliferation and motility, seizure activity, immune responses, cardiovascular responses and insulin receptor-mediated glucose metabolism. Glucose 294-301 insulin receptor Homo sapiens 268-284 18500459-4 2008 Her symptoms responded well to the therapy of predonisolone (30 mg/day) and continuous intravenous glucose as anti-insulin receptor antibody became negative. Glucose 99-106 insulin receptor Homo sapiens 115-131 17003275-9 2006 These data suggest that, in Ir(P1195L/wt) mice, normal levels of plasma glucose were maintained due to high levels of plasma insulin resulting from increased numbers of beta-cells, which in turn was due to increased beta-cell proliferation rather than decreased beta-cell apoptosis. Glucose 72-79 insulin receptor Homo sapiens 28-30 19035155-8 2008 The number and affinity constant of erythrocyte insulin receptor recovered more quickly in intensive glucose controlled group than in hyperglycemia group. Glucose 101-108 insulin receptor Homo sapiens 48-64 19035155-10 2008 Intensive insulin therapy and glucose control may improve function recovery of insulin receptor. Glucose 30-37 insulin receptor Homo sapiens 79-95 18691043-2 2008 Visfatin binds to the insulin receptor at a site distinct from that of insulin and causes hypoglycaemia by reducing glucose release from liver cells and stimulating glucose utilization in adipocytes and myocytes. Glucose 116-123 insulin receptor Homo sapiens 22-38 18691043-2 2008 Visfatin binds to the insulin receptor at a site distinct from that of insulin and causes hypoglycaemia by reducing glucose release from liver cells and stimulating glucose utilization in adipocytes and myocytes. Glucose 165-172 insulin receptor Homo sapiens 22-38 18220662-1 2007 The dissection of mechanisms that regulate glucose transport by insulin has revealed an intricate network of signaling molecules scattered from the insulin receptor to the intracellular glucose transporter GLUT4. Glucose 43-50 insulin receptor Homo sapiens 148-164 16962112-10 2006 Normal fibroblasts respond to increasing glucose concentrations by increasing the expression levels of the IR, IGF-IR, and IGF-I, whereas adhesion fibroblasts respond by decreasing the expression of the IR, IGF-IR, and IGF-I. Glucose 41-48 insulin receptor Homo sapiens 107-109 16962112-10 2006 Normal fibroblasts respond to increasing glucose concentrations by increasing the expression levels of the IR, IGF-IR, and IGF-I, whereas adhesion fibroblasts respond by decreasing the expression of the IR, IGF-IR, and IGF-I. Glucose 41-48 insulin receptor Homo sapiens 115-117 17675299-6 2007 DGK inhibition was also accompanied by increased protein kinase C-alpha (PKCalpha) activity, reduced glucose-induced insulin receptor activation, and GLUT4 translocation. Glucose 101-108 insulin receptor Homo sapiens 117-133 17675299-8 2007 However, antisense silencing of DGKdelta, but not of DGKalpha expression, was sufficient to prevent the effect of high glucose on PKCalpha activity, insulin receptor signaling, and glucose uptake. Glucose 119-126 insulin receptor Homo sapiens 149-165 17675299-9 2007 Thus, the short term exposure of skeletal muscle cells to glucose causes a rapid induction of DGK, followed by a reduction of PKCalpha activity and transactivation of the insulin receptor signaling. Glucose 58-65 insulin receptor Homo sapiens 171-187 17340225-13 2007 These data indicate that the regulation of glucose uptake, proliferation, and type I collagen production by visfatin in human osteoblasts involves IR phosphorylation, the same signal-transduction pathway used by insulin. Glucose 43-50 insulin receptor Homo sapiens 147-149 15764603-0 2005 Differential contribution of insulin receptor substrates 1 versus 2 to insulin signaling and glucose uptake in l6 myotubes. Glucose 93-100 insulin receptor Homo sapiens 29-45 16733497-10 2006 Visfatin binds to the insulin receptor at a site distinct from insulin and exerts hypoglycemic effect by reducing glucose release from hepatocytes and stimulating glucose utilization in peripheral tissues. Glucose 114-121 insulin receptor Homo sapiens 22-38 16733497-10 2006 Visfatin binds to the insulin receptor at a site distinct from insulin and exerts hypoglycemic effect by reducing glucose release from hepatocytes and stimulating glucose utilization in peripheral tissues. Glucose 163-170 insulin receptor Homo sapiens 22-38 16137651-4 2005 Mechanistic studies in adipocytes with alpha-PGG, the more potent of the two anomers, reveal that inhibitors that block the insulin-mediated glucose transport, including one that inhibits the insulin receptor (IR), also completely abolish the glucose transport activated by alpha-PGG. Glucose 141-148 insulin receptor Homo sapiens 192-208 16137651-4 2005 Mechanistic studies in adipocytes with alpha-PGG, the more potent of the two anomers, reveal that inhibitors that block the insulin-mediated glucose transport, including one that inhibits the insulin receptor (IR), also completely abolish the glucose transport activated by alpha-PGG. Glucose 243-250 insulin receptor Homo sapiens 192-208 16137651-4 2005 Mechanistic studies in adipocytes with alpha-PGG, the more potent of the two anomers, reveal that inhibitors that block the insulin-mediated glucose transport, including one that inhibits the insulin receptor (IR), also completely abolish the glucose transport activated by alpha-PGG. Glucose 243-250 insulin receptor Homo sapiens 210-212 16607115-8 2006 The insulin receptor signaling cascade induces anabolic and anticatabolic effects, but its abnormal upregulation under starving conditions potentially compromises glucose and amino acid homeostasis. Glucose 163-170 insulin receptor Homo sapiens 4-20 15581361-1 2004 Cbl is phosphorylated by the insulin receptor and reportedly functions within the flotillin/CAP/Cbl/Crk/C3G/TC10 complex during insulin-stimulated glucose transport in 3T3/L1 adipocytes. Glucose 147-154 insulin receptor Homo sapiens 29-45 15610610-4 2004 As a potential tool to rescue glucose homeostasis at will in both insulin and insulin receptor deficiencies, we developed a recombinant chimeric insulin receptor (LFv2IRE) that can be homodimerized and activated by the small-molecule dimerizer AP20187. Glucose 30-37 insulin receptor Homo sapiens 145-161 15094074-2 2004 In the central nervous system (CNS), insulin and the insulin receptor are found in specific brain regions where they show evidence of participation in a variety of region-specific functions through mechanisms that are different from its direct glucose regulation in the periphery. Glucose 244-251 insulin receptor Homo sapiens 53-69 15118262-0 2004 K(ATP) channel knockout mice crossbred with transgenic mice expressing a dominant-negative form of human insulin receptor have glucose intolerance but not diabetes. Glucose 127-134 insulin receptor Homo sapiens 105-121 12948866-5 2003 Alpha-lipoic acid or insulin-stimulated glucose uptake was inhibited (i) by alkylation of intracellular, but not extracellular, thiol groups downstream of insulin receptor activation, and (ii) by diphenylene iodonium at the level of the insulin receptor autophosphorylation. Glucose 40-47 insulin receptor Homo sapiens 155-171 12948866-7 2003 These findings indicate that oxidants produced by alpha-lipoic acid or insulin are involved in activation of insulin receptor and in inactivation of protein tyrosine phosphatases, which eventually result in elevated glucose uptake into 3T3-L1 adipocytes. Glucose 216-223 insulin receptor Homo sapiens 109-125 15117549-8 2004 These results suggest that ethanol specifically inhibits the association of the insulin receptor and IRS-1 with the p85 subunit of PI3-kinase, which is required for increased glucose uptake, DNA synthesis, and c-Jun expression by insulin. Glucose 175-182 insulin receptor Homo sapiens 80-96 15289656-1 2004 Insulin receptor signal transduction plays a critical role in regulating pancreatic beta-cell function, notably the acute first-phase insulin release in response to glucose. Glucose 165-172 insulin receptor Homo sapiens 0-16 15289656-6 2004 Manipulations aimed at reducing expression of physiologically relevant PTPases acting at a step proximal to the insulin receptor are accompanied by normalization of blood glucose levels and improved insulin sensitivity in both normal and diabetic animals. Glucose 171-178 insulin receptor Homo sapiens 112-128 14690593-1 2003 The adaptor protein APS is a substrate of the insulin receptor and couples receptor activation with phosphorylation of Cbl to facilitate glucose uptake. Glucose 137-144 insulin receptor Homo sapiens 46-62 12948866-5 2003 Alpha-lipoic acid or insulin-stimulated glucose uptake was inhibited (i) by alkylation of intracellular, but not extracellular, thiol groups downstream of insulin receptor activation, and (ii) by diphenylene iodonium at the level of the insulin receptor autophosphorylation. Glucose 40-47 insulin receptor Homo sapiens 237-253 12882906-1 2003 Stimulation of glucose transport by insulin involves tyrosine phosphorylation of the insulin receptor (IR) and IR substrates (IRSs). Glucose 15-22 insulin receptor Homo sapiens 85-101 12882906-1 2003 Stimulation of glucose transport by insulin involves tyrosine phosphorylation of the insulin receptor (IR) and IR substrates (IRSs). Glucose 15-22 insulin receptor Homo sapiens 103-105 12882906-1 2003 Stimulation of glucose transport by insulin involves tyrosine phosphorylation of the insulin receptor (IR) and IR substrates (IRSs). Glucose 15-22 insulin receptor Homo sapiens 111-113 12734794-0 2003 Glucose-mannose-binding lectins isolated from Brazilian beans stimulate the autophosphorylation of the insulin receptor in vitro. Glucose 0-7 insulin receptor Homo sapiens 103-119 12738810-4 2003 Furthermore, we find that alterations in insulin expression and secretion caused by chronic exposure to high glucose are paralleled by decreased insulin receptor expression and increased relative abundance of the Ex11+ isoform in both human islets and RIN beta-cells. Glucose 109-116 insulin receptor Homo sapiens 145-161 11801259-4 2002 Perifusion experiments revealed that both glucose-stimulated and basal insulin secretion were significantly inhibited following human islet insulin receptor activation with L-783,281, and that signalling through phosphatidylinositol 3-kinase (PI 3-kinase) was responsible, at least in part, for this inhibitory effect. Glucose 42-49 insulin receptor Homo sapiens 140-156 12067836-1 2002 Considerable evidence suggests that atypical protein kinase C isoforms (aPKCs), serving downstream of insulin receptor substrates and phosphatidylinositol (PI) 3-kinase, are