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1 Department of Medicine, Division of Renal Diseases and Hypertension, University of Colorado Health Science Center, Denver, Colorado, USA
2 Department of Medicine, Division of Renal Diseases and Hypertension, University of Colorado Health Science Center, Denver, Colorado, USA; Department of Physiology and Biophysics, Division of Renal Diseases and Hypertension, University of Colorado Health Science Center, Denver, Colorado, USA
* To whom correspondence should be addressed. E-mail: jinping.li{at}uchsc.edu.
ChREBP is a rat homologue of human WBSCR14 and, a member of basic helix-loop-helix leucine zipper (bHLHZip) transcription factor family. Its activation was later found to be inducible by carbohydrate in the nuclear extracts from rat liver fed with high-sucrose diet. ChREBP is able to bind to the carbohydrate response element on the promoter of L-type pyruvate kinase and initiate the gene transcription. The detailed expression profile and transcriptional regulation of ChREBP gene in adipocyte has not been characterized. In present study, we provide evidences showing 1) ChREBP gene is expressed in differentiated 3T3 L1 adipocyte and rat adipose tissue; 2) insulin, glucose and the anti-diabetic agent troglitazone can significantly up regulate the gene expression of ChREBP in 3T3 L1 adipocyte, while free fatty acids suppress its expression in this cell type; 3) fasting followed by refeeding with high carbohydrate diet resulted in 10 fold increase of ChREBP mRNA level in rat adipose tissue; and 4) ChREBP expression in adipose tissue is not significantly affected by diabetic state. Taken together, the results we present are consistent with the idea that ChREBP is an important modulator of adipocyte biology and its expression in adipose tissue is subject to the combined regulation by glucose and insulin in vivo. The induction of ChREBP may serve as a novel pharmacological pathway for troglitazone-mediated hypoglycemic effects in vivo.
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