| Tanycytes release glucose using the glucose-6-phosphatase system during hypoglycemia to control hypothalamic energy balance. | Tanycytes release glucose using the glucose-6-phosphatase system during hypoglycemia to control hypothalamic energy balance.
Barahona MJ, Ferrada L, Vera M, Nualart F., Free PMC Article | 05/30/2024 |
| G6PC1 and G6PC2 influence G6P flux but not HSD11B1 activity. | G6PC1 and G6PC2 influence G6P flux but not HSD11B1 activity.
Hawes EM, Boortz KA, Oeser JK, O'Rourke ML, O'Brien RM., Free PMC Article | 10/30/2023 |
| A caveolin-1 dependent glucose-6-phosphatase trafficking contributes to hepatic glucose production. | A caveolin-1 dependent glucose-6-phosphatase trafficking contributes to hepatic glucose production.
Gautier-Stein A, Chilloux J, Soty M, Thorens B, Place C, Zitoun C, Duchampt A, Da Costa L, Rajas F, Lamaze C, Mithieux G., Free PMC Article | 03/23/2023 |
| Hepatocyte-specific glucose-6-phosphatase deficiency disturbs platelet aggregation and decreases blood monocytes upon fasting-induced hypoglycemia. | Hepatocyte-specific glucose-6-phosphatase deficiency disturbs platelet aggregation and decreases blood monocytes upon fasting-induced hypoglycemia.
La Rose AM, Bazioti V, Hoogerland JA, Svendsen AF, Groenen AG, van Faassen M, Rutten MGS, Kloosterhuis NJ, Dethmers-Ausema B, Nijland JH, Mithieux G, Rajas F, Kuipers F, Lukens MV, Soehnlein O, Oosterveer MH, Westerterp M., Free PMC Article | 03/26/2022 |
| Correction of metabolic abnormalities in a mouse model of glycogen storage disease type Ia by CRISPR/Cas9-based gene editing. | Correction of metabolic abnormalities in a mouse model of glycogen storage disease type Ia by CRISPR/Cas9-based gene editing.
Arnaoutova I, Zhang L, Chen HD, Mansfield BC, Chou JY., Free PMC Article | 11/22/2021 |
| The absence of hepatic glucose-6 phosphatase/ChREBP couple is incompatible with survival in mice. | The absence of hepatic glucose-6 phosphatase/ChREBP couple is incompatible with survival in mice.
Rajas F, Dentin R, Cannella Miliano A, Silva M, Raffin M, Levavasseur F, Gautier-Stein A, Postic C, Mithieux G., Free PMC Article | 09/4/2021 |
| The results reveal a previously unrecognized physiological function of NFYA in controlling glucose metabolism by up-regulating the gluconeogenic genes Pck1 and G6pc. | Regulation of hepatic gluconeogenesis by nuclear factor Y transcription factor in mice.
Zhang Y, Guan Q, Liu Y, Zhang Y, Chen Y, Chen J, Liu Y, Su Z., Free PMC Article | 01/5/2019 |
| Hepatic mitochondrial dysfunction is a feature of glycogen storage disease type Ia with glucose-6-phosphatase deficiency. | Hepatic mitochondrial dysfunction is a feature of Glycogen Storage Disease Type Ia (GSDIa).
Farah BL, Sinha RA, Wu Y, Singh BK, Lim A, Hirayama M, Landau DJ, Bay BH, Koeberl DD, Yen PM., Free PMC Article | 11/10/2018 |
| hepatic G6Pase-alpha deficiency causes metabolic reprogramming, leading to enhanced glycolysis and elevated hexose monophosphate shunt that along with impaired autophagy can contribute to hepatocellular adenoma/carcinoma development in glycogen storage disease type Ia. | Hepatic glucose-6-phosphatase-α deficiency leads to metabolic reprogramming in glycogen storage disease type Ia.
Cho JH, Kim GY, Mansfield BC, Chou JY., Free PMC Article | 04/14/2018 |
| We envisage these data and models finding utility when investigating the muscle-specific functions of the 11beta-HSD1/G6PT/H6PDH triad. | Cellular and genetic models of H6PDH and 11β-HSD1 function in skeletal muscle.
Zielinska AE, Fletcher RS, Sherlock M, Doig CL, Lavery GG., Free PMC Article | 08/19/2017 |
| Data show that glucose-6-phosphatase and perilipin-5 (G6PC/PLIN5) are upregulated in notch1 knockout (KO) mice. | Hepatic Notch1 deletion predisposes to diabetes and steatosis via glucose-6-phosphatase and perilipin-5 upregulation.
Bernsmeier C, Dill MT, Provenzano A, Makowska Z, Krol I, Muscogiuri G, Semela D, Tornillo L, Marra F, Heim MH, Duong FH. | 06/24/2017 |
| We conclude that G6PD deficiency at the level of the animals in the present study may not be a risk factor for developing CSN-OT, but this remains to be verified for human subjects | Is glucose-6-phosphate dehydrogenase deficiency a risk factor for hyperbaric oxygen exposure?
