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g6pase-glucose-6-phosphatase

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Schematic diagram of the proposed role of neuronal AR in <span class="search-highlight">glucose</span> homeostati...
Published: 17 January 2013
FIG. 6. Schematic diagram of the proposed role of neuronal AR in glucose homeostatic regulation. G6Pase, glucose-6-phosphatase; PEPCK, phosphoenolpyruvate carboxykinase; TG, triglyceride. FIG. 6. Schematic diagram of the proposed role of neuronal AR in glucose homeostatic regulation. G6Pase, glu... More
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Proposed scheme of hepatic glycogen synthesis. <span class="search-highlight">G6Pase</span>, <span class="search-highlight">glucose</span> <span class="search-highlight">6</span>-phosphatas...
Published: 01 June 2003
FIG. 6. Proposed scheme of hepatic glycogen synthesis. G6Pase, glucose 6-phosphatase; GNG, gluconeogenic pathway. Periportal G6P pools A and B do not communicate directly. Glycogen is formed from glucose via GK (solid arrows, direct pathway). Glycogen can be formed via GNG through pool A, through ... More
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<em>A</em>: Schematic representation of the role of PFK2/FBP2 in th...
Published: 13 April 2012
FIG. 1. A: Schematic representation of the role of PFK2/FBP2 in the F2,6P-mediated regulation of PFK1 in the glycolytic pathway in the liver. G6P, glucose-6-phosphate; TCA, tricarboxylic acid cycle; GK, glucokinase; G6Pase, glucose-6-phosphatase; F6P, fructose-6-phosphate; F2,6P, fructose-2,6-bisphosphate; PPase, protein phosphatase. B: Endogenous expression of PFK1 (PFKL; liver type) and each isoform of PFK2/FBP2 (PFKFB1 through PFKFB4) mRNAs in HuH7 cells analyzed by RT-PCR. The figure shows photographs of the ethidium bromide–stained products using agarose gel electrophoresis. Complementary DNA produced from the reverse transcriptase reaction, using total RNA from the cells, was amplified by PCR with pairs of oligonucleotide primers specific for each mRNA. M, molecular size marker (100-bp ladder). (A high-quality color representation of this figure is available in the online issue.) FIG. 1. A: Schematic representation of the role of PFK2/FBP2 in the F2,6P-mediated regulation of PFK1 in the glycolytic pathway in the liver. G6P, glucose-6-phosphate; TCA, tricarboxylic acid cycle; GK, glucokinase; G6Pase, glucose-6-phosphatase; F6P, fructose-6-phosphate; F2,6P, fructose-2,6-bisphosphate; PPase, protein phosphatase. B: Endogenous expression of PFK1 (PFKL; liver type) and each isoform of PFK2/FBP2 (PFKFB1 through PFKFB4) mRNAs in HuH7 cells analyzed by RT-PCR. The figure shows photographs of the ethidium bromide–stained products using agarose gel electrophoresis. Complementary DNA produced from the reverse transcriptase reaction, using total RNA from the cells, was amplified by PCR with pairs of oligonucleotide primers specific for each mRNA. M, molecular size marker (100-bp ladder). (A high-quality color representation of this figure is available in the online issue.) More
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LXR activation in pancreatic β-cells stimulates the expression of lipogenic...
Published: 01 June 2007
FIG. 2. LXR activation in pancreatic β-cells stimulates the expression of lipogenic genes. A: INS-1 cells were treated with the LXR agonist T0901317 (10 μmol/l) for 36 h. Total RNA was isolated and analyzed by Northern blot analysis. 36B4 was used as a loading control. B and C: cDNAs prepared from primary pancreatic islets (B) or INS-1 cells (C) treated with T0901317 (10 μmol/l) for 36 h were subjected to real-time quantitative RT-PCR analysis. *P < 0.01 versus DMSO control by t test. The relative amount of each mRNA was normalized to cyclophilin levels. G6Pase, glucose-6-phosphatase. FIG. 2. LXR activation in pancreatic β-cells stimulates the expression of lipogenic genes. A: INS-1 cells were treated with the LXR agonist T0901317 (10 μmol/l) for 36 h. Total RNA was isolated and analyzed by Northern blot analysis. 36B4 was used as a loading control. B and C: cDNAs prepared from primary pancreatic islets (B) or INS-1 cells (C) treated with T0901317 (10 μmol/l) for 36 h were subjected to real-time quantitative RT-PCR analysis. *P < 0.01 versus DMSO control by t test. The relative amount of each mRNA was normalized to cyclophilin levels. G6Pase, glucose-6-phosphatase. More
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Hepatic <span class="search-highlight">glucose</span> metabolism. In the postabsorptive state, glucokinase (GK) i...