required for insulin-stimulated glucose transport in skeletal muscle and adipocytes. Glucose 206-213 insulin receptor Homo sapiens 102-118 12169270-10 2002 In summary, these data indicate that PLCgamma, activated at least partially by PI3-kinase, is a link between insulin receptor and PKCzeta through the production of PA and could mediate insulin-induced glucose uptake and GLUT4 translocation. Glucose 201-208 insulin receptor Homo sapiens 109-125 12145261-0 2002 Obesity is a critical risk factor for worsening of glucose tolerance in a family with the mutant insulin receptor. Glucose 51-58 insulin receptor Homo sapiens 97-113 11295170-12 2001 An adaptive coregulation of Glut-4 and insulin receptor content appears to optimize the use of glucose during chronic hypobaric hypoxia within these tissues. Glucose 95-102 insulin receptor Homo sapiens 39-55 11887975-15 2001 These findings may suggest that the effect of rosiglitazone on glucose and lipid metabolism are dependent on the presence of intact IR protein. Glucose 63-70 insulin receptor Homo sapiens 132-134 11423485-10 2001 Interestingly, lack of IR expression in IR-null keratinocytes abolished insulin-induced glucose uptake and partially decreased insulin- and IGF-I-induced proliferation, demonstrating the direct involvement of the IR in these processes. Glucose 88-95 insulin receptor Homo sapiens 23-25 11423485-10 2001 Interestingly, lack of IR expression in IR-null keratinocytes abolished insulin-induced glucose uptake and partially decreased insulin- and IGF-I-induced proliferation, demonstrating the direct involvement of the IR in these processes. Glucose 88-95 insulin receptor Homo sapiens 40-42 11423485-10 2001 Interestingly, lack of IR expression in IR-null keratinocytes abolished insulin-induced glucose uptake and partially decreased insulin- and IGF-I-induced proliferation, demonstrating the direct involvement of the IR in these processes. Glucose 88-95 insulin receptor Homo sapiens 40-42 10909978-1 2000 In patients harboring the IR1152 mutant insulin receptor, hepatic glucose production was normally suppressed by insulin. Glucose 66-73 insulin receptor Homo sapiens 40-56 10927617-1 2000 Recent studies suggest that high glucose concentrations impair insulin receptor phosphorylation and kinase activation in certain cell models. Glucose 33-40 insulin receptor Homo sapiens 63-79 10764799-0 2000 Selective attenuation of metabolic branch of insulin receptor down-signaling by high glucose in a hepatoma cell line, HepG2 cells. Glucose 85-92 insulin receptor Homo sapiens 45-61 10764799-1 2000 The effects of a high concentration of glucose on the insulin receptor-down signaling were investigated in human hepatoma (HepG2) cells in vitro to delineate the molecular mechanism of insulin resistance under glucose toxicity. Glucose 39-46 insulin receptor Homo sapiens 54-70 10909978-9 2000 Thus, the mechanisms controlling insulin receptor internalization differ in liver and skeletal muscle cells and may enable IR1152 to control glucose metabolism selectively in liver. Glucose 141-148 insulin receptor Homo sapiens 33-49 10329994-0 1999 Insulin receptor autophosphorylation in cultured myoblasts correlates to glucose disposal in Pima Indians. Glucose 73-80 insulin receptor Homo sapiens 0-16 10751417-11 2000 Our results suggest that: 1) insulin stimulation of glucose transport in adipocytes requires </=45% of maximal tyrosyl phosphorylation of IR or IRS-1 and <50% of maximal activation of PI3K, 2) a novel PI3K-independent pathway may play a role in insulin-induced glucose transport in adipocytes, and 3) overexpression of PTP1B alone in adipocytes does not impair glucose transport. Glucose 52-59 insulin receptor Homo sapiens 141-143 10544179-5 1999 By extraction with beta-cyclodextrin or destruction with cholesterol oxidase, cholesterol reduction attenuated insulin receptor signaling to protein phosphorylation or glucose transport. Glucose 168-175 insulin receptor Homo sapiens 111-127 10521479-4 1999 The wild-type insulin receptor chimera mediated approximately 2-fold greater phosphorylation of insulin receptor substrate 1 (IRS-1), association of IRS-1 with phosphoinositide 3-kinase, stimulation of glucose uptake, and GLUT4 translocation, compared with the IGF-I receptor chimera. Glucose 202-209 insulin receptor Homo sapiens 14-30 10212828-1 1998 We have achieved significant progress in understanding the central role of the insulin receptor in an increasingly complicated web of intracellular signal transduction leading to the ultimate biological actions of insulin on glucose, lipid, and other metabolic pathways. Glucose 225-232 insulin receptor Homo sapiens 79-95 10338114-2 1999 It is known that supraphysiological levels of D-glucose or 2-deoxyglucose inhibit the insulin receptor and it is speculated that this effect is mediated by serine phosphorylation of the insulin receptor beta-subunit and other proteins of the insulin signaling chain. Glucose 46-55 insulin receptor Homo sapiens 86-102 10338114-2 1999 It is known that supraphysiological levels of D-glucose or 2-deoxyglucose inhibit the insulin receptor and it is speculated that this effect is mediated by serine phosphorylation of the insulin receptor beta-subunit and other proteins of the insulin signaling chain. Glucose 46-55 insulin receptor Homo sapiens 186-202 9345317-1 1997 Two early events downstream of insulin receptor autophosphorylation that are necessary for activation of glucose transport in adipocytes appear to be: (1) The tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1) which (2) recruits and activates phosphatidylinositol 3"-kinase (PI3"-K). Glucose 105-112 insulin receptor Homo sapiens 31-47 8617880-2 1996 Inhibition of insulin receptor signaling by high glucose levels and by TNF-alpha was recently observed in different cell systems. Glucose 49-56 insulin receptor Homo sapiens 14-30 9175764-3 1997 Most likely due to the IR affinity defect analyses of signal transduction pathways showed an impairment of insulin action on glucose uptake, total RNA synthesis and phosphorylation as well as activity of MAP-kinase. Glucose 125-132 insulin receptor Homo sapiens 23-25 9112018-2 1997 Site-directed mutagenesis as well as analyses of the patient"s lymphocytes revealed that this mutation causes a marked decrease in tyrosine kinase activity of the insulin receptor without any defect in insulin binding, which causes severe defects in insulin-stimulated glucose transport, glycogen synthesis and DNA synthesis. Glucose 269-276 insulin receptor Homo sapiens 163-179 9054426-1 1997 L6 myotubes expressing the constitutively active Arg1152-->Gln insulin receptor (L6(1152)) featured a 31% increased glucose consumption as compared with L6 cells expressing wild-type receptors (L6(WT)). Glucose 119-126 insulin receptor Homo sapiens 66-82 8826966-9 1996 Insulin stimulation of muscle glucose transport was negatively related to muscle PC-1 content (r = -0.68, P = 0.001) and positively related to insulin receptor content (r = 0.60, P = 0.005). Glucose 30-37 insulin receptor Homo sapiens 143-159 8617880-4 1996 TNF-alpha (0.5-10 nM) and high glucose (25 mM) showed similar rapid kinetics of inhibition (5-10 min, > 50%) of insulin receptor autophosphorylation in NIH3T3 cells overexpressing the human insulin receptor. Glucose 31-38 insulin receptor Homo sapiens 193-209 8617880-10 1996 In summary, the data suggest that TNF-alpha and high glucose modulate insulin receptor-signaling through different mechanisms: (a) TNF-alpha modulates insulin receptor signals by PTPase activation, whereas glucose acts through activation of PKC. Glucose 53-60 insulin receptor Homo sapiens 70-86 8617880-10 1996 In summary, the data suggest that TNF-alpha and high glucose modulate insulin receptor-signaling through different mechanisms: (a) TNF-alpha modulates insulin receptor signals by PTPase activation, whereas glucose acts through activation of PKC. Glucose 53-60 insulin receptor Homo sapiens 151-167 8617880-10 1996 In summary, the data suggest that TNF-alpha and high glucose modulate insulin receptor-signaling through different mechanisms: (a) TNF-alpha modulates insulin receptor signals by PTPase activation, whereas glucose acts through activation of PKC. Glucose 206-213 insulin receptor Homo sapiens 70-86 8617880-11 1996 (b) Differences in modulation of the insulin receptor signaling cascade are found with TNF-alpha and high glucose: Hyperglycemia-induced insulin receptor inhibition blocks both insulin receptor-dependent tyrosine phosphorylation and dephosphorylation of insulin receptor substrate proteins. Glucose 106-113 insulin receptor Homo sapiens 37-53 8617880-11 1996 (b) Differences in modulation of the insulin receptor signaling cascade are found with TNF-alpha and high glucose: Hyperglycemia-induced insulin receptor inhibition blocks both insulin receptor-dependent tyrosine phosphorylation and dephosphorylation of insulin receptor substrate proteins. Glucose 106-113 insulin receptor Homo sapiens 137-153 8617880-11 1996 (b) Differences in modulation of the insulin receptor signaling cascade are found with TNF-alpha and high glucose: Hyperglycemia-induced insulin receptor inhibition blocks both insulin receptor-dependent tyrosine phosphorylation and dephosphorylation of insulin receptor substrate proteins. Glucose 106-113 insulin receptor Homo sapiens 137-153 8609215-0 1996 Glucose-induced phosphorylation of the insulin receptor. Glucose 0-7 insulin receptor Homo sapiens 39-55 8609215-2 1996 Elevated glucose concentrations have been reported to inhibit insulin receptor kinase activity. Glucose 9-16 insulin receptor Homo sapiens 62-78 7535776-12 1995 In conclusion, exposing cells to high glucose levels desensitizes insulin receptor function, and thiazolidine derivatives can reverse the process via the normalization of cytosolic PTPase, but not of protein kinase C. Glucose 38-45 insulin receptor Homo sapiens 66-82 8624116-0 1996 Brain glucose metabolism is controlled by amplification and desensitization of the neuronal insulin receptor. Glucose 6-13 insulin receptor Homo sapiens 92-108 7537758-9 1995 We conclude that impaired insulin-stimulated glucose uptake in skeletal muscle from severely obese subjects is accompanied by a deficiency in insulin receptor signaling, which may contribute to decreased insulin action. Glucose 45-52 insulin receptor Homo sapiens 142-158 7849042-5 1995 Most of the compounds which inhibit tyrosine phosphorylation of the insulin receptor also inhibited glucose uptake in the same cells. Glucose 100-107 insulin receptor Homo sapiens 68-84 7867639-1 1995 We have previously shown, in rat-1 fibroblasts which stably