Eynan M, Tsitlovsky D, Batit L, Hochman A, Krinsky N, Abramovich A. | 11/3/2012 |
| The results strongly suggested that the increase of glucagon levels could account for the induction of G6pc expression in the kidneys and intestine of L-G6pc-/- mice. | Control of blood glucose in the absence of hepatic glucose production during prolonged fasting in mice: induction of renal and intestinal gluconeogenesis by glucagon.
Mutel E, Gautier-Stein A, Abdul-Wahed A, Amigó-Correig M, Zitoun C, Stefanutti A, Houberdon I, Tourette JA, Mithieux G, Rajas F., Free PMC Article | 02/4/2012 |
| PPARalpha is responsible for glucose production through the up-regulation of hepatic G6Pase gene expression during fasting or type 2 diabetes animal models | Peroxisome proliferator-activated receptor {alpha} is responsible for the up-regulation of hepatic glucose-6-phosphatase gene expression in fasting and db/db Mice.
Im SS, Kim MY, Kwon SK, Kim TH, Bae JS, Kim H, Kim KS, Oh GT, Ahn YH., Free PMC Article | 03/5/2011 |
| HNF-4 and Foxo1 are required for reciprocal transcriptional regulation of glucokinase and glucose-6-phosphatase genes in response to fasting and feeding | A combination of HNF-4 and Foxo1 is required for reciprocal transcriptional regulation of glucokinase and glucose-6-phosphatase genes in response to fasting and feeding.
Hirota K, Sakamaki J, Ishida J, Shimamoto Y, Nishihara S, Kodama N, Ohta K, Yamamoto M, Tanimoto K, Fukamizu A. | 01/21/2010 |
| EGF also inhibits hepatic G6Pase gene expression in vivo | Insulin and epidermal growth factor suppress basal glucose-6-phosphatase catalytic subunit gene transcription through overlapping but distinct mechanisms.
Onuma H, Oeser JK, Nelson BA, Wang Y, Flemming BP, Scheving LA, Russell WE, O'Brien RM., Free PMC Article | 01/21/2010 |
| study identified SRC-2 as a regulator of fasting hepatic glucose release, a function that SRC-2 performs by controlling expression of hepatic G6Pase; SRC-2 modulates G6Pase expression by acting as a coactivator with the orphan nuclear receptor RORalpha | Absence of the SRC-2 coactivator results in a glycogenopathy resembling Von Gierke's disease.
Chopra AR, Louet JF, Saha P, An J, Demayo F, Xu J, York B, Karpen S, Finegold M, Moore D, Chan L, Newgard CB, O'Malley BW., Free PMC Article | 01/21/2010 |
| gene transcription in H4IIE cells mediated by hepatocyte nuclear factor-4 alpha's stimulatory effect of peroxisome proliferator-activated receptor gamma co-activator-1 alpha | Hepatocyte nuclear factor-4 alpha mediates the stimulatory effect of peroxisome proliferator-activated receptor gamma co-activator-1 alpha (PGC-1 alpha) on glucose-6-phosphatase catalytic subunit gene transcription in H4IIE cells.
Boustead JN, Stadelmaier BT, Eeds AM, Wiebe PO, Svitek CA, Oeser JK, O'Brien RM., Free PMC Article | 01/21/2010 |
| G6pc expression was functionally silenced by adenovirus-mediated delivery of short hairpin RNA. | Functional silencing of hepatic microsomal glucose-6-phosphatase gene expression in vivo by adenovirus-mediated delivery of short hairpin RNA.
Huang A, Chen Y, Wang X, Zhao S, Su N, White DW. | 01/21/2010 |
| Hippel Lindau tumor suppressor regulates hepatic glucose metabolism by controlling expression of glucose transporter 2 and glucose 6-phosphatase | von Hippel Lindau tumor suppressor regulates hepatic glucose metabolism by controlling expression of glucose transporter 2 and glucose 6-phosphatase.
Park SK, Haase VH, Johnson RS. | 01/21/2010 |
| Brain contains a functional glucose-6-phosphatase complex capable of endogenous glucose production. | Brain contains a functional glucose-6-phosphatase complex capable of endogenous glucose production.
Ghosh A, Cheung YY, Mansfield BC, Chou JY. | 01/21/2010 |
| Loss of G6pt activity causes neutropenia, and local production of the chemokines KC and macrophage inflammatory protein-2 are defective in G6pt-/- neutrophils. | Impaired glucose homeostasis, neutrophil trafficking and function in mice lacking the glucose-6-phosphate transporter.
Chen LY, Shieh JJ, Lin B, Pan CJ, Gao JL, Murphy PM, Roe TF, Moses S, Ward JM, Lee EJ, Westphal H, Mansfield BC, Chou JY. | 01/21/2010 |
| Evidence for the expression of the catalytic domain of hepatic glucose-6-phosphatase in pancreatic islets. | Evidence for the expression of both the hydrolase and translocase components of hepatic glucose-6-phosphatase in murine pancreatic islets.
Goh BH, Efendić S, Khan A, Portwood N. | 01/21/2010 |
| muscle expresses both Glc-6-Pase-beta and Glc-6-P transporter and that they can couple to form an active Glc-6-Pase complex | A potential new role for muscle in blood glucose homeostasis.
Shieh JJ, Pan CJ, Mansfield BC, Chou JY. | 01/21/2010 |