Published: 01 January 2009
FIG. 1. Hepatic glucose metabolism. In the postabsorptive state, glucokinase (GK) is sequestered in the nucleus bound to GKRP and the liver maintains blood glucose homeostasis by glucose production (red arrows) by glycogenolysis from glycogen and by gluconeogenesis from lactate and other gluconeog... More
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Schematic diagram of the proposed new mechanism by which metformin inhibits...
Published: 14 June 2013
FIG. 3. Schematic diagram of the proposed new mechanism by which metformin inhibits hepatic gluconeogenesis ( 42 ). Up or down arrows next to a metabolite or enzyme show the direction the concentration or activity changes in response to metformin. Metformin (whose uptake into hepatocytes is promot... More
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Overview of the role of the ATF/CREB family in the pathway involved in hepa...
Published: 15 February 2021
Figure 1 Overview of the role of the ATF/CREB family in the pathway involved in hepatic gluconeogenesis. The ATF/CREB family members play central roles in hepatic gluconeogenesis as transcriptional regulators. Under fasting conditions, elevated circulating glucagon binds G-protein–coupled receptor... More
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G0S2 regulates hepatic FFA and <span class="search-highlight">glucose</span> metabolism. Eight-week-old C57BL/6j ...
Published: 13 February 2014
Figure 5 G0S2 regulates hepatic FFA and glucose metabolism. Eight-week-old C57BL/6j female mice were injected with G0S2-specific (G0S2 KD) or control (Ctrl KD) siRNA, and the following analyses were performed 3 days later except for in B. A: After a 16-h fast, plasma levels of 3-hydroxybutyrate were measured (n = 5 per group). *P < 0.05 vs. Ctrl KD. B: Primary hepatocytes were infected with Ad-G0S2 or Ad-Null for 24 h followed by measurement of FA oxidation. The data are representative of three independent experiments. *P < 0.05 vs. Ad-Null. C: Real-time PCR was used to determine the mRNA levels of genes in liver from mice in A. Data normalized to β-actin were expressed relative to the control (n = 5 per group). *P < 0.05 vs. Ctrl KD. D: After a 16-h fast, mice were injected with 2 g/kg pyruvate and blood glucose levels were detected at indicated times (n = 6 per group). *P < 0.05 vs. Ctrl KD. E: After a 16-h fast, the mRNA levels of G6Pase, PEPCK, FPB1, and PC in liver were assessed by real-time PCR (n = 5 per group). G6Pase, glucose-6-phosphatase, catalytic; PEPCK, phosphoenolpyruvate carboxykinase 1, cytosolic; PC, pyruvate carboxylase. *P < 0.05, **P < 0.01 vs. Ctrl KD. F: Hepatic glycogen content was measured at indicated conditions (n = 5–6 per group). *P < 0.05, **P < 0.01 vs. Ctrl KD. Figure 5. G0S2 regulates hepatic FFA and glucose metabolism. Eight-week-old C57BL/6j female mice were injected with G0S2-specific (G0S2 KD) or control (Ctrl KD) siRNA, and the following analyses were performed 3 days later except for in B. A: After a 16-h fast, plasma levels of 3-hydroxybutyrate were measured (n = 5 per group). *P < 0.05 vs. Ctrl KD. B: Primary hepatocytes were infected with Ad-G0S2 or Ad-Null for 24 h followed by measurement of FA oxidation. The data are representative of three independent experiments. *P < 0.05 vs. Ad-Null. C: Real-time PCR was used to determine the mRNA levels of genes in liver from mice in A. Data normalized to β-actin were expressed relative to the control (n = 5 per group). *P < 0.05 vs. Ctrl KD. D: After a 16-h fast, mice were injected with 2 g/kg pyruvate and blood glucose levels were detected at indicated times (n = 6 per group). *P < 0.05 vs. Ctrl KD. E: After a 16-h fast, the mRNA levels of G6Pase, PEPCK, FPB1, and PC in liver were assessed by real-time PCR (n = 5 per group). G6Pase, glucose-6-phosphatase, catalytic; PEPCK, phosphoenolpyruvate carboxykinase 1, cytosolic; PC, pyruvate carboxylase. *P < 0.05, **P < 0.01 vs. Ctrl KD. F: Hepatic glycogen content was measured at indicated conditions (n = 5–6 per group). *P < 0.05, **P < 0.01 vs. Ctrl KD. More
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Interplay of metabolic effects of insulin and LXR. The green areas indicate...
Published: 01 February 2004
FIG. 1. Interplay of metabolic effects of insulin and LXR. The green areas indicate LXR target genes, blue arrows indicate activating effect, and the red arrow indicates inhibitory effects. Activation of LXR leads to increased glucose uptake in muscle and adipose tissue via the GLUT transporters. ... More
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<em>A</em>: The HR-dGTT. <em>Top panel</em>: Time course of...
