PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 25675332-5 2015 This detection limit was further lowered to 5 pM by designing serum insulin conjugates with poly(acrylic acid)-functionalized magnetite nanoparticles (100 nm hydrodynamic diameter) and detecting the binding of MNP-serum insulin conjugate to the surface insulin-antibody on PGE/MWNT/Py electrodes. Prostaglandins E 273-276 insulin Homo sapiens 68-75 25675332-5 2015 This detection limit was further lowered to 5 pM by designing serum insulin conjugates with poly(acrylic acid)-functionalized magnetite nanoparticles (100 nm hydrodynamic diameter) and detecting the binding of MNP-serum insulin conjugate to the surface insulin-antibody on PGE/MWNT/Py electrodes. Prostaglandins E 273-276 insulin Homo sapiens 220-227 25675332-5 2015 This detection limit was further lowered to 5 pM by designing serum insulin conjugates with poly(acrylic acid)-functionalized magnetite nanoparticles (100 nm hydrodynamic diameter) and detecting the binding of MNP-serum insulin conjugate to the surface insulin-antibody on PGE/MWNT/Py electrodes. Prostaglandins E 273-276 insulin Homo sapiens 220-227 23118029-8 2013 In vitro C5a and C3a (100 nM) exhibited novel insulin-like effects on 3T3-L1 adipocytes, promoting energy conservation by increasing glucose and fatty acid uptake while inhibiting cAMP signaling and lipolysis, and induced PGE(2) release from macrophages, effects all blocked by each respective antagonist (10 muM). Prostaglandins E 222-225 insulin Homo sapiens 46-53 20022932-9 2010 Similarly, COX-2 inhibition impaired insulin-stimulated Akt phosphorylation and 2-deoxy-D-[(14)C]glucose uptake in palmitate-exposed skeletal muscle cells, and this effect was abolished in the presence of PGE(2). Prostaglandins E 205-208 insulin Homo sapiens 37-44 19575453-7 2009 In hepatocytes, insulin-stimulated glycogen synthesis and insulin-dependent phosphorylation of Akt-kinase were attenuated synergistically by prior incubation with IL-6 and/or PGE(2) while insulin receptor autophosphorylation was barely affected. Prostaglandins E 175-178 insulin Homo sapiens 16-23 19575453-7 2009 In hepatocytes, insulin-stimulated glycogen synthesis and insulin-dependent phosphorylation of Akt-kinase were attenuated synergistically by prior incubation with IL-6 and/or PGE(2) while insulin receptor autophosphorylation was barely affected. Prostaglandins E 175-178 insulin Homo sapiens 58-65 19575453-11 2009 In HepG2 cells expressing a recombinant EP3-receptor, PGE(2) pre-incubation activated ERK1/2, caused a serine phosphorylation of insulin receptor substrate 1 (IRS1), and reduced the insulin-dependent Akt-phosphorylation. Prostaglandins E 54-57 insulin Homo sapiens 129-136 19575453-12 2009 CONCLUSION: PGE(2) might contribute to hepatic insulin resistance via an EP3-receptor-dependent ERK1/2 activation resulting in a serine phosphorylation of insulin receptor substrate, thereby preventing an insulin-dependent activation of Akt and glycogen synthesis. Prostaglandins E 12-15 insulin Homo sapiens 47-54 19575453-12 2009 CONCLUSION: PGE(2) might contribute to hepatic insulin resistance via an EP3-receptor-dependent ERK1/2 activation resulting in a serine phosphorylation of insulin receptor substrate, thereby preventing an insulin-dependent activation of Akt and glycogen synthesis. Prostaglandins E 12-15 insulin Homo sapiens 155-162 16157560-5 2005 Inhibition of glucose-stimulated insulin secretion by prostaglandin E (PGE1) is pertussis-toxin insensitive, indicating that other G alpha(i) family members are not involved in this process in this beta-cell line. Prostaglandins E 54-69 insulin Homo sapiens 33-40 10531320-0 1999 Prostaglandin E(2) mediates inhibition of insulin secretion by interleukin-1beta. Prostaglandins E 0-15 insulin Homo sapiens 42-49 10531320-6 1999 Both drugs prevented IL-1beta from inducing PGE(2) synthesis and inhibiting insulin secretion; adding back exogenous PGE(2) re-established inhibition of insulin secretion in the presence of IL-1beta. Prostaglandins E 117-120 insulin Homo sapiens 153-160 7800581-0 1994 [Effect of misoprostol, a synthetic prostaglandin E analog, on levels of serum C-peptide in serum and glucose tolerance]. Prostaglandins E 36-51 insulin Homo sapiens 79-88 3073092-5 1988 Play in favor of this hypothesis the fact that the administration of PGE inhibits the insulin response to arginine in type-2 diabetics but not in normal subject and the fact that the administration of salicylates could improve the insulin response to glucose in some of these patients. Prostaglandins E 69-72 insulin Homo sapiens 86-93 3443962-21 1987 Fetal hypoglycaemia induced by fetal infusion of insulin increased fetal concentrations of plasma PGE without any apparent change in maternal plasma PGE values. Prostaglandins E 98-101 insulin Homo sapiens 49-56 3936737-3 1985 Met-enkephalin, catecholamines and prostaglandin E (PGE) have all been reported to inhibit the acute insulin response to glucose in normal