overexpress high levels of human insulin receptor (HIR), that high glucose levels induce an inhibition of insulin receptor tyrosine kinase (IRK) activity [Berti, L., Mosthaf, L., Kellerer, M., Tippmer, S., Mushack, J., Seffer, E., Seedorf, K., Haring, H. (1994) J. Biol. Glucose 127-134 insulin receptor Homo sapiens 93-109 7835273-1 1995 Insulin-stimulated glucose transport in adipocytes is mediated by the insulin receptor. Glucose 19-26 insulin receptor Homo sapiens 70-86 7867639-1 1995 We have previously shown, in rat-1 fibroblasts which stably overexpress high levels of human insulin receptor (HIR), that high glucose levels induce an inhibition of insulin receptor tyrosine kinase (IRK) activity [Berti, L., Mosthaf, L., Kellerer, M., Tippmer, S., Mushack, J., Seffer, E., Seedorf, K., Haring, H. (1994) J. Biol. Glucose 127-134 insulin receptor Homo sapiens 166-182 7835273-12 1995 These data suggest that the insulin and EGF signaling pathways that lead to glucose transport converge in these adipocytes down-stream of the insulin receptor, and that activation of this pathway requires signaling motifs in the carboxy-terminus of the EGFR. Glucose 76-83 insulin receptor Homo sapiens 142-158 7867639-13 1995 To test whether serine residues 955/956 and 962/964 in the juxtamembrane region of the insulin receptor are involved in the inhibitory effect of glucose, 293 cells transiently transfected either with wild-type HIR or HIR with a juxtamembrane deletion spanning amino acids 954-965 [des-(954-965)-HIR] were studied in parallel. Glucose 145-152 insulin receptor Homo sapiens 87-103 8048939-1 1994 Specific insulin binding by the fetal lung insulin receptor is reduced in vitro by a combination of high glucose and insulin. Glucose 105-112 insulin receptor Homo sapiens 43-59 7983789-4 1994 The same mutation in the insulin receptor does not always necessarily show the same phenotypes of skin lesion or the same glucose intolerance. Glucose 122-129 insulin receptor Homo sapiens 25-41 7983803-5 1994 In these cases, despite having a same mutation in the insulin receptor gene, some individuals exhibited significant clinical differences (e.g. insulin resistance or glucose tolerance). Glucose 165-172 insulin receptor Homo sapiens 54-70 7826318-0 1995 Glucose-induced stimulation of human insulin-receptor mRNA and tyrosine kinase activity in cultured cells. Glucose 0-7 insulin receptor Homo sapiens 37-53 7826318-1 1995 The effects of high glucose on insulin-receptor tyrosine kinase activity and gene expression were investigated in 3T3-HIR cells. Glucose 20-27 insulin receptor Homo sapiens 31-47 7826318-8 1995 In cells challenged with high glucose plus inhibitor, insulin-receptor mRNA half-life was increased from 1 to 3 h, indicating that posttranscriptional mechanisms are involved in these processes of glucose regulation. Glucose 30-37 insulin receptor Homo sapiens 54-70 7826318-8 1995 In cells challenged with high glucose plus inhibitor, insulin-receptor mRNA half-life was increased from 1 to 3 h, indicating that posttranscriptional mechanisms are involved in these processes of glucose regulation. Glucose 197-204 insulin receptor Homo sapiens 54-70 7826318-9 1995 Inhibition of protein synthesis by cycloheximide induced an overexpression of insulin-receptor mRNA levels in the presence of glucose, suggesting that labile repressor protein(s) could be implicated in the effects of glucose. Glucose 126-133 insulin receptor Homo sapiens 78-94 7826318-9 1995 Inhibition of protein synthesis by cycloheximide induced an overexpression of insulin-receptor mRNA levels in the presence of glucose, suggesting that labile repressor protein(s) could be implicated in the effects of glucose. Glucose 217-224 insulin receptor Homo sapiens 78-94 7826318-10 1995 We conclude that (1) long-term culture with high glucose increases the amount of insulin receptors and their tyrosine kinase activity and (2) the glucose-induced increase in insulin-receptor mRNA levels can be accounted for, at least in part, by posttranscriptional events. Glucose 49-56 insulin receptor Homo sapiens 174-190 7826318-10 1995 We conclude that (1) long-term culture with high glucose increases the amount of insulin receptors and their tyrosine kinase activity and (2) the glucose-induced increase in insulin-receptor mRNA levels can be accounted for, at least in part, by posttranscriptional events. Glucose 146-153 insulin receptor Homo sapiens 174-190 8048939-4 1994 Insulin-receptor mRNA abundance was reduced by high glucose + insulin to 37 +/- 6% of control values (p < .05). Glucose 52-59 insulin receptor Homo sapiens 0-16 1905936-5 1991 The predominant abnormality in brain glucose utilization in incipient late-onset DAT may be associated with an impairment of its control mechanism(s), which are assumed to be either an influence of brain insulin action, or brain insulin receptor function, or both. Glucose 37-44 insulin receptor Homo sapiens 229-245 7927191-2 1994 Insulin receptor activity, as assessed by [125I Tyr A14] insulin binding, was significantly lower in erythrocyte preparations from the obese group when compared with similar preparations from non-obese subjects, with either normal glucose tolerance or NIDDM. Glucose 231-238 insulin receptor Homo sapiens 0-16 7927191-4 1994 Insulin receptor tyrosine kinase activity, measured in the absence (basal) and presence of insulin (0.3-3000 nM), was decreased in obese and NIDDM subjects with normal glucose tolerance and in patients with NIDDM. Glucose 168-175 insulin receptor Homo sapiens 0-16 8088709-11 1994 In a rat-1 fibroblast cell line overexpressing human insulin receptor, inhibition of the tyrosine kinase activity of the receptor can be induced by high glucose levels. Glucose 153-160 insulin receptor Homo sapiens 53-69 8419945-0 1993 Activation of glucose transport by a natural mutation in the human insulin receptor. Glucose 14-21 insulin receptor Homo sapiens 67-83 8419945-3 1993 However, fibroblasts cultured from a patient with intrauterine growth restriction and severe insulin resistance (leprechaun Atl-1) had normal amounts of insulin receptor protein and defective insulin binding but constitutive activation of insulin-receptor autophosphorylation and kinase activity and of glucose transport. Glucose 303-310 insulin receptor Homo sapiens 239-255 8419945-17 1993 These results suggest that the R86P mutation in the insulin receptor activates glucose transport without promoting cell growth and that distinct cell types process this mutant insulin receptor differently. Glucose 79-86 insulin receptor Homo sapiens 52-68 1426762-7 1992 Insulin receptor antibodies, however, have been reported to increase glucose transport without increasing kinase activity. Glucose 69-76 insulin receptor Homo sapiens 0-16 1619013-9 1992 We conclude that in vivo activation of the insulin receptor tyrosine kinase in human skeletal muscle is a rapid process, related to insulin action on glucose disposal, and that circulating insulin primes inactive insulin receptor molecules for subsequent tyrosine kinase activation by a mechanism that remains to be elucidated. Glucose 150-157 insulin receptor Homo sapiens 43-59 1290322-4 1992 Idiopathic insulin resistance in type 2 diabetes is additionally characterized by reduced glucose storage, the basis of which may reside in an insulin receptor defect, in the presence of insulin receptor antibodies, in a postreceptor defect or in the synthesis of abnormal insulin molecules. Glucose 90-97 insulin receptor Homo sapiens 143-159 1308998-0 1992 Mutations in the insulin receptor and their effect on glucose transport. Glucose 54-61 insulin receptor Homo sapiens 17-33 1680759-1 1991 In searching for a genetic marker of type 2 diabetes we estimated the frequency of alleles of the Bgl II restriction fragment length polymorphism (RFLP) of the insulin receptor gene in a group of type II diabetic patients (n = 50), characterized by OGTT (glucose, insulin, C-peptide) and insulin receptor binding parameters. Glucose 255-262 insulin receptor Homo sapiens 160-176 1676686-0 1991 Screening for insulin receptor gene DNA polymorphisms associated with glucose intolerance in a Scandinavian population. Glucose 70-77 insulin receptor Homo sapiens 14-30 7524845-5 1994 The existence of the common epitope leads to competition of insulin and apoprotein B for an insulin receptor and reduces tissue glucose uptake. Glucose 128-135 insulin receptor Homo sapiens 92-108 8421104-4 1993 In this study we investigated the ability of the monocyte insulin receptor to acutely alter its affinity in response to oral glucose. Glucose 125-132 insulin receptor Homo sapiens 58-74 1618850-0 1992 Differential role of insulin receptor autophosphorylation sites 1162 and 1163 in the long-term insulin stimulation of glucose transport, glycogenesis, and protein synthesis. Glucose 118-125 insulin receptor Homo sapiens 21-37 1619960-12 1992 When insulin receptor protein is confined to small areas of the cell membrane through aggregation, any potential inhibitory function is negated and glucose entry increases dramatically. Glucose 148-155 insulin receptor Homo sapiens 5-21 1547686-1 1992 OBJECTIVE: To evaluate insulin receptor binding characteristics of urbanized South African black women with normal glucose tolerance and of patients with newly diagnosed untreated non-insulin-dependent diabetes mellitus (NIDDM). Glucose 115-122 insulin receptor Homo sapiens 23-39 1547686-6 1992 CONCLUSIONS: Our study of urban South African black women showed decreasing insulin-receptor activity with obesity and glucose intolerance. Glucose 119-126 insulin receptor Homo sapiens 76-92 2019259-8 1991 Insulin receptor down-regulation (18%) was observed after 24 h (but not 5 h) in insulin-treated cells; however, the major portion of the decrease in insulin sensitivity was due to uncoupling of occupied insulin receptors from stimulation of the glucose transport system. Glucose 245-252 insulin receptor Homo sapiens 0-16 2229049-0 1990 Glucose regulation of insulin receptor affinity in primary cultured adipocytes. Glucose 0-7 insulin receptor Homo sapiens 22-38 2250023-0 1990 Insulin receptor tyrosine residues 1162 and 1163 control insulin stimulation of myristoyl-diacylglycerol generation and subsequent activation of glucose transport. Glucose 145-152 insulin receptor Homo sapiens 0-16 2229049-1 1990 Treatment of primary cultured adipocytes with 20 mM glucose resulted in a progressive increase in specific 125I-insulin binding that began almost immediately (no lag period) and culminated in a 60% increase by 24 h. This effect was dose-dependent (glucose ED50 of 4.6 mM) and mediated by an