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gk-glucokinase

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Schematic representation of the signaling network regulated by PKCζ in gluc...
Published: 11 February 2016
Figure 8 Schematic representation of the signaling network regulated by PKCζ in glucose- and insulin resistance–mediated β-cell replication. GK, glucokinase. Figure 8. Schematic representation of the signaling network regulated by PKCζ in glucose- and insulin resistance–mediated β-cell replicati... More
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Serum, pancreas, and muscle insulin in AAV-treated mice. <em>A</em>...
Published: 01 June 2006
FIG. 4. Serum, pancreas, and muscle insulin in AAV-treated mice. A: Serum insulin concentration. Mouse insulin concentration was low in all STZ-administered mice. Increased levels of total insulin (mouse plus human) were noted in STZ-administered mice that received a single injection of AAV-Ins+GK vectors (3.6 × 1010 vector genomes). B: Pancreatic insulin content and insulin immunostaining in islets of pancreatic sections were greatly reduced 4 months after STZ administration. Arrowheads indicate mouse islets (×100). Expression of insulin and glucokinase (C) in skeletal muscle and hepatic expression of PEPCK (D) 4 months after a single injection of AAV-Ins+GK vectors (3.6 × 1010 vector genomes). Total RNA was obtained from either skeletal muscle or liver, analyzed by Northern blot, and hybridized with insulin, glucokinase, or PEPCK probes. A representative Northern blot is shown. All results are the means ± SE of 10 mice in each group. *P < 0.05 vs. STZ-control. Con, control; GK, glucokinase; Ins, insulin. FIG. 4. Serum, pancreas, and muscle insulin in AAV-treated mice. A: Serum insulin concentration. Mouse insulin concentration was low in all STZ-administered mice. Increased levels of total insulin (mouse plus human) were noted in STZ-administered mice that received a single injection of AAV-Ins+GK vectors (3.6 × 1010 vector genomes). B: Pancreatic insulin content and insulin immunostaining in islets of pancreatic sections were greatly reduced 4 months after STZ administration. Arrowheads indicate mouse islets (×100). Expression of insulin and glucokinase (C) in skeletal muscle and hepatic expression of PEPCK (D) 4 months after a single injection of AAV-Ins+GK vectors (3.6 × 1010 vector genomes). Total RNA was obtained from either skeletal muscle or liver, analyzed by Northern blot, and hybridized with insulin, glucokinase, or PEPCK probes. A representative Northern blot is shown. All results are the means ± SE of 10 mice in each group. *P < 0.05 vs. STZ-control. Con, control; GK, glucokinase; Ins, insulin. More
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Calculated thresholds for glucose-stimulated insulin release (GSIR) in acti...
Published: 31 March 2009
FIG. 5. Calculated thresholds for glucose-stimulated insulin release (GSIR) in activating and inactivating mutations of glucokinase. Thresholds are plotted against the inverse of the mutant enzyme activity index relative to wild-type (WT) enzyme. Because relative expression of the glucokinase form... More
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Immunofluorescence analyses of protein expression in FH-B-TPN cells treated...
Published: 01 September 2005
FIG. 3. Immunofluorescence analyses of protein expression in FH-B-TPN cells treated with SFM for 6 days followed by Act-A in SFM for 3 days (Treated) compared with cells grown in complete medium (Untreated). Indicated antigens were visualized with Cy2- (green) and Cy3- (red) conjugated secondary antibodies. All nuclei were labeled blue with DAPI. The percent of positive cells shown on each panel is based on counting >300 cells in multiple fields. Bar = 10 μm. GK, glucokinase. FIG. 3. Immunofluorescence analyses of protein expression in FH-B-TPN cells treated with SFM for 6 days followed by Act-A in SFM for 3 days (Treated) compared with cells grown in complete medium (Untreated). Indicated antigens were visualized with Cy2- (green) and Cy3- (red) conjugated secondary antibodies. All nuclei were labeled blue with DAPI. The percent of positive cells shown on each panel is based on counting >300 cells in multiple fields. Bar = 10 μm. GK, glucokinase. More
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Changes in hepatic gene expression in L-<em>Pdk1</em>KO mice. The a...