Published: 01 December 2006
FIG. 2. A: The HR-dGTT. Top panel: Time course of the [6,6-2H2]glucose (M2) isotopomers using 1 mg/g body wt of a 1:1 mixture of [2-2H]- and [6,6-2H2]glucose for the ipGTT. Data are presented as means ± SE. *P < 0.05 between Pten+/+ and Pten+/− mice, determined by Student’s t test. M2 glucose levels are significantly lower for Pten+/− versus Pten+/+ mice, suggesting increased peripheral disposal of glucose for the Pten+/− mice. B: Time course of the percent difference between the plasma [2-2H1]- and [6,6-2H2] glucose enrichments during the deuterated glucose HR-dGTT. The HR-dGTT was performed using 1 mg/g body wt of a 1:1 mixture of [2-2H1]- and [6,6-2H2]glucose on Pten+/− (n = 5) and Pten+/− (n = 7) mice after a 15-h overnight fast. The data are presented as means ± SE. The percent difference between the plasma enrichments of the two tracers reflects the relative rate of de-deuteration of [2-2H1]- versus [6,6-2H2]glucose, which is a measure of net hepatic glucose phosphorylation or, equivalently, glucose/glucose-6-P futile cycling. At all time points during the IPGTT, the percent difference between the plasma enrichments of the two tracers is greater for the Pten+/+ than for the Pten+/− mouse, indicating a much smaller amount of glucose/glucose-6-P futile cycling for the Pten+/− mice. The slope is 16.2 ± 0.53% for the Pten+/+ mice versus 7.4 ± 0.35% for Pten+/− mice. C: Illustrative diagram of pathways for hepatic metabolism of the deuterium-labeled [2-2H1]/[6,6-2H2]glucose. De-deuteration of [2-2H1]glucose occurs during the equilibration of glucose-6-P (G-6-P) with fructose-6-P (F-6-P), which is theoretically two orders of magnitude faster than any other glycolytic or gluconeogenic flux. De-deuteration of [6,6-2H1]glucose does not occur until the deuterated glucose reaches the level of pyruvate. F-1,6-P2, fructose-1,6-bisphosphate; GK, glucokinase; G6Pase, glucose-6-phosphatase; PK, pyruvate kinase. FIG. 2. A: The HR-dGTT. Top panel: Time course of the [6,6-2H2]glucose (M2) isotopomers using 1 mg/g body wt of a 1:1 mixture of [2-2H]- and [6,6-2H2]glucose for the ipGTT. Data are presented as means ± SE. *P < 0.05 between Pten+/+ and Pten+/− mice, determined by Student’s t test. M2 glucose levels are significantly lower for Pten+/− versus Pten+/+ mice, suggesting increased peripheral disposal of glucose for the Pten+/− mice. B: Time course of the percent difference between the plasma [2-2H1]- and [6,6-2H2] glucose enrichments during the deuterated glucose HR-dGTT. The HR-dGTT was performed using 1 mg/g body wt of a 1:1 mixture of [2-2H1]- and [6,6-2H2]glucose on Pten+/− (n = 5) and Pten+/− (n = 7) mice after a 15-h overnight fast. The data are presented as means ± SE. The percent difference between the plasma enrichments of the two tracers reflects the relative rate of de-deuteration of [2-2H1]- versus [6,6-2H2]glucose, which is a measure of net hepatic glucose phosphorylation or, equivalently, glucose/glucose-6-P futile cycling. At all time points during the IPGTT, the percent difference between the plasma enrichments of the two tracers is greater for the Pten+/+ than for the Pten+/− mouse, indicating a much smaller amount of glucose/glucose-6-P futile cycling for the Pten+/− mice. The slope is 16.2 ± 0.53% for the Pten+/+ mice versus 7.4 ± 0.35% for Pten+/− mice. C: Illustrative diagram of pathways for hepatic metabolism of the deuterium-labeled [2-2H1]/[6,6-2H2]glucose. De-deuteration of [2-2H1]glucose occurs during the equilibration of glucose-6-P (G-6-P) with fructose-6-P (F-6-P), which is theoretically two orders of magnitude faster than any other glycolytic or gluconeogenic flux. De-deuteration of [6,6-2H1]glucose does not occur until the deuterated glucose reaches the level of pyruvate. F-1,6-P2, fructose-1,6-bisphosphate; GK, glucokinase; G6Pase, glucose-6-phosphatase; PK, pyruvate kinase. More
Meeting Abstracts
Journal: Diabetes
Diabetes 1999;48(8):1579–1585
Published: 01 August 1999
... littermates (db/+m). The results were compared with those after troglitazone administration under the same conditions. Despite hyperinsulinemia, hepatic glucose-6-phosphatase (G6Pase) and fructose-1,6-bisphosphatase (FBPase) activities are higher in db/db than in db/+m mice. Dietary administration of DHEA...