increase in insulin receptor affinity. Glucose 52-59 insulin receptor Homo sapiens 303-319 2229049-1 1990 Treatment of primary cultured adipocytes with 20 mM glucose resulted in a progressive increase in specific 125I-insulin binding that began almost immediately (no lag period) and culminated in a 60% increase by 24 h. This effect was dose-dependent (glucose ED50 of 4.6 mM) and mediated by an increase in insulin receptor affinity. Glucose 248-255 insulin receptor Homo sapiens 303-319 2229049-2 1990 Moreover, it appears that glucose modulates insulin receptor affinity through de novo protein synthesis rather than through covalent modification of receptors, since cycloheximide selectively inhibited the glucose-induced increase in insulin binding capacity (ED50 of 360 ng/ml) and restored receptor affinity to control values. Glucose 26-33 insulin receptor Homo sapiens 44-60 2229049-2 1990 Moreover, it appears that glucose modulates insulin receptor affinity through de novo protein synthesis rather than through covalent modification of receptors, since cycloheximide selectively inhibited the glucose-induced increase in insulin binding capacity (ED50 of 360 ng/ml) and restored receptor affinity to control values. Glucose 206-213 insulin receptor Homo sapiens 44-60 2229049-5 1990 On the basis of these studies, we conclude that 1) insulin binding is subject to dual regulation (glucose controls insulin action by enhancing receptor affinity, whereas insulin controls the number of cell surface receptors); and 2) glucose appears to modulate insulin receptor affinity through the rapid biosynthesis of an affinity regulatory protein. Glucose 233-240 insulin receptor Homo sapiens 261-277 1694071-2 1990 In this work (i) we stably cultured three human cell lines in media containing different glucose concentrations (from 0 to 25 mM), (ii) we characterized glucose effects on insulin receptor gene expression, (iii) we investigated the mechanism by which glucose produces these effects. Glucose 153-160 insulin receptor Homo sapiens 172-188 1697168-3 1990 We found that (i) forskolin reduces insulin receptor mRNA levels; (ii) the effects of either forskolin or dexamethasone on insulin receptor mRNA levels are near completely abolished in glucose-starved cells; (iii) 2-mercaptoethanol and heat shock, besides previously described stress conditions (glycosylatyon inhibitors), reduce insulin receptor mRNA levels. Glucose 185-192 insulin receptor Homo sapiens 123-139 1697168-3 1990 We found that (i) forskolin reduces insulin receptor mRNA levels; (ii) the effects of either forskolin or dexamethasone on insulin receptor mRNA levels are near completely abolished in glucose-starved cells; (iii) 2-mercaptoethanol and heat shock, besides previously described stress conditions (glycosylatyon inhibitors), reduce insulin receptor mRNA levels. Glucose 185-192 insulin receptor Homo sapiens 123-139 1694071-2 1990 In this work (i) we stably cultured three human cell lines in media containing different glucose concentrations (from 0 to 25 mM), (ii) we characterized glucose effects on insulin receptor gene expression, (iii) we investigated the mechanism by which glucose produces these effects. Glucose 153-160 insulin receptor Homo sapiens 172-188 1694071-4 1990 Our data indicate that glucose affects insulin receptor gene expression in human cells and that protein glycosylation plays a role in this regulatory mechanism. Glucose 23-30 insulin receptor Homo sapiens 39-55 2156441-2 1990 In both species, IGF-II has been reported to stimulate glucose transport by interacting with the insulin receptor. Glucose 55-62 insulin receptor Homo sapiens 97-113 33777737-3 2021 The aim of this study is to explore the association of triglyceride glucose (TyG) index, a simple surrogate marker of IR, with NSCLC risk. Glucose 68-75 insulin receptor Homo sapiens 118-120 2210055-5 1990 The sequences of the gene and oligonucleotide primers will facilitate studies of genetic variation in the hINSR gene and thereby increase our understanding of the role of this gene in the development of insulin-resistant states and glucose intolerance. Glucose 232-239 insulin receptor Homo sapiens 106-111 34969688-3 2021 An in vitro model of IR cleavage shows that extracellular calpain 2 directly cleaves IR, which generates sIR, and sequential cleavage of the IRbeta subunit by gamma-secretase impairs insulin signaling in a glucose concentration-dependent manner. Glucose 206-213 insulin receptor Homo sapiens 21-23 33776919-5 2021 The aim of the present study was to measure the content of IR and IGF-1R and their phosphorylation in the placenta of women with type 1 diabetes mellitus (T1D) or with gestational diabetes mellitus (GDM) compared to women with normal glucose tolerance (NGT) during pregnancy. Glucose 234-241 insulin receptor Homo sapiens 59-61 33033446-12 2020 Several parameter values were affected by the INSR genotype, particularly W/H ratio, lipid, insulin and glucose levels and insulin resistance in PCOS patients. Glucose 104-111 insulin receptor Homo sapiens 46-50 34944530-3 2021 Insulin receptor stimulation is correlated with multiple physiological and biochemical functions, including glucose transport, glucose homeostasis, food intake, proliferation, glycolysis, and lipogenesis. Glucose 108-115 insulin receptor Homo sapiens 0-16 34944530-5 2021 Signal transducers such as protein kinases or the GLUT4-induced influx of glucose connect insulin receptor stimulation with transcription. Glucose 74-81 insulin receptor Homo sapiens 90-106 33805872-11 2021 CONCLUSIONS: An increase of fasting glucose and more frequent incidence of metabolic syndrome, diabetes, and cardiovascular diseases in subjects with IR are associated with the prevalence of cardiovascular risk factors. Glucose 36-43 insulin receptor Homo sapiens 150-152 33776919-13 2021 A positive correlation was observed between phosphorylation of placental IR and the glucose levels during the third trimester of GDM and T1D pregnancy (R-squared 0.21, p=0.003). Glucose 84-91 insulin receptor Homo sapiens 73-75 7821730-11 1994 We have found that in rat-1 fibroblasts which overexpressing human insulin receptor an inhibition of the tyrosine kinase activity of the receptor may be induced by high glucose levels. Glucose 169-176 insulin receptor Homo sapiens 67-83 34165135-6 2021 However, clinical trials and systematic reviews show statistical differences on glucose, insulin, and glycated hemoglobin levels of patients with T2DM, associated with activation mechanisms of transcription factors related to genes of the glucide metabolism and the insulin receptor, and the regulation of intracellular Ca2+ insulin concentrations. Glucose 80-87 insulin receptor Homo sapiens 266-282 34438601-7 2021 IR was calculated by using the homeostasis model assessment for IR in patients with obesity and the estimated glucose disposal rate in T1D. Glucose 110-117 insulin receptor Homo sapiens 0-2 34207541-1 2021 Insulin acts by binding with a specific receptor called an insulin receptor (INSR), ending up with glucose transporter activation and glucose uptake. Glucose 99-106 insulin receptor Homo sapiens 77-81 34203120-2 2021 LRP1 is a scaffold protein for insulin receptor involved in the insulin-induced glucose transporter type 4 (GLUT4) translocation to plasma membrane and glucose uptake in different types of cells. Glucose 152-159 insulin receptor Homo sapiens 31-47 34207541-1 2021 Insulin acts by binding with a specific receptor called an insulin receptor (INSR), ending up with glucose transporter activation and glucose uptake. Glucose 99-106 insulin receptor Homo sapiens 59-75 34207541-1 2021 Insulin acts by binding with a specific receptor called an insulin receptor (INSR), ending up with glucose transporter activation and glucose uptake. Glucose 134-141 insulin receptor Homo sapiens 59-75 34207541-1 2021 Insulin acts by binding with a specific receptor called an insulin receptor (INSR), ending up with glucose transporter activation and glucose uptake. Glucose 134-141 insulin receptor Homo sapiens 77-81 35223937-7 2021 In addition, we illustrated our cellular and molecular model consisting of studying the functional activity of CM fractions on IR and its downstream signaling pathways in the hepatocarcinoma (HepG2) and the human embryonic kidney (HEK293) cells using the bioluminescence resonance energy transfer (BRET), phosphorylation, and glucose uptake assays. Glucose 326-333 insulin receptor Homo sapiens 127-129 35073186-10 2022 Conclusions: We developed a simple and affordable method of identifying IR in children with overweight or OB based on anthropometric variables and routine blood tests for metabolic indicators, such as glucose and triglycerides, which can be implemented in underserved sites. Glucose 201-208 insulin receptor Homo sapiens 72-74 2558650-5 1989 We previously demonstrated that insulin receptor gene expression in human cell lines in enhanced by glucose. Glucose 100-107 insulin receptor Homo sapiens 32-48 35225010-8 2022 High glucose can influence on GBM progression through the promotion of the following parameters: cell viability, dispersal, InsR expression and cell proliferation (Ki-67). Glucose 5-12 insulin receptor Homo sapiens 124-128 2551760-9 1989 However, IGF-I stimulates glucose transport predominantly by interacting with the insulin receptor. Glucose 26-33 insulin receptor Homo sapiens 82-98 2753889-1 1989 Recently, we have described a COOH-terminal deletion mutation of the human insulin receptor (HIR delta CT) that exhibits normal insulin-mediated kinase activity and endocytosis, but is inefficient in stimulating glucose transport and glycogen synthase (McClain, D. A., Maegawa, H., Levy, J., Huecksteadt, T., Dull, T. J., Lee, J., Ullrich, A., and Olefsky, J.M. Glucose 212-219 insulin receptor Homo sapiens 75-91 2834414-0 1988 Alterations in insulin receptor autophosphorylation in insulin resistance: correlation with altered sensitivity to glucose transport and antilipolysis to insulin. Glucose 115-122 insulin receptor Homo sapiens 15-31 2543399-0 1989 Effect of two different glucose concentrations on insulin receptor mRNA levels in human hepatoma HepG2 cells. Glucose 24-31 insulin receptor Homo sapiens 50-66 2543399-3 1989 Insulin receptor mRNA levels and insulin binding activity were reduced in HepG2 cultured at lower glucose concentrations. Glucose 98-105 insulin receptor Homo sapiens 0-16 2543399-4 1989 These data suggest that glucose affects insulin receptor gene expression. Glucose 24-31 insulin receptor Homo sapiens 40-56 2546845-5 1989 After corticoids and immunosuppressive therapy by azathioprine, the patient