Published: 01 April 2007
FIG. 4. Changes in hepatic gene expression in L-Pdk1KO mice. The amounts of the indicated mRNAs in the liver of L-Pdk1KO (▪) or Pdk1flox/flox (□) mice in the randomly fed state (A) or at the indicated times of refeeding after food deprivation for 24 h (B and C) were determined. GK, glucokinase. Data are means ± SEM (n = 5–6 or n = 4, respectively, in A and B, and n = 4 in each genotype in C) and are expressed relative to the amount of 36B4 mRNA. *P < 0.05, **P < 0.01 (Student's t test) vs. corresponding value for Pdk1flox/flox mice. FIG. 4. Changes in hepatic gene expression in L-Pdk1KO mice. The amounts of the indicated mRNAs in the liver of L-Pdk1KO (▪) or Pdk1flox/flox (□) mice in the randomly fed state (A) or at the indicated times of refeeding after food deprivation for 24 h (B and C) were determined. GK, glucokinase. Data are means ± SEM (n = 5–6 or n = 4, respectively, in A and B, and n = 4 in each genotype in C) and are expressed relative to the amount of 36B4 mRNA. *P < 0.05, **P < 0.01 (Student's t test) vs. corresponding value for Pdk1flox/flox mice. More
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RT-PCR analysis of gene expression in FH-B and FH-B-TPN cells treated with ...
Published: 01 September 2005
FIG. 2. RT-PCR analysis of gene expression in FH-B and FH-B-TPN cells treated with various culture media. Cells were grown for >7 days in complete medium (CM), 3 days in CM containing Act-A, 6 days in SFM, 6 days in SFM, and then 3 days in Act-A in SFM, or tested for phenotypic stability (Stb) ... More
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Nonapoptotic function of Bcl-2 family members as energystat of mitochondria...
Published: 13 December 2012
FIG. 1. Nonapoptotic function of Bcl-2 family members as energystat of mitochondrial metabolism. Through multiple interactions with mitochondrial proteins (cyan), antiapoptotic (yellow) as well as proapoptotic (orange) Bcl-2 family members regulate glucose-driven mitochondrial ATP synthesis, there... More
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Effect of EPA on energy metabolism–related genes in the HF/HS groups. <ital
Published: 03 August 2010
FIG. 3. Effect of EPA on energy metabolism–related genes in the HF/HS groups. A and B: Liver. C and D: Skeletal muscle. E: Epididymal WAT. F: Hepatic SREBP-1 protein in the HF/HS group. n = 7–10. †P < 0.05; ††P < 0.01 vs. control group. *P < 0.05; **P < 0.01 vs. HF/HS group. ACO, acyl-CoA oxidase; ATGL, adipose triglyceride lipase; CPT-1a, carnitine palmitoyltransferase-1a; CS, citrate synthase; GK, glucokinase; HAD, hydroxyacyl-CoA dehydrogenase; HK-2, hexokinase-2; HSL, hormone-sensitive lipase; MCAD, acetyl-CoA dehydrogenase, medium chain; PFKL, phosphofructokinase, liver; PFKM, phosphofructokinase, muscle, B-type. FIG. 3. Effect of EPA on energy metabolism–related genes in the HF/HS groups. A and B: Liver. C and D: Skeletal muscle. E: Epididymal WAT. F: Hepatic SREBP-1 protein in the HF/HS group. n = 7–10. †P < 0.05; ††P < 0.01 vs. control group. *P < 0.05; **P < 0.01 vs. HF/HS group. ACO, acyl-CoA oxidase; ATGL, adipose triglyceride lipase; CPT-1a, carnitine palmitoyltransferase-1a; CS, citrate synthase; GK, glucokinase; HAD, hydroxyacyl-CoA dehydrogenase; HK-2, hexokinase-2; HSL, hormone-sensitive lipase; MCAD, acetyl-CoA dehydrogenase, medium chain; PFKL, phosphofructokinase, liver; PFKM, phosphofructokinase, muscle, B-type. More
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Gene expression analysis. <em>A</em>: mRNA levels of genes involved...