humans. Prostaglandins E 35-50 insulin Homo sapiens 101-108 3936737-3 1985 Met-enkephalin, catecholamines and prostaglandin E (PGE) have all been reported to inhibit the acute insulin response to glucose in normal humans. Prostaglandins E 52-55 insulin Homo sapiens 101-108 3908178-0 1985 Interaction between epinephrine, prostaglandin E, and met-enkephalin in the regulation of insulin release in man. Prostaglandins E 33-48 insulin Homo sapiens 90-97 6419621-6 1983 On the basis of these results, it is hypothesized that endogenous PGE released in response to glucose stimulation exert an inhibiting effect on insulin release that becomes biphasic in appearance. Prostaglandins E 66-69 insulin Homo sapiens 144-151 6419621-0 1983 A role for endogenous prostaglandin E in biphasic pattern of insulin release in humans. Prostaglandins E 22-37 insulin Homo sapiens 61-68 6419621-1 1983 These studies were undertaken to evaluate in humans the possible physiological role of prostaglandins of the E series (PGE) in modulating insulin release and to assess whether endogenous PGE synthesis may account for the biphasic pattern of insulin secretion. Prostaglandins E 119-122 insulin Homo sapiens 138-145 6419621-3 1983 Infusion of lysine acetylsalicylate to block the synthesis of endogenous PGE increased by twofold total insulin response to glucose and also converted insulin release to a multiphasic pattern. Prostaglandins E 73-76 insulin Homo sapiens 104-111 6419621-3 1983 Infusion of lysine acetylsalicylate to block the synthesis of endogenous PGE increased by twofold total insulin response to glucose and also converted insulin release to a multiphasic pattern. Prostaglandins E 73-76 insulin Homo sapiens 151-158 6337902-6 1983 When acute insulin responses to glucose specifically are examined and data from indomethacin studies are excluded, the available information consistently indicates that prostaglandin E has adverse effects on glucose homeostasis and insulin secretion. Prostaglandins E 169-184 insulin Homo sapiens 11-18 6798594-4 1981 At lease one arachidonate derivative (prostaglandin E) inhibits insulin secretion, and several inhibitors of prostaglandin synthesis augment glucose-induced insulin release in normal subjects and type II diabetics. Prostaglandins E 38-53 insulin Homo sapiens 64-71 7018961-5 1981 Both PGE synthesis inhibitors shifted the glucose dose-insulin response curves to the left at low glucose concentrations and augmented maximal insulin release at high glucose concentrations. Prostaglandins E 5-8 insulin Homo sapiens 55-62 7018961-5 1981 Both PGE synthesis inhibitors shifted the glucose dose-insulin response curves to the left at low glucose concentrations and augmented maximal insulin release at high glucose concentrations. Prostaglandins E 5-8 insulin Homo sapiens 143-150 6998800-7 1980 The effect of furosemide on insulin and glucagon secretion might be mediated through enhanced release of endogenous prostaglandin E. Prostaglandins E 116-131 insulin Homo sapiens 28-35 394200-2 1979 This report compares the effects of four inhibitors of PGE synthesis on the acute insulin response to glucose and subsequent glucose disappearance rates. Prostaglandins E 55-58 insulin Homo sapiens 82-89 467810-1 1979 Prostaglandin E (PGE) infusion in normal man inhibits the acute insulin response to glucose. Prostaglandins E 0-15 insulin Homo sapiens 64-71 467810-1 1979 Prostaglandin E (PGE) infusion in normal man inhibits the acute insulin response to glucose. Prostaglandins E 17-20 insulin Homo sapiens 64-71 467810-9 1979 It is suggested that furosemide acts via the release of endogenous PGEs, which are known to inhibit insulin responses in man. Prostaglandins E 67-71 insulin Homo sapiens 100-107 353256-7 1978 However, during insulin stimulation there was significantly more pepsin output per unit PGE or PGF output than during either pentagastrin or histamine stimulation. Prostaglandins E 88-91 insulin Homo sapiens 16-23 353256-9 1978 The correlations between the outputs of gastric acid and both PGE and PGF were similar during pentagastrin and insulin stimulation whereas those between acid and PGE and PGF altered during the infusion of histamine. Prostaglandins E 62-65 insulin Homo sapiens 111-118 330566-1 1977 Prostaglandin E(2) (PGE(2)) infusion in normal humans inhibited acute insulin responses to a glucose (5 g i.v.) Prostaglandins E 20-23 insulin Homo sapiens 70-77 330566-10 1977 These findings uniquely demonstrate that (a) PGE(2) inhibits glucose-induced acute insulin responses and decreases glucose disposal in nondiabetic humans and (b) SS restores acute insulin responses, augments second phase insulin secretion, and accelerates glucose disposal in hyperglycemic, adultonset diabetics. Prostaglandins E 45-48 insulin Homo sapiens 83-90 33694300-3 2021 Prostaglandin E receptor (EP) subfamily agonists and antagonists have been shown to influence beta-cell insulin secretion, replication, and/or survival. Prostaglandins E 0-15 insulin Homo sapiens 104-111