hypoglycaemic episodes disappeared, and concomitantly, the antibodies to insulin receptor were no longer detected, as judged by both immunoprecipitation of insulin receptor and stimulation of glucose transport. Glucose 268-275 insulin receptor Homo sapiens 149-165 2972576-8 1988 These results indicate that 1) the defect is specific to the insulin-receptor binding in these patients, 2) insulin and IGF-I activate glucose incorporation and alpha-aminoisobutyric acid uptake mainly through their own specific receptors, but 3) the IGF-I receptor appears to have a more important role in stimulating thymidine incorporation than the insulin receptor in physiological condition or, alternatively, an unknown postreceptor process with cascade signal transmission may overcome the decreased insulin-receptor binding to produce a normal dose-response curve. Glucose 135-142 insulin receptor Homo sapiens 61-77 2972576-8 1988 These results indicate that 1) the defect is specific to the insulin-receptor binding in these patients, 2) insulin and IGF-I activate glucose incorporation and alpha-aminoisobutyric acid uptake mainly through their own specific receptors, but 3) the IGF-I receptor appears to have a more important role in stimulating thymidine incorporation than the insulin receptor in physiological condition or, alternatively, an unknown postreceptor process with cascade signal transmission may overcome the decreased insulin-receptor binding to produce a normal dose-response curve. Glucose 135-142 insulin receptor Homo sapiens 352-368 2972576-8 1988 These results indicate that 1) the defect is specific to the insulin-receptor binding in these patients, 2) insulin and IGF-I activate glucose incorporation and alpha-aminoisobutyric acid uptake mainly through their own specific receptors, but 3) the IGF-I receptor appears to have a more important role in stimulating thymidine incorporation than the insulin receptor in physiological condition or, alternatively, an unknown postreceptor process with cascade signal transmission may overcome the decreased insulin-receptor binding to produce a normal dose-response curve. Glucose 135-142 insulin receptor Homo sapiens 507-523 3045261-8 1988 We conclude that (1) cultured neurons from fetal chicken brain express the same subtype of insulin receptor previously identified in adult rat and human brain, (2) the neuronal subtype of insulin receptor undergoes internalization and down-regulation in response to insulin, and (3) neuronal insulin receptors do not acutely regulate glucose metabolism but mediate growth in neurons. Glucose 334-341 insulin receptor Homo sapiens 188-204 2546561-5 1989 Similarly, insulin receptor tyrosine kinase as assessed by receptor autophosphorylation and phosphorylation of the substrate poly-(Glu/Tyr) was not fully activated by treatment of cells with the insulin dimer (31 and 42% of the effect of insulin, respectively) in concentrations which maximally activate glucose transport and give rise to full insulin receptor occupancy (5 X 10(-7) M). Glucose 304-311 insulin receptor Homo sapiens 11-27 2834414-5 1988 These data indicate a significant correlation between changes in sensitivity of glucose transport and antilipolysis to insulin and receptor kinase activity in those patients and suggest that defective coupling of insulin binding to insulin action at the level of phosphorylation of the insulin receptor may cause the insulin resistance in this group of patients. Glucose 80-87 insulin receptor Homo sapiens 286-302 3320694-6 1987 These changes in the membrane phospholipids would then theoretically increase both insulin receptor binding affinity and sensitivity, thus enhancing glucose transport across their membranes. Glucose 149-156 insulin receptor Homo sapiens 83-99 3144155-6 1988 Adipocyte insulin receptor binding was comparable before and after therapy, both in the fasting state and following glucose intake. Glucose 116-123 insulin receptor Homo sapiens 10-26 3680872-3 1987 The results obtained clearly demonstrate that dexamethasone increases insulin receptor concentration while glucose ingestion increases both insulin receptor affinity and concentration on young RBCs. Glucose 107-114 insulin receptor Homo sapiens 140-156 3550798-2 1987 It has been shown previously that phenylarsine oxide, an agent that complexes vicinal dithiols, interrupts signal transmission from the insulin receptor to the glucose transport system. Glucose 160-167 insulin receptor Homo sapiens 136-152 3549468-2 1987 A reduction in the biologic action of insulin, at a point beyond the insulin receptor (postbinding site), is primarily responsible for the reduced rate of glucose utilization. Glucose 155-162 insulin receptor Homo sapiens 69-85 3033648-0 1987 Monoclonal antibodies to the human insulin receptor that activate glucose transport but not insulin receptor kinase activity. Glucose 66-73 insulin receptor Homo sapiens 35-51 3550798-3 1987 Several lines of evidence presented here indicate the involvement of pp15 in insulin receptor-initiated signal transduction to the glucose transport system. Glucose 131-138 insulin receptor Homo sapiens 77-93 3101064-0 1987 Replacement of lysine residue 1030 in the putative ATP-binding region of the insulin receptor abolishes insulin- and antibody-stimulated glucose uptake and receptor kinase activity. Glucose 137-144 insulin receptor Homo sapiens 77-93 3440445-11 1987 Thus, this inborn error of the insulin receptor offers unique insight into a regulatory signal by its alpha subunit which, when altered, results in constitutively increased glucose transport. Glucose 173-180 insulin receptor Homo sapiens 31-47 3541915-13 1986 The findings demonstrate that vanadate stimulates glucose transport by an effect at a level distal to the insulin receptor. Glucose 50-57 insulin receptor Homo sapiens 106-122 6599719-7 1984 In the long term, non-diabetics may maintain normal glucose tolerance on thiazide diuretics by increasing insulin receptor numbers. Glucose 52-59 insulin receptor Homo sapiens 106-122 3005370-4 1986 The functions of the insulin receptor were examined by measuring specific 125I-insulin binding (receptor concentration, affinity, specificity, pH-, time-, and temperature dependence), insulin-induced down-regulation of the receptor, insulin-stimulated autophosphorylation of the beta-subunit, and phosphorylation of exogenous substrates as well as insulin-stimulated glucose uptake in glioblastoma cells. Glucose 367-374 insulin receptor Homo sapiens 21-37 6331454-0 1984 Effect of glucose on beta-adrenergic induced downregulation of insulin receptor binding in human fat cells. Glucose 10-17 insulin receptor Homo sapiens 63-79 6384270-4 1984 In these studies, the glucose clamp technique was employed to isolate perturbations in plasma glucose and plasma insulin as potential mediators of the regulation of the mitogen-induced T lymphocyte insulin receptor. Glucose 22-29 insulin receptor Homo sapiens 198-214 6384270-4 1984 In these studies, the glucose clamp technique was employed to isolate perturbations in plasma glucose and plasma insulin as potential mediators of the regulation of the mitogen-induced T lymphocyte insulin receptor. Glucose 94-101 insulin receptor Homo sapiens 198-214 6331454-6 1984 In conclusion, low amounts of glucose prevent catecholamine induced down-regulation of insulin receptor binding in human fat cells at physiological temperature. Glucose 30-37 insulin receptor Homo sapiens 87-103 7028773-9 1981 Finally, the enhanced neonatal glucose tolerance of these babies may be related not only to the hyperinsulinemia but also to increased insulin sensitivity mediated, in part, by the increased insulin receptor binding. Glucose 31-38 insulin receptor Homo sapiens 191-207 6732235-7 1984 These results indicate that the subcellular distribution of internalized insulin and of intracellular glucose transport activity are different, suggesting that the pathways of intracellular processing of the insulin receptor and the glucose transport mechanism are different. Glucose 102-109 insulin receptor Homo sapiens 208-224 6732235-7 1984 These results indicate that the subcellular distribution of internalized insulin and of intracellular glucose transport activity are different, suggesting that the pathways of intracellular processing of the insulin receptor and the glucose transport mechanism are different. Glucose 233-240 insulin receptor Homo sapiens 208-224 6801160-1 1982 Characteristic of insulin receptor in human placental villi with relation to glucose uptake and glycogenesis was studied in vitro. Glucose 77-84 insulin receptor Homo sapiens 18-34 6801160-6 1982 Collectively, the data suggest the presence of insulin receptor in placental villi varying its concentration with gestational age, where insulin plays a role in adjusting glucose uptake and glycogenesis. Glucose 171-178 insulin receptor Homo sapiens 47-63 6389294-1 1984 We have examined insulin binding to the erythrocyte insulin receptor in normal males following a short fast and a test meal or glucose load. Glucose 127-134 insulin receptor Homo sapiens 52-68 7041848-2 1982 Unlike most previously reported cases of islet cell hyperplasia, where the islet cell hyperactivity produced disturbed glucose metabolism (hypoglycemia, this case illustrates compensatory islet cell hyperplasia in response to a perturbation in glucose metabolism by insulin-receptor blockade with resultant hyperglycemia. Glucose 244-251 insulin receptor Homo sapiens 266-282 33569729-7 2021 RESULTS: In the longitudinal study, significant relationships were found between remission of IR and changes in visceral adiposity index (VAI) (r = 0.452, P < 0.05) and triglyceride-glucose index (TyG) (r = 0.650, P < 0.01). Glucose 182-189 insulin receptor Homo sapiens 94-96 279910-1 1978 Exposure of adipocytes to antibodies to the insulin receptor results in a blockade of (125)I-labeled insulin binding, stimulation of glucose oxidation, and many more insulin-like effects. Glucose 133-140 insulin receptor Homo sapiens 44-60 34001235-5 2021 The involvement of CAV1 in glucose/lipid homeostasis is revealed and could modify the signaling of the insulin receptor. Glucose 27-34 insulin receptor Homo sapiens 103-119 7018254-6 1981 Maximal effects of insulin on glucose production and utilization occurred at plasma insulin concentrations causing 11 and 49% insulin receptor occupancy, respectively. Glucose 30-37 insulin receptor Homo sapiens 126-142 1165235-4 1975 Termination of the glucose transport action of insulin (which includes insulin-receptor disassociation and all other steps leading to decelerated glucose entry) began within 2 min and