Published: 01 October 2006
FIG. 5. Gene expression analysis. A: mRNA levels of genes involved in glucose metabolism were determined by real-time PCR in RNA samples from isolated islets. mRNA levels were normalized to mRNA levels of hypoxanthine phosphoribosyl transferase (HPRT). *P < 0.05 (n = 5 for each experiment). GADPH, glyceraldehyde 3-phosphate dehydrogenase; GK, glucokinase; l-PK, liver pyruvate kinase; OGDH, oxoglutarate dehydrogenase; PFK-2, phosphofruktokinase 2; UCP2, uncoupling protein 2. B: Mitochondrial membrane potential in Foxa1+/+ and Foxa1−/− isolated islets. MitoSensor aggregates in the mitochondria with high membrane potential of wild-type Foxa1+/+ islets produce red fluorescence. The absence of red fluorescence in Foxa1−/− islets is indicative of reduced mitochondrial membrane potential. FIG. 5. Gene expression analysis. A: mRNA levels of genes involved in glucose metabolism were determined by real-time PCR in RNA samples from isolated islets. mRNA levels were normalized to mRNA levels of hypoxanthine phosphoribosyl transferase (HPRT). *P < 0.05 (n = 5 for each experiment). GADPH, glyceraldehyde 3-phosphate dehydrogenase; GK, glucokinase; l-PK, liver pyruvate kinase; OGDH, oxoglutarate dehydrogenase; PFK-2, phosphofruktokinase 2; UCP2, uncoupling protein 2. B: Mitochondrial membrane potential in Foxa1+/+ and Foxa1−/− isolated islets. MitoSensor aggregates in the mitochondria with high membrane potential of wild-type Foxa1+/+ islets produce red fluorescence. The absence of red fluorescence in Foxa1−/− islets is indicative of reduced mitochondrial membrane potential. 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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Metabolic pathways for hepatic lipogenesis in mice refed with glucose and/o...
Published: 01 March 2004
FIG. 8. Metabolic pathways for hepatic lipogenesis in mice refed with glucose and/or fructose. Major pathways for lipogenesis after ingestion of glucose or fructose are highlighted by bold lines. 6PG, 6-phosphogluconate; 6PGD, 6-phosphogluconate dehydrogenase; ACAS, acetyl-CoA synthase; ACL, ATP c... More
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Effect of insulin on the protein and mRNA levels in livers of control (C), ...
Published: 01 March 2004
FIG. 6. Effect of insulin on the protein and mRNA levels in livers of control (C), STZ-administered (S), and STZ-administered mice injected with insulin (S + I) refed with glucose. A: Plasma glucose levels from the control (C), STZ-administered (S), and STZ-administered mice injected with insulin (S + I). Results are the mean ± SE of four male mice. B: Immunoblot analysis of SREBP-1 and -1c in nuclear extracts from pooled livers of each group. The primary antibodies used were polyclonal anti-mouse SREBP-1 and anti-mouse SREBP-1c. The blots are representative of two different experiments. C: Northern blot analysis of different mRNAs in livers of each experimental group. Total RNA isolated from the livers of four male mice was pooled, and 10-μg aliquots were subjected to electrophoresis and Northern blotting, followed by hybridization with the indicated 32P-labeled cDNA probes. The blots are representative of three different experiments. 36B4, acidic ribosomal phosphoprotein p0; GK, glucokinase. FIG. 6. Effect of insulin on the protein and mRNA levels in livers of control (C), STZ-administered (S), and STZ-administered mice injected with insulin (S + I) refed with glucose. A: Plasma glucose levels from the control (C), STZ-administered (S), and STZ-administered mice injected with insulin (S + I). Results are the mean ± SE of four male mice. B: Immunoblot analysis of SREBP-1 and -1c in nuclear extracts from pooled livers of each group. The primary antibodies used were polyclonal anti-mouse SREBP-1 and anti-mouse SREBP-1c. The blots are representative of two different experiments. C: Northern blot analysis of different mRNAs in livers of each experimental group. Total RNA isolated from the livers of four male mice was pooled, and 10-μg aliquots were subjected to electrophoresis and Northern blotting, followed by hybridization with the indicated 32P-labeled cDNA probes. The blots are representative of three different experiments. 36B4, acidic ribosomal phosphoprotein p0; GK, glucokinase. More
Journal Articles
Journal: Diabetes
Diabetes 1997;46(2):179–186
Published: 01 February 1997
...Karen S Brown; Stephen S Kalinowski; John R Megill; Stephen K Durham; Kasim A Mookhtiar Glucokinase (GK) plays a central role in the sensing of glucose in pancreatic β-cells and parenchymal cells of the liver. Glucokinase regulatory protein is a physiological inhibitor of GK in the liver...
