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G6PC — INS

Text-mined interactions from Literome

Guignot et al., Am J Physiol 1999 (Hyperglycemia...) : Therefore, 1 ) insulin suppresses HGP in euglycemia by solely decreasing the G-6-P concentration ; 2 ) when combining both hyperinsulinemia and hyperglycemia, the suppression of HGP involves the inhibition of the G-6-Pase activity ; and 3 ) a sustained glucose-phosphorylation flux might be a crucial determinant in the inhibition of G-6-Pase and of HGP
Iizuka et al., J Endocrinol 2000 (Diabetes Mellitus) : To study the role of G-6-Pase in glucose stimulated insulin secretion from beta cells, we have introduced rat G-6-Pase catalytic subunit cDNA and have established permanent clones with 3-, 7- and 24-fold G-6-Pase activity of the mouse beta-cell line, MIN6
Chen et al., Gene Ther 2000 (Diabetes Mellitus, Type 1...) : Glucose stimulated as well as self limiting insulin production was achieved in vector transduced hepatoma cells in which expression of the insulin gene was controlled by the G6Pase promoter ... While insulin strongly inhibited the G6Pase promoter activity under low glucose conditions, its inhibitory capacity was attenuated when glucose levels were elevated
Schmoll et al., Biochem J 2001 : With that, PMA mimics the effect of insulin on G6Pase gene expression by a different signalling pathway
Hornbuckle et al., Am J Physiol Endocrinol Metab 2001 (Hyperinsulinism) : The regulation of glucose-6-phosphatase (G-6-Pase) catalytic subunit and glucose 6-phosphate ( G-6-P ) transporter gene expression by insulin in conscious dogs in vivo and in tissue culture cells in situ were compared
Patel et al., Biochem J 2001 : This mechanism has been proposed to underlie insulin action on G6Pase and IGFBP-1 gene transcription ... However, we find that treatment of cells with phorbol esters mimics the effect of insulin on G6Pase , but not IGFBP-1, gene expression
Patel et al., J Biol Chem 2002 : Insulin inhibits the expression of the hepatic insulin-like growth factor binding protein-1 ( IGFBP-1 ) and glucose-6-phosphatase (G6Pase) genes ... In addition, rapamycin did not affect insulin regulation of G6Pase expression or Akt activation
Vander Kooi et al., J Biol Chem 2003 (Carcinoma, Hepatocellular) : In HepG2 cells, the maximum repression of basal glucose-6-phosphatase catalytic subunit ( G6Pase ) gene transcription by insulin requires two distinct promoter regions, designated A ( located between -231 and -199 ) and B ( located between -198 and -159 ), that together form an insulin response unit
Patel et al., FEBS Lett 2003 : Insulin rapidly and completely inhibits expression of the hepatic insulin-like growth factor binding protein-1 ( IGFBP-1 ), phosphoenolpyruvate carboxykinase ( PEPCK ) and glucose-6-phosphatase (G6Pase) genes ... However, we recently found that the regulation of the IGFBP1 but not the PEPCK or G6Pase genes by insulin was sensitive to rapamycin, an inhibitor of mTOR
Salgado et al., J Mol Endocrinol 2004 : Transcriptional regulation of glucose-6-phosphatase catalytic subunit promoter by insulin and glucose in the carnivorous fish, Sparus aurata ... In vivo, glucose and insulin reduced G6Pase mRNA levels in the fish liver ... Transfection experiments in HepG2 cells showed that insulin repressed S. aurata G6pc under high-glucose conditions ... Interestingly, insulin hardly affected G6pc promoter activity in the absence of glucose, suggesting that a reduced capacity of insulin dependent repression of piscine G6pc may lead to insulin resistance in carnivorous fish
Liu et al., BMC molecular biology 2006 : Pharmacological inhibition of GSK3 mimics the effect of insulin on Phosphoenolpyruvate Carboxykinase ( PEPCK ), Glucose-6 Phosphatase (G6Pase) and IGF binding protein-1 (IGFBP1) gene expression