was complete within 30 min. Glucose 19-26 insulin receptor Homo sapiens 71-87 33293347-7 2021 Hepatocellular insulin signaling, assessed for the first time in humans, exhibited a proximal block in insulin-resistant subjects: Signaling was attenuated from the level of the insulin receptor through both glucose and lipogenesis pathways. Glucose 208-215 insulin receptor Homo sapiens 178-194 33634518-5 2021 We present the current literature on the importance of the insulin receptor with respect to regulating glucose and energy homeostasis and mood-related behaviours. Glucose 103-110 insulin receptor Homo sapiens 59-75 33096618-5 2020 Insulin is a protein hormone secreted from pancreatic beta-cells that stimulates glucose uptake and metabolism via insulin receptor signaling. Glucose 81-88 insulin receptor Homo sapiens 115-131 32936988-2 2021 Triglyceride-glucose index (TyG), a simple, inexpensive and easily accessible IR marker, is calculated by fasting serum glucose and triglyceride values. Glucose 13-20 insulin receptor Homo sapiens 78-80 32936988-2 2021 Triglyceride-glucose index (TyG), a simple, inexpensive and easily accessible IR marker, is calculated by fasting serum glucose and triglyceride values. Glucose 120-127 insulin receptor Homo sapiens 78-80 33384765-8 2020 Such studies revealed that all three parameters (insulin receptor, insulin receptor substrate 1, and protein kinase B) were inactivated by high glucose, indicating a disruption of the signal pathway. Glucose 144-151 insulin receptor Homo sapiens 49-65 32733189-4 2020 Here, we explore the relationship between insulin receptor signaling and glucose metabolism using similar methods. Glucose 73-80 insulin receptor Homo sapiens 42-58 32583238-2 2020 A time delay was considered to represent the time required for performing various cellular mechanisms between activation of insulin receptor and subsequent glucose entry from extracellular region into intracellular region of a cardiac cell. Glucose 156-163 insulin receptor Homo sapiens 124-140 32409919-6 2020 Insulin-resistant Huh7 (Huh7-IR) showed a reduction in Glut2, glycogen levels, and glucose uptake stimulated by insulin or tyrosine phosphorylation from the beta-fraction of insulin receptor post-insulin stimulation, with an increase of glucose production and lipid intracellular content. Glucose 83-90 insulin receptor Homo sapiens 174-190 32409919-6 2020 Insulin-resistant Huh7 (Huh7-IR) showed a reduction in Glut2, glycogen levels, and glucose uptake stimulated by insulin or tyrosine phosphorylation from the beta-fraction of insulin receptor post-insulin stimulation, with an increase of glucose production and lipid intracellular content. Glucose 237-244 insulin receptor Homo sapiens 174-190 32427889-6 2020 We also found that the effects of N6-adenine methylation on lipid production involved the regulation of INSR signaling pathway, which promotes glucose up-taking and lipid production in the terminal differentiation stage. Glucose 143-150 insulin receptor Homo sapiens 104-108 31969308-4 2019 In conclusion, SES has the ameliorating effect on L02 hepatocyte model of insulin resistance induced by high glucose/high insulin, which might be related to its effect on promoting expression of insulin receptor and its associated proteins of IRS-PI3K-Akt passway, and thus promoting insulin sensitivity. Glucose 109-116 insulin receptor Homo sapiens 195-211 32332780-4 2020 In muscle, LRP2 is necessary for insulin-dependent IR internalization, an initial trigger for insulin signaling, that is crucial in regulating downstream signaling and glucose uptake. Glucose 168-175 insulin receptor Homo sapiens 51-53 31825461-1 2020 The surfacing of the glucose transporter GLUT4 driven by insulin receptor activation provides the prototypic example of a homeostasis response dependent on mobilization of an intracellular storage compartment. Glucose 21-28 insulin receptor Homo sapiens 57-73 31721020-6 2019 Both IR and ADIPO signaling pathways simultaneously affect the glucose homeostasis regulation effect of DNJ, whereas the key response target located in AMPK and its effect on subsequent GLUT4 mRNA expression. Glucose 63-70 insulin receptor Homo sapiens 5-7 31588494-0 2020 Thyroid Hormone Effects on Glucose Disposal in Patients With Insulin Receptor Mutations. Glucose 27-34 insulin receptor Homo sapiens 61-77 31872693-2 2019 Insulin stimulation causes autophosphorylation of the insulin receptor( IR),which then activates tyrosine phosphorylation of insulin receptor substrate( IRS).Phosphorylation of IRS can induce and activate phosphatidylinositol 3-kinase( PI3 K),subsequently activate downstream 3-phosphoinositide-dependent protease 1( PDK1) and Akt/PKB,and finally promote expression and translocation of glucose transporter 4 to increase glucose uptake of insulin-sensitive tissues and alleviate insulin resistance. Glucose 387-394 insulin receptor Homo sapiens 54-70 31872693-2 2019 Insulin stimulation causes autophosphorylation of the insulin receptor( IR),which then activates tyrosine phosphorylation of insulin receptor substrate( IRS).Phosphorylation of IRS can induce and activate phosphatidylinositol 3-kinase( PI3 K),subsequently activate downstream 3-phosphoinositide-dependent protease 1( PDK1) and Akt/PKB,and finally promote expression and translocation of glucose transporter 4 to increase glucose uptake of insulin-sensitive tissues and alleviate insulin resistance. Glucose 421-428 insulin receptor Homo sapiens 54-70 29262294-1 2018 The insulin receptor is an important regulator of metabolic processes in the body, and in particular of glucose homeostasis, including glucose uptake into peripheral tissues. Glucose 104-111 insulin receptor Homo sapiens 4-20 30576640-7 2019 Here, we provide a review of contemporary literature on brain insulin resistance, highlight the rationale for improving memory function using intranasal insulin, and describe initial results from experiments using a molecular approach to more directly measure the impact of insulin receptor activation and signaling on glucose uptake in neurons. Glucose 319-326 insulin receptor Homo sapiens 274-290 30718702-4 2019 The increased glucose uptake was accompanied by enhanced phosphorylation of the insulin receptor (IR), insulin receptor substrate-1 (IRS-1), the serine/threonine kinase Akt and Akt substrate of 160 kDa (AS160). Glucose 14-21 insulin receptor Homo sapiens 80-96 30718702-4 2019 The increased glucose uptake was accompanied by enhanced phosphorylation of the insulin receptor (IR), insulin receptor substrate-1 (IRS-1), the serine/threonine kinase Akt and Akt substrate of 160 kDa (AS160). Glucose 14-21 insulin receptor Homo sapiens 98-100 30718702-7 2019 Taken together, these results establish that apoA-I increases glucose disposal in skeletal muscle by activating the IR/IRS-1/PI3K/Akt/AS160 signal transduction pathway. Glucose 62-69 insulin receptor Homo sapiens 116-118 30040480-11 2018 Additionally, IGF-II reduced mRNA expression of the insulin receptor in adipocytes and downregulated insulin receptor isoform A and glucose transporter 4 abundance and corresponding glucose uptake in visceral adipocytes. Glucose 132-139 insulin receptor Homo sapiens 52-68 30661991-4 2019 Using CHIP-RIP, we demonstrate that GAS5 binds to promoter of insulin receptor to regulate its expression, and its depletion inhibits glucose uptake and insulin signaling. Glucose 134-141 insulin receptor Homo sapiens 62-78 29543533-3 2018 The inhibition of the transcriptional activity of Egr-1 enhanced the phosphorylation of the insulin receptor (InsR) and Akt, thus increasing glucose uptake in L6 myotubes after insulin stimulation, whereas overexpression of Egr-1 decreased insulin sensitivity. Glucose 141-148 insulin receptor Homo sapiens 92-108 29543533-3 2018 The inhibition of the transcriptional activity of Egr-1 enhanced the phosphorylation of the insulin receptor (InsR) and Akt, thus increasing glucose uptake in L6 myotubes after insulin stimulation, whereas overexpression of Egr-1 decreased insulin sensitivity. Glucose 141-148 insulin receptor Homo sapiens 110-114 29168473-9 2018 Before treatment, the fasting and postprandial levels of the insulin receptor were significantly lower in patients with impaired glucose tolerance compared with those in patients with normal glucose tolerance and healthy children. Glucose 129-136 insulin receptor Homo sapiens 61-77 29330302-7 2018 Holo-IGF1R and HybR both promoted cell proliferation and glucose uptake, whereas holo-InsR only promoted glucose uptake, and only holo-IGF1R showed anti-apoptotic effects. Glucose 105-112 insulin receptor Homo sapiens 86-90 29610518-2 2018 Here we show that the amount of biologically active IR is regulated by the cleavage of its ectodomain, by the beta-site amyloid precursor protein cleaving enzyme 1 (BACE1), in a glucose concentration-dependent manner. Glucose 178-185 insulin receptor Homo sapiens 52-54 29500363-4 2018 We find that by improving insulin sensitivity at the level of the insulin receptor (IR), either by IR over-expression or by knocking down the negative regulator of IR activity, protein tyrosine-phosphatase 1B (PTP1B), podocytes are protected from ER stress caused by fatty acids or diabetic media containing high glucose, high insulin and inflammatory cytokines TNFalpha and IL-6. Glucose 313-320 insulin receptor Homo sapiens 66-82 29500363-4 2018 We find that by improving insulin sensitivity at the level of the insulin receptor (IR), either by IR over-expression or by knocking down the negative regulator of IR activity, protein tyrosine-phosphatase 1B (PTP1B), podocytes are protected from ER stress caused by fatty acids or diabetic media containing high glucose, high insulin and inflammatory cytokines TNFalpha and IL-6. Glucose 313-320 insulin receptor Homo sapiens 84-86 28122381-6 2017 In addition, this review highlights insulin transport into the brain, signaling pathways associated with hypothalamic insulin receptor expression in the regulation of hepatic glucose production, and finally the perturbation of systemic glucose homeostasis as a consequence of central insulin resistance. Glucose 175-182 insulin receptor Homo sapiens 118-134 29321379-6 2018 These studies demonstrate that a glucose-dependent locus of insulin clearance and, hence, insulin action can be achieved by targeting MR and IR concurrently. Glucose 33-40 insulin receptor Homo sapiens 141-143 30151293-9 2017 Irisin is found to improve insulin resistance and type 2 diabetes by increasing sensitization of the insulin receptor in skeletal muscle and heart by improving hepatic glucose and lipid metabolism, promoting pancreatic