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Time-course changes of hepatic mRNA levels of SREBP-1 and lipogenic enzymes...
Published: 01 March 2004
FIG. 1. Time-course changes of hepatic mRNA levels of SREBP-1 and lipogenic enzymes in the mice refed with glucose (G, ○), fructose (F, □), or sucrose (S, ▵). A: Northern blot analysis of different mRNAs in livers of mice. For each experimental group, total RNA isolated from the livers of three male mice was pooled, and 10-μg aliquots were subjected to electrophoresis and Northern blotting, followed by hybridization with the indicated 32P-labeled cDNA probes. The blots are representative of three different experiments. B: Quantification of hepatic mRNAs for SREBP-1 and FAS. The data in panel A were quantified as described in research design and methods and normalized relative to the 36B4 (acidic ribosomal phosphoprotein p0) mRNA signal. The fold change is the relative ratio of each signal versus the corresponding fasted control mice, corrected for the signal from 36B4 as loading control. C: Plasma glucose and insulin levels of the mice fasted for 24 h and refed glucose, fructose, or sucrose for 6, 9, or 12 h. Results are the means ± SE of four male mice. GK, glucokinase; L-PK, l-pyruvate kinase. FIG. 1. Time-course changes of hepatic mRNA levels of SREBP-1 and lipogenic enzymes in the mice refed with glucose (G, ○), fructose (F, □), or sucrose (S, ▵). A: Northern blot analysis of different mRNAs in livers of mice. For each experimental group, total RNA isolated from the livers of three male mice was pooled, and 10-μg aliquots were subjected to electrophoresis and Northern blotting, followed by hybridization with the indicated 32P-labeled cDNA probes. The blots are representative of three different experiments. B: Quantification of hepatic mRNAs for SREBP-1 and FAS. The data in panel A were quantified as described in research design and methods and normalized relative to the 36B4 (acidic ribosomal phosphoprotein p0) mRNA signal. The fold change is the relative ratio of each signal versus the corresponding fasted control mice, corrected for the signal from 36B4 as loading control. C: Plasma glucose and insulin levels of the mice fasted for 24 h and refed glucose, fructose, or sucrose for 6, 9, or 12 h. Results are the means ± SE of four male mice. GK, glucokinase; L-PK, l-pyruvate kinase. More
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Liver weight, glycogen content, and gene expression analysis of Hep-M3-KO m...
Published: 14 September 2009
FIG. 3. Liver weight, glycogen content, and gene expression analysis of Hep-M3-KO mice (■) and control littermates (□) maintained on regular diet. A: Liver weight. B: Liver glycogen content of Hep-M3-KO mice and control littermates (freely fed 8-month-old males, n = 6 per group). C: Liver gene expression analysis. Gene expression was studied by real-time qRT-PCR using total hepatic RNA prepared from Hep-M3-KO mice and control littermates (freely fed 3-month-old males). Data from three independent experiments were normalized relative to the expression of cyclophilin A, which served as an internal control. Results are presented as percent change in gene expression in Hep-M3-KO mice relative to control littermates (100%). Acly, ATP citrate lyase; AOX, acyl-CoA oxidase; CPT, carnitine palmitoyltransferase; CREB, cAMP-response element binding protein; FAS, fatty acid synthase; GK, glucokinase; IR, insulin receptor; IRS1, IR substrate 1; PC, pyruvate carboxylase; PGC, PPAR coactivator; PPAR, peroxisome proliferator–activated receptor. FIG. 3. Liver weight, glycogen content, and gene expression analysis of Hep-M3-KO mice (■) and control littermates (□) maintained on regular diet. A: Liver weight. B: Liver glycogen content of Hep-M3-KO mice and control littermates (freely fed 8-month-old males, n = 6 per group). C: Liver gene expression analysis. Gene expression was studied by real-time qRT-PCR using total hepatic RNA prepared from Hep-M3-KO mice and control littermates (freely fed 3-month-old males). Data from three independent experiments were normalized relative to the expression of cyclophilin A, which served as an internal control. Results are presented as percent change in gene expression in Hep-M3-KO mice relative to control littermates (100%). Acly, ATP citrate lyase; AOX, acyl-CoA oxidase; CPT, carnitine palmitoyltransferase; CREB, cAMP-response element binding protein; FAS, fatty acid synthase; GK, glucokinase; IR, insulin receptor; IRS1, IR substrate 1; PC, pyruvate carboxylase; PGC, PPAR coactivator; PPAR, peroxisome proliferator–activated receptor. More
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Hepatic protein and gene expression analysis. Total protein and RNA were ex...
