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Originally published In Press as doi:10.1074/jbc.M004388200 on June 13, 2000

J. Biol. Chem., Vol. 275, Issue 35, 27117-27122, September 1, 2000
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Regulation of the Liver Fatty Acid-binding Protein Gene by Hepatocyte Nuclear Factor 1alpha (HNF1alpha )
ALTERATIONS IN FATTY ACID HOMEOSTASIS IN HNF1alpha -DEFICIENT MICE*

Taro E. AkiyamaDagger , Jerrold M. Ward§, and Frank J. GonzalezDagger

From the Dagger  Laboratory of Metabolism, National Institutes of Health, Bethesda, Maryland 20892 and the § Veterinary and Tumor Pathology Section, Office of Laboratory Animal Science, NCI-Frederick Cancer Research and Development Center, National Institutes of Health, Frederick, Maryland 21702

Hepatocyte nuclear factor 1alpha (HNF1alpha )-null mice have enlarged fatty livers and alterations in the expression of genes encoding enzymes involved in the synthesis, catabolism, and transport of fatty acids. Elevations in the expression of genes encoding fatty acid synthetic enzymes (fatty acid synthase and acyl-CoA carboxylase) and peroxisomal beta -oxidation enzymes (CYP4A3, bifunctional enzyme, and thiolase) were observed in the livers of HNF1alpha -null mice, whereas hepatic mitochondrial beta -oxidation gene (medium and short chain acyl-CoA dehydrogenase) expression levels remain unchanged relative to HNF1alpha -heterozygous controls. An elevation in the levels of fatty acid transporter gene expression was also observed. In contrast, there was a marked reduction of liver fatty acid-binding protein (L-FABP) gene expression in the livers of HNF1alpha -null mice. Isolation and sequence analysis of the 5'-flanking region of the mouse L-FABP gene revealed the presence of two HNF1alpha regulatory elements. The results of transient transfection studies indicate that HNF1alpha is required to trans-activate the expression of the L-FABP promoter. Taken together, these data define a critical role for HNF1alpha in the pathogenesis of a phenotype marked by fatty infiltration of the liver and in the regulation of the L-FABP gene, the expression of which may have a direct impact on the maintenance of fatty acid homeostasis.

* 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: Laboratory of Metabolism, National Institutes of Health, 9000 Rockville Pike, Bethesda, MD 20892. Tel.: 301-496-9067; Fax: 301-496-8419; E-mail: fjgonz@helix.nih.gov.

Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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