beta cell functions, and transforming white adipose tissue to brown adipose tissue. Glucose 168-175 insulin receptor Homo sapiens 101-117 28507217-1 2017 Regulation of Glucose Uptake and Enteroendocrine Function by the Intestinal Epithelial Insulin Receptor. Glucose 14-21 insulin receptor Homo sapiens 87-103 28507218-1 2017 Regulation of Glucose Uptake and Enteroendocrine Function by the Intestinal Epithelial Insulin Receptor. Glucose 14-21 insulin receptor Homo sapiens 87-103 28677502-4 2017 Its binding to insulin receptor on the surface of diverse cells allows glucose entry into cells, and activates a variety of cellular actions. Glucose 71-78 insulin receptor Homo sapiens 15-31 29321379-5 2018 When the blood glucose level is elevated, as in individuals with diabetes mellitus, MR binding diminishes due to glucose competition, leading to reduced MR-mediated clearance and increased partitioning for IR binding and consequent glucose lowering. Glucose 15-22 insulin receptor Homo sapiens 206-208 29321379-5 2018 When the blood glucose level is elevated, as in individuals with diabetes mellitus, MR binding diminishes due to glucose competition, leading to reduced MR-mediated clearance and increased partitioning for IR binding and consequent glucose lowering. Glucose 113-120 insulin receptor Homo sapiens 206-208 29321379-5 2018 When the blood glucose level is elevated, as in individuals with diabetes mellitus, MR binding diminishes due to glucose competition, leading to reduced MR-mediated clearance and increased partitioning for IR binding and consequent glucose lowering. Glucose 113-120 insulin receptor Homo sapiens 206-208 27695899-10 2016 CONCLUSIONS/INTERPRETATION: Sequential cleavage of IR by calpain 2 and gamma-secretase may contribute to insulin signalling in cells and its inhibition may be partly responsible for the glucose-lowering effects of metformin. Glucose 186-193 insulin receptor Homo sapiens 51-53 27514532-2 2016 When tyrosine is phosphorylated by the activated insulin receptor, IRS proteins recruit downstream effectors, such as phosphoinositide 3-kinase and mitogen-activated protein kinase, in order to elicit cellular responses such as glucose uptake, lipid metabolism and cell proliferation. Glucose 228-235 insulin receptor Homo sapiens 49-65 27695899-1 2016 AIMS/HYPOTHESIS: Soluble insulin receptor (sIR), the ectodomain of the insulin receptor (IR), has been detected in human plasma and its concentration paralleled that of blood glucose. Glucose 175-182 insulin receptor Homo sapiens 25-41 27695899-1 2016 AIMS/HYPOTHESIS: Soluble insulin receptor (sIR), the ectodomain of the insulin receptor (IR), has been detected in human plasma and its concentration paralleled that of blood glucose. Glucose 175-182 insulin receptor Homo sapiens 71-87 27695899-1 2016 AIMS/HYPOTHESIS: Soluble insulin receptor (sIR), the ectodomain of the insulin receptor (IR), has been detected in human plasma and its concentration paralleled that of blood glucose. Glucose 175-182 insulin receptor Homo sapiens 44-46 27695899-4 2016 METHODS: Using the in vitro model, we investigated the molecular mechanisms of IR cleavage, which is accelerated by high-glucose treatment. Glucose 121-128 insulin receptor Homo sapiens 79-81 27470565-8 2016 In conclusion, our findings indicate that simvastatin suppresses glucose uptake activity and GLUT4 translocation via IR-dependent IRS-1/PI3K/Akt pathway. Glucose 65-72 insulin receptor Homo sapiens 117-119 27733843-4 2016 In this study, we assessed alterations in the IR-A and IR-B isoform ratio and associated changes in cell proliferation and migration of PCa cell lines following exposure to altered concentrations of glucose and treatment with IGF-II and insulin. Glucose 199-206 insulin receptor Homo sapiens 46-48 27470565-5 2016 Mechanistically, the inhibition of glucose uptake and GLUT4 translocation elicited by simvastatin were associated with the suppression of the insulin receptor (IR)/IR substrate (IRS)/Akt signaling cascade. Glucose 35-42 insulin receptor Homo sapiens 142-158 27470565-5 2016 Mechanistically, the inhibition of glucose uptake and GLUT4 translocation elicited by simvastatin were associated with the suppression of the insulin receptor (IR)/IR substrate (IRS)/Akt signaling cascade. Glucose 35-42 insulin receptor Homo sapiens 160-162 27733843-4 2016 In this study, we assessed alterations in the IR-A and IR-B isoform ratio and associated changes in cell proliferation and migration of PCa cell lines following exposure to altered concentrations of glucose and treatment with IGF-II and insulin. Glucose 199-206 insulin receptor Homo sapiens 55-57 26934053-8 2016 Indeed, we found reduced levels of insulin receptor, PI3K, AKT, all important molecules in insulin signaling and glucose uptake by cells. Glucose 113-120 insulin receptor Homo sapiens 35-51 27291139-2 2016 Efficient glucose uptake by the endothelium requires insulin receptor activation to deliver GLUT receptors to the cell surface. Glucose 10-17 insulin receptor Homo sapiens 53-69 27281820-3 2016 Further refinement has yielded, in particular, a 36-residue Site 2-Site 1 fusion peptide, S519, that binds the insulin receptor with subnanomolar affinity and exhibits agonist activity in both lipogenesis and glucose uptake assays. Glucose 209-216 insulin receptor Homo sapiens 111-127 26485752-2 2016 In skeletal muscle, binding of the insulin to insulin receptor (IR) initiates a signaling cascade that results in the translocation of the insulin-sensitive glucose transporter protein 4 (GLUT4) to the plasma membrane which leads to facilitated diffusion of glucose into the cell. Glucose 157-164 insulin receptor Homo sapiens 46-62 26485752-2 2016 In skeletal muscle, binding of the insulin to insulin receptor (IR) initiates a signaling cascade that results in the translocation of the insulin-sensitive glucose transporter protein 4 (GLUT4) to the plasma membrane which leads to facilitated diffusion of glucose into the cell. Glucose 157-164 insulin receptor Homo sapiens 64-66 27506738-6 2016 RESULTS: The basal autophagy level decreased under the high glucose conditions, which was accompanied by a decrease in the glucose uptake and phosphorylation of the insulin receptor in the human podocytes. Glucose 60-67 insulin receptor Homo sapiens 165-181 27422524-6 2016 Furthermore, beating-rate in Cor.4U( ) human cardiomyocytes, glucose uptake in HL-1 cells, and prevention from H2O2 induced caspase 3/7 activation in cardiac cells overexpressing the human insulin receptor (H9c2-E2) were analysed. Glucose 61-68 insulin receptor Homo sapiens 189-205 25808283-2 2015 We have previously characterized an allosteric monoclonal antibody to the human insulin receptor (IR), XMetA, that activated metabolic signaling leading to enhanced glucose transport in cultured cells, and chronically reduced fasting blood glucose levels in mouse models of diabetes mellitus. Glucose 165-172 insulin receptor Homo sapiens 80-96 26888756-5 2016 Efficient knockdown of either Insr or Irs1/2 was achieved by conditional shRNA expression, severely attenuating insulin-stimulated AKT phosphorylation and glucose uptake. Glucose 155-162 insulin receptor Homo sapiens 30-34 26467793-2 2016 In insulin-targeted cells, such as hepatocytes, proper glucose utilization requires an elaborate interplay between the insulin receptor, the glucose transporter, and mitochondria that involves the participation of actin microfilaments and microtubules. Glucose 55-62 insulin receptor Homo sapiens 119-135 26514725-4 2015 By virtue of its ability to directly bind the InsR, IRS1 and PI3K, GIV enhances the InsR-IRS1-Akt-AS160 (RabGAP) signaling cascade and cellular glucose uptake via its GEF function. Glucose 144-151 insulin receptor Homo sapiens 46-50 26378251-4 2015 By virtue of its ability to directly bind InsR, IRS1, and phosphoinositide 3-kinase, GIV serves as a key hub in the immediate postreceptor level, which coordinately enhances the metabolic insulin response and glucose uptake in myotubes via its GEF function. Glucose 209-216 insulin receptor Homo sapiens 42-46 25808283-2 2015 We have previously characterized an allosteric monoclonal antibody to the human insulin receptor (IR), XMetA, that activated metabolic signaling leading to enhanced glucose transport in cultured cells, and chronically reduced fasting blood glucose levels in mouse models of diabetes mellitus. Glucose 165-172 insulin receptor Homo sapiens 98-100 25808283-2 2015 We have previously characterized an allosteric monoclonal antibody to the human insulin receptor (IR), XMetA, that activated metabolic signaling leading to enhanced glucose transport in cultured cells, and chronically reduced fasting blood glucose levels in mouse models of diabetes mellitus. Glucose 240-247 insulin receptor Homo sapiens 80-96 25808283-2 2015 We have previously characterized an allosteric monoclonal antibody to the human insulin receptor (IR), XMetA, that activated metabolic signaling leading to enhanced glucose transport in cultured cells, and chronically reduced fasting blood glucose levels in mouse models of diabetes mellitus. Glucose 240-247 insulin receptor Homo sapiens 98-100 25476247-3 2015 Consequently, the exon 11-deleted IR isoform that is less sensitive to insulin is predominantly produced, leading to glucose intolerance in DM1. Glucose 117-124 insulin receptor Homo sapiens 34-36 26021696-6 2015 These results suggest that VOSO4-induced OH radical, which is a signaling species, promotes glucose uptake via the IR/Akt signaling pathway. Glucose 93-100 insulin receptor Homo sapiens 116-118 25848166-1 2015 Normal blood glucose level depends on the availability of insulin and its ability to bind insulin receptor (IR) that regulates the downstream signaling pathway. Glucose 13-20 insulin receptor Homo sapiens 90-106 26021696-0 2015 Oxidovanadium(IV) sulfate-induced glucose uptake in HepG2 cells through IR/Akt pathway and hydroxyl radicals. Glucose 34-41 insulin receptor Homo sapiens 72-74 25613982-6 2015 The metabolic selectivity of partial IR agonists like XMetA, if recapitulated in vivo, may be a desirable feature of therapeutic agents designed to regulate blood glucose levels while minimizing undesirable outcomes of excessive IR mitogenic activation. Glucose 163-170 insulin receptor Homo sapiens 37-39 25848166-1 2015 Normal blood glucose level depends on the availability of insulin and its ability to bind insulin receptor (IR) that regulates the downstream signaling pathway. Glucose 13-20 insulin receptor Homo sapiens 108-110 24196191-2 2014 INSR-A promotes cell growth whereas INSR-B predominantly regulates glucose homeostasis. Glucose 67-74 