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J. Biol. Chem., Vol. 281, Issue 42, 31268-31278, October 20, 2006

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Transcriptional Regulation of the Glucose-6-phosphatase Gene by cAMP/Vasoactive Intestinal Peptide in the Intestine

ROLE OF HNF4, CREM, HNF1, and C/EBP^*

Amandine Gautier-Stein^¶||1, Carine Zitoun^¶||, Enzo Lalli^**, Gilles Mithieux^¶||, and Fabienne Rajas^¶||

From the INSERM, U.449, F-69372 Lyon, France, INRA, U1235, F-69372 Lyon, France, ^¶Université Lyon 1, F-69372 Lyon, France, ^||Institut Fédératif de Recherche Laennec 62, F-69372 Lyon, France, and ^**Institut de Pharmacologie Moléculaire et Cellulaire CNRS, UMR 6097, F-06560 Valbonne Sophia-Antipolis, France

Gluconeogenesis is induced in both the liver and intestine by increased cAMP levels. However, hepatic and intestinal glucose production can have opposite effects on glucose homeostasis. Glucose release into the portal vein by the intestine increases glucose uptake and reduces food intake. In contrast, glucose production by the liver contributes to hyperglycemia in type II diabetes. Glucose-6-phosphatase (Glc6Pase) is the key enzyme of gluconeogenesis in both the liver and intestine. Here we specify the cAMP/protein kinase A regulation of the Glc6Pase gene in the intestine compared with the liver. Similarly to the liver, the molecular mechanism of cAMP/protein kinase A regulation involves cAMP-response element-binding protein, HNF4, CAAT/enhancer-binding protein, and HNF1. In contrast to the situation in the liver, we find that different isoforms of CAAT/enhancer-binding protein and HNF1 contribute to the specific regulation of the Glc6Pase gene in the intestine. Moreover, we show that cAMP-response element binding modulator specifically contributes to the regulation of the Glc6Pase gene in the intestine but not in the liver. These results allow us to identify intestine-specific regulators of the Glc6Pase gene and to improve the understanding of the differences in the regulation of gluconeogenesis in the intestine compared with the liver.

Received for publication, April 5, 2006 , and in revised form, July 11, 2006.

^* The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ Recipient of a grant from Nestlé. To whom correspondence and reprint requests should be addressed: INSERM U.449-Faculté deMédecine Laennec, Rue Guillaume Paradin-69372 Lyon cedex 08 France. Tel.: 33-478-77-86-29; Fax: 33-478-77-87-62; E-mail: Amandine.Gautier{at}univ-lyon1.fr.

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