ChREBP: A Glucose-activated Transcription Factor Involved in the Development of Metabolic Syndrome

Iizuka, Katsumi; Horikawa, Yukio

doi:10.1507/endocrj.k07e-110

Cited by 180 publications

(130 citation statements)

References 49 publications

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“…Recently, it has been reported that glucose activates ChREBP, a carbohydrate responsive element binding protein identified as a key regulator of glucose and lipid metabolism. 33 Specifically, a diet rich in glucose has been shown to activate hepatic ChREBP in animal models leading to an increased expression of enzymes involved in the formation of triglycerides. 34,35 In this study, we confirmed these results and showed an elevated mRNA expression of ChREBP associated with increased levels of FAS and triglycerides in the liver of mice fed a 30% glucose solution.…”

Section: Discussionmentioning

confidence: 99%

Treatment with the 5-HT3 antagonist tropisetron modulates glucose-induced obesity in mice

et al. 2009

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Objective: Sugar consumption has increased markedly over the last few decades and parallels the dramatic increase in overweight and obesity. Data obtained from animal studies suggest that the intestinal serotonergic system and herein particularly the serotonin receptor 3 (5-HT3R) may be involved in sugar detection and short-term control of food intake. Using a mouse model, we tested the hypothesis that blocking 5-HT3R prevents the development of sugar-induced obesity. Design: For 8 weeks, C57BL/J6 mice were offered either water containing 30% glucose or plain water in addition to normal chow. The effect of oral treatment with the 5-HT3R antagonist, tropisetron (0.2 mg kg À1 body weight), on body weight and caloric intake was studied. Results: Total caloric intake and weight gain were significantly increased in mice fed glucose compared with the control group. Tropisetron treatment reduced intestinal motility and almost completely blocked weight gain associated with glucose feeding; however, total caloric intake was not affected. The effect of tropisetron was not associated with a decreased expression of the intestinal and hepatic glucose transporters, SGLT1 (sodium-dependent glucose cotransporter) and Glut2 (glucose transporter 2); instead, the expression of these transporters was slightly increased by the 5-HT3R antagonist. However, expressions of carbohydrate responsive element binding protein and fatty acid synthase, as well as triglyceride levels in the liver were only enhanced in mice fed glucose, but remained unchanged at the level of the control group when mice were treated concomitantly with tropisetron. At the same time, b-hydroxybutyrate dehydrogenase mRNA expression and plasma levels of ketone bodies were significantly increased. Conclusion: Our results suggest that 5-HT3R is a new target for the modulation of hepatic glucose metabolism and for the prevention of obesity.

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Section: Discussionmentioning

confidence: 99%

Treatment with the 5-HT3 antagonist tropisetron modulates glucose-induced obesity in mice

et al. 2009

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“…PKLR is a rate-limiting enzyme in the glycolytic pathway and plays an important role in the regulation of glycolysis and lipogenesis [6,7]. TXNIP has an important role in glucose toxicity in pancreatic β cells [26].…”

Section: Dg Can Induce Pklr and Txnip Mrna Expression In A Time-and mentioning

confidence: 99%

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

Horikawa

et al. 2013

Endocr J

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“…Carbohydrate response element-binding protein (ChREBP) as well as SREBP-1c plays a pivotal role in the generation of hepatic lipogenesis in response to changes in glucose in the liver [66][67][68]. We have demonstrated that ChREBP gene expression is positively regulated by thyroid hormone [69].…”

Section: Carbohydrate Response Element-binding Protein (Chrebp)mentioning

confidence: 99%

Crosstalk of thyroid hormone receptor and liver X receptor in lipid metabolism and beyond [Review]

Hashimoto

Mori

2011

Endocr J

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Abstract. Thyroid hormone receptors (TRs) and liver X receptors (LXRs) are members of the nuclear receptor superfamily. Although LXRs and TRs belong to two distinct receptor subgroups with respect to ligand-binding affinity, the two receptor systems show similarity with respect to molecular mechanism, target genes, and physiological roles. Since both TRs and LXRs play an important role in metabolic regulation, form heterodimers with retinoid X receptors (RXRs), and bind to direct repeat-4 (DR-4) with identical geometry and polarity, crosstalk between these two receptors has been reported, especially on lipid metabolism-related genes. Recently, several types of crosstalk between TRs and LXRs have been identified and crosstalk has also been observed in other physiological systems such as central nervous system rather than lipid metabolism. In this review, recent advances in elucidating the molecular mechanisms of the crosstalk between these two nuclear receptors are discussed, with the aim of finding a perspective on unknown roles of TRs and LXRs.

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ChREBP: A Glucose-activated Transcription Factor Involved in the Development of Metabolic Syndrome

Cited by 180 publications

References 49 publications

Treatment with the 5-HT3 antagonist tropisetron modulates glucose-induced obesity in mice

Treatment with the 5-HT3 antagonist tropisetron modulates glucose-induced obesity in mice

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

Crosstalk of thyroid hormone receptor and liver X receptor in lipid metabolism and beyond [Review]

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