insulin receptor Homo sapiens 36-40 25458098-1 2015 PURPOSE: Insulin/insulin receptor (INSR) signaling plays diverse roles in the central nervous system, including regulation of blood glucose, synaptic plasticity, dendritic growth, modulation of electrophysiological activity, proliferation of astrocytes and neuronal apoptosis. Glucose 132-139 insulin receptor Homo sapiens 9-33 25458098-1 2015 PURPOSE: Insulin/insulin receptor (INSR) signaling plays diverse roles in the central nervous system, including regulation of blood glucose, synaptic plasticity, dendritic growth, modulation of electrophysiological activity, proliferation of astrocytes and neuronal apoptosis. Glucose 132-139 insulin receptor Homo sapiens 35-39 25123125-27 2014 The results from these studies demonstrate that the well-established abnormalities in insulin action on glucose uptake and glycogen synthesis are reflected by defects in insulin signaling to these cellular processes in type 2 diabetes, obesity, and PCOS, and as expected also in inherited insulin resistance caused by a mutation in INSR. Glucose 104-111 insulin receptor Homo sapiens 332-336 24568842-0 2014 Human biliverdin reductase-based peptides activate and inhibit glucose uptake through direct interaction with the kinase domain of insulin receptor. Glucose 63-70 insulin receptor Homo sapiens 131-147 24651808-6 2014 Through binding to the extracellular domain of the IR, 4548-G05 induces activation of the receptor and initiates the downstream Akt and extracellular signal-related kinase pathways to trigger glucose uptake in C2C12 myotubes. Glucose 192-199 insulin receptor Homo sapiens 51-53 24508798-0 2014 Development of in vitro model of insulin receptor cleavage induced by high glucose in HepG2 cells. Glucose 75-82 insulin receptor Homo sapiens 33-49 24703981-1 2014 The hepatic insulin signaling mediated by insulin receptor substrates IRS1 and IRS2 plays a central role in maintaining glucose homeostasis under different physiological conditions. Glucose 120-127 insulin receptor Homo sapiens 42-58 25114673-3 2014 OBJECTIVE: To examine whether the exon 17 of INSR gene contributes to genetic susceptibility to PCOS in Iraqi women and its effects on glucose tolerance test and lipid profile. Glucose 135-142 insulin receptor Homo sapiens 45-49 23448488-1 2013 Insulin resistance is associated with the impairment of the response of insulin receptor to insulin, resulting in the reduction of glucose uptake, leading to the alteration of myocardial glucose metabolism, impairment of cardiac electrophysiology, and increased susceptibility to ischemia-induced myocardial injury. Glucose 131-138 insulin receptor Homo sapiens 72-88 23052216-1 2013 The insulin signaling pathway regulates whole-body glucose homeostasis by transducing extracellular signals from the insulin receptor (IR) to downstream intracellular targets, thus coordinating a multitude of biological functions. Glucose 51-58 insulin receptor Homo sapiens 117-133 23052216-1 2013 The insulin signaling pathway regulates whole-body glucose homeostasis by transducing extracellular signals from the insulin receptor (IR) to downstream intracellular targets, thus coordinating a multitude of biological functions. Glucose 51-58 insulin receptor Homo sapiens 135-137 23052216-5 2013 Accordingly, our review will focus on roles for IR substrates as they pertain to three primary areas: metabolism/glucose uptake, mitogenesis/growth, and aging/longevity. Glucose 113-120 insulin receptor Homo sapiens 48-50 23052216-6 2013 While IR functions in a seemingly pleiotropic manner in many cell types, through these three main roles in fat and skeletal muscle cells, IR multi-tasks to regulate whole-body glucose homeostasis to impact healthspan and lifespan. Glucose 176-183 insulin receptor Homo sapiens 6-8 23052216-6 2013 While IR functions in a seemingly pleiotropic manner in many cell types, through these three main roles in fat and skeletal muscle cells, IR multi-tasks to regulate whole-body glucose homeostasis to impact healthspan and lifespan. Glucose 176-183 insulin receptor Homo sapiens 138-140 23471249-4 2013 The insulin receptor within the central nervous system is widely distributed, reflecting insulin"s diverse range of actions, including acting as an adiposity signal to reduce food intake and increase energy expenditure, regulation of systemic glucose responses, altering sympathetic activity, and involvement in cognitive function. Glucose 243-250 insulin receptor Homo sapiens 4-20 23395167-4 2013 LRP6 mutation carriers exhibited hyperinsulinemia and reduced insulin sensitivity compared to noncarrier relatives in response to oral glucose ingestion, which correlated with a significant decline in tissue expression of the insulin receptor and insulin signaling activity. Glucose 135-142 insulin receptor Homo sapiens 226-242 23425024-2 2013 "Hydrogen sulfide treatment promotes glucose uptake by increasing insulin receptor sensitivity and ameliorates kidney lesions in type 2 diabetes." Glucose 37-44 insulin receptor Homo sapiens 66-82 23592917-0 2013 Reduced insulin receptor signaling in retinal Muller cells cultured in high glucose. Glucose 76-83 insulin receptor Homo sapiens 8-24 23225242-2 2013 Tyrosine phosphorylation of the insulin receptor (IR) by insulin promotes glucose uptake by activating the PI3K/Akt pathway. Glucose 74-81 insulin receptor Homo sapiens 32-48 23225242-2 2013 Tyrosine phosphorylation of the insulin receptor (IR) by insulin promotes glucose uptake by activating the PI3K/Akt pathway. Glucose 74-81 insulin receptor Homo sapiens 50-52 22862558-5 2012 EXPERT OPINION: Mechanisms of TCM in treating DM are concluded: i) to promote insulin secretion and increase serum insulin levels; ii) to increase the sensitivity of insulin and improve its resistance; iii) to inhibit glucose absorption; iv) to affect glucose metabolism of insulin receptor; and v) to scavenge radicals and prevent lipid peroxidation. Glucose 218-225 insulin receptor Homo sapiens 274-297 24296476-9 2013 CONCLUSION: The results of the present study indicate that stearic acid serves as a potent PTP1B inhibitor, possibly causing an enhancement in the insulin receptor signaling to stimulate glucose uptake into adipocytes. Glucose 187-194 insulin receptor Homo sapiens 147-163 23569395-8 2013 RESULTS: High Glc indeed led to inactivation of IR, IRS-1, and subsequent Akt in myotubes, indicating an interruption of the signal pathway. Glucose 14-17 insulin receptor Homo sapiens 48-50 23705494-9 2013 Mutations of INSR induce insulin resistance, lipodystrophy, other pathology, and suggest an important role of insulin in glucose level regulation and in stimulation of fat accumulation as well. Glucose 121-128 insulin receptor Homo sapiens 13-17 23363253-9 2013 Moreover, hypoxia and glucose or glutamine deprivation are controlled by the expression of insulin receptor and related to insulin signaling genes mostly via ERN1 enzyme signaling. Glucose 22-29 insulin receptor Homo sapiens 91-107 22974639-3 2012 Moreover, a high extracellular concentration of glucose activated DGKdelta in skeletal muscle cells, which was followed by a reduction in the intracellular diacylglycerol levels and the inactivation of protein kinase Calpha, the enzyme that phosphorylates and inactivates the insulin receptor. Glucose 48-55 insulin receptor Homo sapiens 276-292 21671008-0 2011 Insulin receptor signaling activated by penta-O-galloyl-alpha-D: -glucopyranose induces p53 and apoptosis in cancer cells. Glucose 66-79 insulin receptor Homo sapiens 0-16 22928576-4 2012 Rodents with tissue-specific knockout of the insulin receptor in the beta-cell (betaIRKO) show reduced first-phase glucose-stimulated insulin secretion (GSIS) and with aging develop glucose intolerance and diabetes, phenotypically similar to the process seen in human T2D. Glucose 115-122 insulin receptor Homo sapiens 45-61 22775283-3 2012 SUBJECTS AND METHODS: The INSR gene was sequenced in 25 normal glucose-tolerant (NGT) and 25 T2D subjects, and the variant found was genotyped by polymerase chain reaction-restriction fragment length polymorphism in 1,016 NGT and 1,010 T2D subjects, randomly selected from the Chennai Urban Rural Epidemiology Study. Glucose 63-70 insulin receptor Homo sapiens 26-30 22278734-1 2012 The insulin receptor (IR) and low-density lipoprotein receptor (LDLR) maintain glucose and lipid metabolism, respectively. Glucose 79-86 insulin receptor Homo sapiens 4-20 22278734-1 2012 The insulin receptor (IR) and low-density lipoprotein receptor (LDLR) maintain glucose and lipid metabolism, respectively. Glucose 79-86 insulin receptor Homo sapiens 22-24 22775461-3 2012 The aim of this work was to investigate the insulin receptor expression in B and T cells under incubation with pathological glucose concentrations, respond hyperglycemia and hypoglycemia. Glucose 124-131 insulin receptor Homo sapiens 44-60 22434934-5 2012 Pharmacological blockade or genetic deficiency of CB1 receptors enhanced insulin receptor signaling after injury, leading to reduced blood glucose concentrations and activation of Bad, which increased beta-cell survival. Glucose 139-146 insulin receptor Homo sapiens 73-89 23056614-4 2012 But the mechanism integrating insulin receptor signaling to glucose utilization with lipogenesis is unknown. Glucose 60-67 insulin receptor Homo sapiens 30-46 22110065-6 2011 RESULTS: TNF-alpha-only treatments of Muller cells resulted in significant decreases of tyrosine phosphorylation of the insulin receptor and Akt in high-glucose conditions. Glucose 153-160 insulin receptor Homo sapiens 120-136 21354844-7 2011 In islets maintained at 5.5 mmol/L of glucose, insulin receptor (IR) expression was reduced by low RHI, while phosphatidylinositol-3 kinase p110-alpha (PI3K) was enhanced by both concentrations of glulisine and aspart, and by high RHI. Glucose 38-45 insulin receptor Homo sapiens 47-63 21354844-7 2011 In islets maintained at 5.5 mmol/L of glucose, insulin receptor (IR) expression was reduced by low RHI, while phosphatidylinositol-3 kinase p110-alpha (PI3K) was enhanced by both concentrations of glulisine and aspart, and by high RHI. Glucose 38-45 insulin receptor Homo sapiens 65-67 21354844-8 2011 In islets preexposed to high glucose, IR expression was increased by both concentrations of aspart and RHI, but not by glulisine. Glucose 29-36 insulin receptor Homo sapiens 38-40 21324373-0 2011 Expression and function of the insulin receptor in normal and osteoarthritic human chondrocytes: modulation of anabolic gene expression, glucose transport and GLUT-1 content by insulin. Glucose 137-144 insulin receptor Homo sapiens 31-47