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Diabetes 51:2536-2545, 2002
© 2002 by the American Diabetes Association, Inc.

Stimulation of Acetyl-CoA Carboxylase Gene Expression by Glucose Requires Insulin Release and Sterol Regulatory Element Binding Protein 1c in Pancreatic MIN6 ß-Cells

Chrysovalantis Andreolas1, Gabriela da Silva Xavier1, Frederique Diraison1, Chao Zhao1, Aniko Varadi1, Fernando Lopez-Casillas2, Pascal Ferré3, Fabienne Foufelle3, and Guy A. Rutter1

1 Department of Biochemistry, University of Bristol, Bristol, U.K.
2 Instituto de Fisiologia Celular, Universidad Nacional Autonoma de Mexico, Mexico City, Mexico
3 Unit 465 INSERM, Centre Biomedical des Cordeliers, Paris, France

Acetyl-CoA carboxylase I (ACCI) is a key lipogenic enzyme whose induction in islet ß-cells may contribute to glucolipotoxicity. Here, we provide evidence that enhanced insulin release plays an important role in the activation of this gene by glucose. Glucose (30 vs. 3 mmol/l) increased ACCI mRNA levels ~4-fold and stimulated ACCI (pII) promoter activity >30-fold in MIN6 cells. The latter effect was completely suppressed by blockade of insulin release or of insulin receptor signaling. However, added insulin substantially, but not completely, mimicked the effects of glucose, suggesting that intracellular metabolites of glucose may also contribute to transcriptional stimulation. Mutational analysis of the ACCI promoter, and antibody microinjection, revealed that the effect of glucose required sterol response element binding protein (SREBP)-1c. Moreover, adenoviral transduction with dominant-negative-acting SREBP1c blocked ACCI gene induction, whereas constitutively active SREBP1c increased ACCI mRNA levels. Finally, glucose also stimulated SREBP1c transcription, although this effect was independent of insulin release. These data suggest that glucose regulates ACCI gene expression in the ß-cell by complex mechanisms that may involve the covalent modification of SREBP1c. However, overexpression of SREBP1c also decreased glucose-stimulated insulin release, implicating SREBP1c induction in ß-cell lipotoxicity in some forms of type 2 diabetes.


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