JBC Focus on PI3-Kinase with Echelon

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Originally published In Press as doi:10.1074/jbc.M101557200 on February 28, 2001

J. Biol. Chem., Vol. 276, Issue 19, 16033-16039, May 11, 2001
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Glucose Regulation of the Acetyl-CoA Carboxylase Promoter PI in Rat Hepatocytes*

Brennon L. O'CallaghanDagger , Seung-Hoi KooDagger , Yue Wu§, Hedley C. Freake§, and Howard C. TowleDagger §

From the Dagger  Department of Biochemistry, Molecular Biology & Biophysics, University of Minnesota, Minneapolis, Minnesota 55455 and the § Department of Nutritional Sciences, University of Connecticut, Storrs, Connecticut 06269

The rat acetyl-CoA carboxylase (ACC) alpha  gene is transcribed from two promoters, denoted PI and PII, that direct regulated expression in a tissue-specific manner. Induction of ACC, the rate-controlling enzyme of fatty acid biosynthesis, occurs in the liver in response to feeding of a high carbohydrate, low fat diet, conditions that favor enhanced lipogenesis. This induction is mainly due to increases in PI promoter activity. We have used primary cultured hepatocytes from the rat to investigate glucose regulation of ACC expression. Glucose and insulin synergistically activated expression of ACC mRNAs transcribed from the PI promoter with little or no effect on PII mRNAs. Glucose treatment stimulated PI promoter activity in transfection assays and a glucose-regulated element was identified (-126/-102), homologous to those previously described in other responsive genes, including L-type pyruvate kinase, S14 and fatty acid synthase. Mutation of this element eliminated the response to glucose. This region of the ACC PI promoter was able to bind a liver nuclear factor designated ChoRF that interacts with other conserved glucose-regulated elements. This ACC PI element is also capable of conferring a strong response to glucose when linked to a heterologous promoter. We conclude that induction of ACC gene expression under lipogenic conditions in hepatocytes is mediated in part by the activation of a glucose-regulated transcription factor, ChoRF, which stimulates transcription from the PI promoter. Similar mechanisms operate on related genes permitting the coordinate induction of the lipogenic pathway.

* This work was supported by National Institutes of Health Grant DK26919 (to H. C. T.) and United States Department of Agriculture Hatch Grant CONS00665 (to H. C. F.).The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

To whom correspondence should be addressed: Dept. of Biochemistry, Molecular Biology & Biophysics, 6-155 Jackson Hall, 321 Church St. SE., Minneapolis, MN 55455. Tel.: 612-625-3662; Fax: 612-625-5476; E-mail: towle@mail.ahc.umn.edu.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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