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Originally published In Press as doi:10.1074/jbc.M101764200 on July 31, 2001

J. Biol. Chem., Vol. 276, Issue 43, 39522-39532, October 26, 2001
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Characterization of the Rodent Genes for Arylacetamide Deacetylase, a Putative Microsomal Lipase, and Evidence for Transcriptional Regulation*,

Jeffrey I. TrickettDagger §, Dilip D. Patel||**, Brian L. Knight||**, E. David SaggersonDagger , Geoffrey F. Gibbons**Dagger Dagger , and Richard J. PeaseDagger §§

From the Dagger  Department of Biochemistry and Molecular Biology, University College London, Gower Street, London WC1E 6BT, || Lipoprotein Group, Medical Research Council Clinical Sciences Center, Hammersmith Hospital, Ducane Road, London W12 ONN, and Dagger Dagger  Metabolic Research Laboratory, Nuffield Department of Clinical Medicine, Radcliffe Infirmary, Woodstock Road, Oxford OX2 6HE, United Kingdom

In the current study, we have determined the cDNA and the genomic sequences of the arylacetamide deacetylase (AADA) gene in mice and rats. The AADA genes in the rat and mouse consist of five exons and have 2.4 kilobases of homologous promoter sequence upstream of the initiating ATG codon. AADA mRNA is expressed in hepatocytes, intestinal mucosal cells (probably enterocytes), the pancreas and also the adrenal gland. In mice, there is a diurnal rhythm in hepatic AADA mRNA concentration, with a maximum 10 h into the light (post-absorptive) phase. This diurnal regulation is attenuated in peroxisome proliferator-activated receptor alpha  knockout mice. Intestinal but not hepatic AADA mRNA was increased following oral administration of the fibrate, Wy-14,643. The homology of AADA with hormone-sensitive lipase and the tissue distribution of AADA are consistent with the view that AADA plays a role in promoting the mobilization of lipids from intracellular stores and in the liver for assembling VLDL. This hypothesis is supported by parallel changes in AADA gene expression in animals with insulin-deficient diabetes and following treatment with orotic acid.

* 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.

The on-line version of this article (available at http://www.jbc.org) contains the complete promoter sequence in Fig. 4S.

The nucleotide sequence(s) reported in this paper has been submitted to the GenBankTM/EMBL Data Bank with accession number(s) AF182426 (rat cDNA), AF264017 (rat genomic DNA), and AF306788 (mouse genomic DNA).

§ Supported by a British Heart Foundation research studentship.

Each of these authors made a similar contribution to this work.

** Supported by the Medical Research Council, UK.

§§ Supported by a British Heart Intermediate Research Fellowship and a Wellcome Trust project grant. To whom correspondence should be addressed. Tel.: 44-207-679-2185; Fax: 44-207-679-7193.

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