Published: 01 January 2009
FIG. 4. Hepatic protein and gene expression analysis. Total protein and RNA were extracted from frozen liver samples of mice fed standard diet and administered vehicle (open bars, SD), fed high-fat diet and administered vehicle (open bars, HFD), FGF21 (striped bars; 0.1, 1, and 10 mg · kg−1 · day−1 doses), or rosiglitazone (black bars; ∼4 mg · kg−1 · day−1) for 6 weeks. Western analyses and RT-PCRs were conducted on pooled protein and RNA extracts (n = 5 per group). A: FGF21 reduced the amount of mature SREBP-1 without changing its precursor content in liver. Vehi, vehicle; Rosi, rosiglitazone. B: FGF21 reduced protein expression levels of total ACC, FAS, and PPARγ in liver. C: FGF21 reduced mRNAs encoding enzymes involved in hepatic lipogenesis without changing SREBP-1 mRNA expression. GK, glucokinase; PK, pyruvate kinase; SCD1, stearoyl-CoA desaturase 1; Elovl6, long-chain fatty acid elongase 6; DGAT1 and MOGAT2, diacylgycerol and monoacyglycerol acyltransferases. D: FGF21 reduced mRNA expression of PPARγ and its target genes, aP2 and CD36, in liver. E: FGF21 reduced glucose-6-phosphatase (G6Pase) mRNA expression. FIG. 4. Hepatic protein and gene expression analysis. Total protein and RNA were extracted from frozen liver samples of mice fed standard diet and administered vehicle (open bars, SD), fed high-fat diet and administered vehicle (open bars, HFD), FGF21 (striped bars; 0.1, 1, and 10 mg · kg−1 · day−1 doses), or rosiglitazone (black bars; ∼4 mg · kg−1 · day−1) for 6 weeks. Western analyses and RT-PCRs were conducted on pooled protein and RNA extracts (n = 5 per group). A: FGF21 reduced the amount of mature SREBP-1 without changing its precursor content in liver. Vehi, vehicle; Rosi, rosiglitazone. B: FGF21 reduced protein expression levels of total ACC, FAS, and PPARγ in liver. C: FGF21 reduced mRNAs encoding enzymes involved in hepatic lipogenesis without changing SREBP-1 mRNA expression. GK, glucokinase; PK, pyruvate kinase; SCD1, stearoyl-CoA desaturase 1; Elovl6, long-chain fatty acid elongase 6; DGAT1 and MOGAT2, diacylgycerol and monoacyglycerol acyltransferases. D: FGF21 reduced mRNA expression of PPARγ and its target genes, aP2 and CD36, in liver. E: FGF21 reduced glucose-6-phosphatase (G6Pase) mRNA expression. More
Journal Articles
Journal: Diabetes
Diabetes 2004;53(suppl_1):S66–S70
Published: 01 February 2004
.... Recently it was reported that glucokinase (GK) expression was increased by TZDs in the liver of diabetic ZDF rats. However, the mechanism whereby TZDs increase GK expression is not yet studied. We have assumed that liver type glucokinase (LGK) induction by TZDs could be achieved by direct transcriptional...
Journal Articles
Journal: Diabetes
Diabetes 2004;53(8):2164–2168
Published: 01 August 2004
...Antonio L. Cuesta-Muñoz; Hanna Huopio; Timo Otonkoski; Juan M. Gomez-Zumaquero; Kirsti Näntö-Salonen; Jacques Rahier; Soledad López-Enriquez; Maria A. García-Gimeno; Pascual Sanz; Federico C. Soriguer; Markku Laakso Glucokinase (GK) is a glycolytic key enzyme that functions as a glucose sensor...