Logie et al., Diabetes 2007 (Carcinoma, Hepatocellular...) : Complete inhibition of PKB activity is achieved in liver cells incubated with 1-10 mumol/l Akti-1/2, and this blocks insulin regulation of PEPCK and G6Pase expression ... This work establishes the requirement for PKB activity in the insulin regulation of PEPCK, G6Pase , and a third insulin regulated gene, IGF binding protein-1 (IGFBP1) ; suggests a high degree of functional reserve ; and identifies Akti-1/2 as a useful tool to delineate PKB function in the liver
Hirota et al., J Biol Chem 2008 : Interestingly, HNF-4 binding elements ( HBEs ) in the GK and G6Pase promoters were required both for the insulin stimulated GK gene activation and insulin mediated G6Pase gene repression
Onuma et al., Biochem J 2009 : Insulin and epidermal growth factor suppress basal glucose-6-phosphatase catalytic subunit gene transcription through overlapping but distinct mechanisms ... Several studies have shown that insulin represses basal mouse G6Pase fusion gene transcription through FOXO1 ( forkhead box O1 ), but Stoffel and colleagues have recently suggested that insulin can also regulate gene transcription through FOXA2 ( forkhead box A2 ) [ Wolfrum, Asilmaz, Luca, Friedman and Stoffel ( 2003 ) Proc. Natl. Acad. Sci. 100, 11624-11629 ]
Mues et al., Horm Metab Res 2009 (Diabetes Mellitus, Type 2) : We have found that both metformin and insulin inhibit the basal and dexamethasone/cAMP stimulated G6Pase promoter activity in hepatoma cells ... These data indicate a differential AMPK dependent regulation of G6Pase gene expression by insulin and metformin under basal and dexamethasone/cAMP stimulated conditions
Li et al., Diabetes 2009 : Glucokinase (GCK) and glucose-6-phosphatase catalytic subunit 2 ( G6PC2 ) regulate the glucose cycling step in pancreatic beta-cells and may regulate insulin secretion
Kong et al., Eur J Pharmacol 2013 (Diabetes Mellitus) : We found that both insulin and FGF21 suppressed gene expression of G6Pase and PEPCK
Streeper et al., J Biol Chem 1997 : The transcription of the gene encoding the catalytic subunit of G6Pase is stimulated by glucocorticoids, whereas insulin strongly inhibits both basal G6Pase gene transcription and the stimulatory effect of glucocorticoids ... To identify the insulin response sequence (IRS) in the G6Pase promoter through which insulin mediates its action, we have analyzed the effect of insulin on the basal expression of mouse G6Pase-chloramphenicol acetyltransferase (CAT) fusion genes transiently expressed in hepatoma cells ... The presence of this multicomponent IRS may explain why insulin potently inhibits basal G6Pase-CAT expression
Dickens et al., J Biol Chem 1998 : We have explored the signaling pathways by which insulin mediates the repression of G6Pase transcription in H4IIE cells ... These results imply the existence of a novel signaling pathway downstream of PtdIns 3 kinase that is involved in the regulation of G6Pase expression by insulin
Streeper et al., Proc Natl Acad Sci U S A 1998 : Transcription of the gene encoding the glucose-6-phosphatase catalytic subunit ( G6Pase ) is stimulated by cAMP and glucocorticoids whereas insulin strongly inhibits both this induction and basal G6Pase gene transcription ... Previously, we have demonstrated that the maximum repression of basal G6Pase gene transcription by insulin requires two distinct promoter regions, designated A ( from -271 to -199 ) and B ( from -198 to -159 ) ... By contrast, region A fails to mediate an insulin response in a heterologous context, and the mutation of region B within an otherwise intact promoter almost completely abolishes the effect of insulin on basal G6Pase gene transcription