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GPI — INS

Text-mined interactions from Literome

Müller et al., Biochemistry 2000 : GPI-PLC was most pronouncedly stimulated by authentic human insulin compared to various insulin analogues and insulin-like growth factor I
Müller et al., Biochem Pharmacol 2005 : In contrast, blockade of the moderate insulin activation of the GPI-PLC and of lipid raft protein redistribution by GPI-2350 slightly reduced insulin signalling and metabolic action, only
Wood et al., J Endocrinol 1992 : pH(i) in the presence of both TSH and insulin was 7.81 +/- 0.03 ( n = 60 )
Gunawardana et al., BMC endocrine disorders 2005 : Nutrient stimulated insulin secretion ( NSIS ) requires a specific pHi-range , and is dramatically enhanced by forced intracellular acidification with DMA
Yoon et al., Arch Pharm Res 2007 : Taken together, these results suggest that insulin , in part, may activate a GPI-PLC , via PI-PLC/intracellular Ca2+, which may consequently stimulate the release of RDPase
Axelrod et al., Diabetes 1991 (Hyperinsulinism...) : Thus, insulin may regulate PGI2 and PGE2 production by adipose tissue ( and possibly other tissues ) through a wide range of concentrations with important physiological and clinical consequences
Rosenthal et al., J Surg Res 1990 : The results of these experiments indicate that human insulin inhibits both basal and arachidonic acid stimulated production of PGI2 from HUVEC in a dose dependent manner ... We therefore conclude that insulin , in locally high concentrations, inhibits endothelial PGI2 production in vitro
Axelrod et al., Endocrinology 1986 : Insulin selectively inhibited isoproterenol stimulated PGI2 production and triglyceride lipolysis at physiological concentrations, but had no effect on angiotensin II-stimulated PGI2 production ... We conclude that : angiotensin II stimulates PGI2 production rapidly and independently of cAMP, but isoproterenol stimulates PGI2 production more slowly, an effect that is cAMP dependent ; insulin inhibits the cAMP dependent beta-adrenergic stimulation of PGI2 production ( and triglyceride lipolysis ), but not the cAMP independent angiotensin II-induced stimulation of PGI2 production ( this suggests that the former effect is mediated by a decrease in cAMP levels in the adipocyte ) ; and dexamethasone inhibits both mechanisms of PGI2 production
Ahrén et al., Peptides 1989 : Since VIP and PHI both stimulate insulin and glucagon secretion, we investigated the effects of helodermin on insulin and glucagon secretion in the mouse, both in the basal state and during administration of glucose and the cholinergic agonist carbachol
Ahrén et al., Neuropeptides 1988 : It was found that PHI did not affect basal levels of insulin of glucagon ... When injected together with glucose ( 2.8 nmol/kg ), PHI ( 1.0 and 4.0 nmol/kg ) potentiated the insulin response by approximately 35 % ( P less than 0.05 ) and 50 % ( P less than 0.01 ), respectively ... In contrast, the insulin response to the cholinergic agonist carbachol ( 0.16 mumol/kg ) or the beta 2-adrenoceptor agonist terbutaline ( 3.6 mumol/kg ) was not affected by PHI
Cook et al., J Biol Chem 1988 (Liver Neoplasms, Experimental) : Insulin and serum, alone or in combination, did not cause pHi to increase in either 4- ( 2-hydroxyethyl ) -1-piperazineethanesulfonic acid ( HEPES ) ( pHi 7.17 ) - or HCO3/CO2 ( pHi 7.19 ) - buffered media
Yanaihara et al., Peptides 1986 : Replacement of amino-terminal decapeptide portion of the PHI molecule with the corresponding part of VIP resulted in a drastic decrease of the potentiating effect of PHI on insulin release
Stith et al., Dev Biol 1985 : Sodium-free medium decreased basal pHi by 0.3 unit and prevented increases in pHi in response to both insulin and progesterone, but S6 phosphorylation occurred normally with both hormones
Szczeklik et al., Prostaglandins 1980 (Arteriosclerosis...) : PGI2 repressed glucose induced insulin release in some normoglycemic patients but in others it either increased it or did not affect it
Szecówka et al., Am J Physiol 1983 : PHI increased the release of insulin , glucagon, and somatostatin ... In the presence of 16.7 mmol/liter glucose, only insulin secretion was increased by PHI ... When arginine was used as a secretagogue, PHI ( 10 nmol/liter ) potentiated secretion of insulin , glucagon, and somatostatin
Lasché et al., Diabetes 1982 : Suppression of insulin production in presence of PGI2 in high glucose medium resembles the action of other prostaglandins and suggests it may inhibit insulin secretion after a glucose load
Patrono et al., Prostaglandins 1981 : Thus, in contrast to PGE2, PGI2 does not affect insulin secretion nor glucose disposal at doses producing platelet and vascular changes
Fidelman et al., Am J Physiol 1982 : The results support the model that the acute effect of insulin on glycolysis is mediated by a change in pHi , consequent to activation by insulin of Na : H exchange at the plasma membrane
Morris et al., J Biol Chem 1995 : Glucosaminyl ( alpha 1 -- > 6 ) -D-myo-inositol ( GlcN ( alpha 1 -- > 6 ) Ins ), GlcN ( alpha 1 -- > 6 ) Ins 1,2-cyclic phosphate, GlcN ( alpha 1 -- > 6 ) -2-deoxy-Ins , and GlcN ( alpha 1 -- > 6 ) Ins 1-dodecyl phosphonate inhibited GPI-PLC
Müller et al., J Cell Biol 1994 : Inhibition of glucose transport or incubation of rat adipocytes in glucose-free medium completely abolished stimulation of GPI-PL by either insulin or glimepiride
Takahashi et al., Hypertens Res 1996 : The insulin induced pHi increase was almost completely inhibited by 10 ( -3 ) mol/l amiloride in the lumen, indicating that insulin activates luminal Na/H exchange in PST