Journal Articles
Journal: Diabetes
Diabetes 2006;55(6):1546–1553
Published: 01 June 2006
... of AAV-Ins+GK vectors (3.6 × 1010 vector genomes). B: Pancreatic insulin content and insulin immunostaining in islets of pancreatic sections were greatly reduced 4 months after STZ administration. Arrowheads indicate mouse islets (×100). Expression of insulin and glucokinase...
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Time-course changes of various mRNA levels in livers of the control and STZ...
Published: 01 March 2004
FIG. 5. Time-course changes of various mRNA levels in livers of the control and STZ-administered mice refed with glucose (Glu), fructose (Fru), or sucrose (Suc). A: Northern blot analysis of key genes in the regulation of lipogenesis in livers of control (C) and STZ-administered (S) mice refed with glucose (Glu), fructose (Fru), or sucrose (Suc) for 6 or 12 h. B: Northern blot analysis of key genes in the regulation of glycolysis and gluconeogenesis in livers of control (C) and STZ-administered (S) mice refed with glucose (Glu), fructose (Fru), or sucrose (Suc) for 6 or 12 h. C: Northern blot analysis of key genes in the regulation of insulin signaling, glucose transport, cholesterol synthesis, and 36B4 in livers of control (C) and STZ-administered (S) mice refed with glucose (Glu), fructose (Fru), or sucrose (Suc) for 6 or 12 h. D: Northern blot analysis of key genes in the regulation of glycolysis, gluconeogenesis, and SREBP-1 in livers of control (C) and STZ-administered (S) mice refed with glucose (Glu), fructose (Fru), or sucrose (Suc) for 3 h. For each experimental group, total RNA isolated from the livers of three male mice was pooled, and 10-μg aliquots were subjected to electrophoresis and Northern blotting, followed by hybridization with the indicated 32P-labeled cDNA probes. The blots are representative of three different experiments. 36B4, acidic ribosomal phosphoprotein p0; 6PGD, 6-phosphogluconate dehydrogenase; ACL, ATP citrate lyase; Ald, aldolase; G6PD, glucose-6-phosphate dehydrogenase; GK, glucokinase; L-PK, pyruvate kinase; ChREBP, carbohydrate response element-binding protein; HMGCoA Syn, 3-hydroxy-3-methylglutaryl CoA synthase. FIG. 5. Time-course changes of various mRNA levels in livers of the control and STZ-administered mice refed with glucose (Glu), fructose (Fru), or sucrose (Suc). A: Northern blot analysis of key genes in the regulation of lipogenesis in livers of control (C) and STZ-administered (S) mice refed with glucose (Glu), fructose (Fru), or sucrose (Suc) for 6 or 12 h. B: Northern blot analysis of key genes in the regulation of glycolysis and gluconeogenesis in livers of control (C) and STZ-administered (S) mice refed with glucose (Glu), fructose (Fru), or sucrose (Suc) for 6 or 12 h. C: Northern blot analysis of key genes in the regulation of insulin signaling, glucose transport, cholesterol synthesis, and 36B4 in livers of control (C) and STZ-administered (S) mice refed with glucose (Glu), fructose (Fru), or sucrose (Suc) for 6 or 12 h. D: Northern blot analysis of key genes in the regulation of glycolysis, gluconeogenesis, and SREBP-1 in livers of control (C) and STZ-administered (S) mice refed with glucose (Glu), fructose (Fru), or sucrose (Suc) for 3 h. For each experimental group, total RNA isolated from the livers of three male mice was pooled, and 10-μg aliquots were subjected to electrophoresis and Northern blotting, followed by hybridization with the indicated 32P-labeled cDNA probes. The blots are representative of three different experiments. 36B4, acidic ribosomal phosphoprotein p0; 6PGD, 6-phosphogluconate dehydrogenase; ACL, ATP citrate lyase; Ald, aldolase; G6PD, glucose-6-phosphate dehydrogenase; GK, glucokinase; L-PK, pyruvate kinase; ChREBP, carbohydrate response element-binding protein; HMGCoA Syn, 3-hydroxy-3-methylglutaryl CoA synthase. More