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Vol. 63, Issue 3, 722-731, March 2003
-Hydroxysteroid Dehydrogenase Type 1: A
cDNA Array Analysis
Department of Biochemistry and Molecular Biology, the University of
Louisville School of Medicine, Louisville, Kentucky
Dehydroepiandrosterone (DHEA) is a C-19 adrenal steroid precursor to
the gonadal steroids. In humans, circulating levels of DHEA, as its
sulfated conjugate, are high at puberty and throughout early adulthood
but decline with age. Dietary supplementation to maintain high levels
of DHEA purportedly has beneficial effects on cognitive memory, the
immune system, and fat and carbohydrate metabolism. In rodents, DHEA is
a peroxisome proliferator that induces genes for the classical
peroxisomal and microsomal enzymes associated with this response. These
effects are mediated through activation of peroxisome
proliferator-activated receptor 
(PPAR). However, DHEA can affect
the expression of genes independently of PPAR, including the gene
for the major inducible drug and xenobiotic metabolizing enzyme,
cytochrome P450 3A23. To elucidate the biochemistry associated with
DHEA treatment, we employed a cDNA gene expression array using liver
RNA from rats treated with DHEA or the classic peroxisome proliferator
nafenopin. Principal components analysis identified 30 to 35 genes
whose expression was affected by DHEA and/or nafenopin. Some were genes
previously identified as PPAR-responsive genes. Changes in expression
of several affected genes were verified by quantitative reverse
transcriptase-polymerase chain reaction. These included
aquaporin 3, which was induced by DHEA and to a lesser extent
nafenopin, nuclear tyrosine phosphatase, which was induced by both
agents, and 11
-hydroxysteroid dehydrogenase 1, which was decreased
by treatment with DHEA in a dose-dependent fashion. Regulation of
11-hydroxysteroid dehydrogenase 1 expression is important since the
enzyme is believed to amplify local glucocorticoid signaling, and its
repression may cause some of the metabolic effects associated with
DHEA.
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