Meeting Abstracts
Journal: Diabetes
Diabetes 2000;49(6):969–974
Published: 01 June 2000
... that increased EGP is mediated in part by increased G6Pase flux in type 2 diabetes. Glucose-6-Phosphatase Flux In Vitro Is Increased in Type 2 Diabetes John N. Clore, Julie Stillman, and Harvey Sugerman Despite the effects of hyperinsulinemia and hypergly- Type 2 diabetes is characterized in part by cemia, 2...
Journal Articles
Journal: Diabetes
Diabetes 1994;43(11):1284–1290
Published: 01 November 1994
... ± 13 nmol/g, P < 0.01). Maximal activities of glucose-6-phosphatase (G6Pase) (from 17.6 ± 0.8 to 19.6 ± 2.6 U/g) and glucokinase (from 1.1 ± 0.2 to 1.0 ± 0.2 U/g) did not change. Insulin infusion resulted in a threefold increase (P < 0.05) in the activity of glycogen synthase (active form...
Journal Articles
Journal: Diabetes
Diabetes 2001;50(11):2591–2597
Published: 01 November 2001
...Robert H.J. Bandsma; Coen H. Wiegman; Andreas W. Herling; Hans-Joerg Burger; Anke ter Harmsel; Alfred J. Meijer; Johannes A. Romijn; Dirk-Jan Reijngoud; Folkert Kuipers Glucose-6-phosphatase (G6Pase) is a key enzyme in hepatic glucose metabolism. Altered G6Pase activity in glycogen storage disease...
Meeting Abstracts
Journal: Diabetes
Diabetes 2000;49(6):896–903
Published: 01 June 2000
...P A Lochhead; I P Salt; K S Walker; D G Hardie; C Sutherland Insulin regulates the rate of expression of many hepatic genes, including PEPCK, glucose-6-phosphatase (G6Pase), and glucose-6-phosphate dehydrogenase (G6PDHase). The expression of these genes is also abnormally regulated in type 2...
Journal Articles
Journal: Diabetes
Diabetes 2005;54(7):1958–1967
Published: 01 July 2005
... the reduced phosphorylation was restored in ΔIP-SHIP2–expressing db/db mice. The abundance of mRNA for glucose-6-phosphatase (G6Pase) and PEPCK was increased, that for glucokinase (GK) was unchanged, and that for sterol regulatory element–binding protein 1 (SREBP)-1 was decreased in hepatic WT-SHIP2...
Journal Articles
Journal: Diabetes
Diabetes 2006;55(7):2042–2050
Published: 01 July 2006
... gluconeogenesis. The transcription factor Foxo1 links insulin signaling to decreased transcription of PEPCK and glucose-6-phosphatase (G6Pase) and provides a possible therapeutic target in insulin-resistant states. Synthetic, optimized antisense oligonucleotides (ASOs) specifically inhibit Foxo1 expression. Here...
Journal Articles
Journal: Diabetes
Diabetes 2006;55(9):2479–2490
Published: 01 September 2006
... exhibited persistent endogenous glucose production (EGP) despite marked hyperglycemia. Gluconeogenesis and glucose cycling (GC) were responsible for 46 and 51% of glucose-6-phosphatase (G6Pase) flux, respectively. Net incorporation of plasma glucose into hepatic glycogen was negligible. Glucokinase (GK...
Journal Articles
Journal: Diabetes
Diabetes 2001;50(3):502–514
Published: 01 March 2001
...Larry J. Bischof; Cyrus C. Martin; Christina A. Svitek; Beth T. Stadelmaier; Lauri A. Hornbuckle; Joshua K. Goldman; James K. Oeser; John C. Hutton; Richard M. O’Brien Glucose-6-phosphatase (G6Pase) is a multicomponent system located in the endoplasmic reticulum comprising a catalytic subunit...
Journal Articles
Journal: Diabetes
Diabetes 2007;56(9):2218–2227
Published: 01 September 2007
...Lisa Logie; Antonio J. Ruiz-Alcaraz; Michael Keane; Yvonne L. Woods; Jennifer Bain; Rudolfo Marquez; Dario R. Alessi; Calum Sutherland OBJECTIVE— Abnormal expression of the hepatic gluconeogenic genes (glucose-6-phosphatase [G6Pase] and PEPCK) contributes to hyperglycemia. These genes are repressed...
Includes: Supplementary data