Role of glucose-6-phosphate and xylulose-5-phosphate in the regulation of glucose-stimulated gene expression in the pancreatic β cell line, INS-1E

Iizuka, Katsumi; Wu, Wudelehu; Horikawa, Yukio; Takeda, Jun

doi:10.1507/endocrj.ej12-0413

Cited by 30 publications

(45 citation statements)

References 38 publications

(69 reference statements)

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“…It may be speculated, in light of previous findings and the present findings, that two or more pathways lead to the activation of ChoRE, resulting in changes of variable relative magnitude in the mRNA expression of distinct glucose-responsive genes in the same or different cell types. In a recent study (26), it was proposed that, even in the case of glucose-induced gene expression, further investigation is required to understand the involvement of distinct potential mediators in pancreatic insulin-producing cells, as well as in rat primary hepatocytes.…”

Section: Discussionmentioning

confidence: 99%

D-glucose- and 3-O-methyl-D-glucose-induced upregulation of selected genes in rat hepatocytes and INS1E cells: Re-evaluation of the possible role of hexose phosphorylation

Svoboda

Tastenoy

Zhang

et al. 2013

Molecular Medicine Reports

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Abstract. The biochemical events involved in the upregulation of selected glucose-responsive genes by 3-O-methyl-D-glucose (3-MG) remain to be elucidated. The present study mainly aimed to re-evaluate the possible role of 3-MG phosphorylation in the upregulation of the thioredoxin interacting protein (TXNIP) and liver pyruvate kinase (LPK) genes in rat hepatocytes and INS1E cells. 3 H] glucose by intact INS1E cells was also measured. In rat hepatocytes, a rise in the D-glucose concentration increased the TXNIP/hypoxanthine-guanine phosphoribosyl transferase (HPRT) and LPK/HPRT ratios, while 2-DG and 3-MG also increased the TXNIP/HPRT ratio, but not the LPK/HPRT ratio. In INS1E cells, the TXNIP/HPRT and LPK/HPRT ratios were increased in response to the addition of D-glucose, 2-DG and 3-MG. Furthermore, D-mannoheptulose abolished the response to D-glucose and 2-DG, but not to 3-MG, in these cells. Liver cell homogenates catalyzed the phosphorylation of 3-MG to a modest extent, whilst INS1E and rat pancreatic islet cell homogenates did not. Moreover, 3-MG marginally decreased D-glucose phosphorylation in INS1E cell homogenates but not in liver cell homogenates. D- [5-3 H]glucose utilization by intact INS1E cells was decreased by 2-DG, but not by 3-MG. These findings reinforce the view that the upregulation of the TXNIP and LPK genes induced by 3-MG is not attributable to its phosphorylation or any favorable effect on D-glucose metabolism.

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Section: Discussionmentioning

confidence: 99%

D-glucose- and 3-O-methyl-D-glucose-induced upregulation of selected genes in rat hepatocytes and INS1E cells: Re-evaluation of the possible role of hexose phosphorylation

Svoboda

Tastenoy

Zhang

et al. 2013

Molecular Medicine Reports

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“…As mentioned above, ChREBP has two isoforms, ChREBP-α and -β [25,39]. Previously, we reported that overexpression of dominant negative Mlx (dnMlx), a ChREBP antagonist, inhibits glucose induction of Chrebp mRNA expression in rat primary hepatocytes [12].…”

Section: Chrebp Isoforms Chrebp-α and -βmentioning

confidence: 95%

“…In addition, in rat primary hepatocytes, glucose increases the mRNA levels of Chrebp and transketolase (Tkt), which catalyzes the production of X5P, a candidate activator of ChREBP (Fig. 3) [39]. We hypothesized that there is a feedforward mechanism ChREBP transactivity, and gene ablation of FoxO1 increases ChREBP transactivity through enhanced O-glycosylation and increased ChREBP protein levels [33].…”

Section: Chrebp Isoforms Chrebp-α and -βmentioning

confidence: 99%

“…3). X5P is an intermediate molecule in the pentose phosphate pathway [12,23,39]. Transketolase (TKT) is the enzyme that produces X5P from two glycolytic intermediates, glyceraldehyde 3-P (GAP) and fructose-6-P (F6P) (GAP + F6P ↔ X5P + erythrose 4-P).…”

Section: Pedersen Et Al Identified That the Chore In The Ratmentioning

confidence: 99%

“…Moreover, Chrebpa mRNA is regulated by insulin, LXR, and thyroid hormone, but not glucose [40][41][42]. Recently, it has been reported that ChREBP-β, a novel isoform of ChREBP, is increased by glucose in a dose-dependent manner, while Chrebpa mRNA expression is not affected by glucose [25,39], and that Chrebpa and Chrebpb mRNA are regulated by two different promoters [25]. Moreover, ChoRE of ChREBP-β was found to be located near exon1b in the ChREBP target genes [25].…”

Section: Feedback Control (Crosstalk Between Chrebp and Its Target Gementioning

confidence: 99%

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Recent progress on the role of ChREBP in glucose and lipid metabolism [Review]

Iizuka

2013

Endocr J

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Abstract. Carbohydrate response element binding protein (ChREBP) is a transcription factor activated by glucose that is highly expressed in liver, pancreatic β-cells, brown and white adipose tissues, and muscle. We reported that hepatic suppression of the Chrebp gene improves hepatic steatosis, glucose intolerance, and obesity in genetically obese mice. Moreover, we have studied the role of ChREBP with special reference to feedforward and feedback looping in liver and pancreatic β-cells. Recently, several groups reported that (1) glucose activates ChREBP-α transactivity and in turn ChREBP-α induces ChREBP-β on both transcriptional and translational levels in adipose tissues, and (2) ChREBP regulates glucose transporter type 4 mRNA levels, which may affect glucose uptake in adipose tissues. Moreover, in adipose tissues of obese patients, Chrebpb mRNA levels were much lower than those in lean subjects, while the levels were much higher in liver of obese patients than those in lean subjects. These findings suggest that Chrebpb mRNA levels are different in various tissues and probably in the stages of diabetes mellitus. Herein, we review recent progress in the study of ChREBP with special references to (1) the mechanisms regulating ChREBP transactivity (posttranslational modifications, intramolecular glucose sensing module, feedforward mechanism, and the feedback loop between ChREBP and its target genes), and (2) the role of ChREBP in liver, pancreatic islets and adipose tissues. Understanding the role of ChREBP in each tissue will provide important insight into the pathogenesis of metabolic syndrome.

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The Role of Carbohydrate Response Element–Binding Protein in the Development of Liver Diseases

Iizuka

2019

Dietary Interventions in Liver Disease

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Role of glucose-6-phosphate and xylulose-5-phosphate in the regulation of glucose-stimulated gene expression in the pancreatic β cell line, INS-1E

Cited by 30 publications

References 38 publications

D-glucose- and 3-O-methyl-D-glucose-induced upregulation of selected genes in rat hepatocytes and INS1E cells: Re-evaluation of the possible role of hexose phosphorylation

D-glucose- and 3-O-methyl-D-glucose-induced upregulation of selected genes in rat hepatocytes and INS1E cells: Re-evaluation of the possible role of hexose phosphorylation

Recent progress on the role of ChREBP in glucose and lipid metabolism [Review]

The Role of Carbohydrate Response Element–Binding Protein in the Development of Liver Diseases

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