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The effect of dehydroepiandrosterone on lipogenic gene mRNA expression in cultured primary chicken hepatocytes
Author(s) -
Tang Xue,
Ma Haitian,
Huang Guoqing,
Miao Jinfeng,
Zou Sixiang
Publication year - 2009
Publication title -
european journal of lipid science and technology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.614
H-Index - 94
eISSN - 1438-9312
pISSN - 1438-7697
DOI - 10.1002/ejlt.200800169
Subject(s) - dehydroepiandrosterone , carnitine , gene expression , endocrinology , medicine , biology , messenger rna , peroxisome proliferator activated receptor , peroxisome , chemistry , receptor , gene , hormone , biochemistry , androgen
The effects of dehydroepiandrosterone (DHEA) on lipogenic gene mRNA expression were examined using cultured primary chicken hepatocytes. Cell samples were equilibrated to culture conditions for 24 h and then exposed to DHEA (1, 10 and 100 µM) dissolved in DMSO. The expression of sterol regulatory element‐binding protein‐1 (SREBP‐1) mRNA in cultured primary hepatocytes did not vary with time, except for a significant decrease in gene expression when cells were treated with 10 or 100 µM DHEA for either 1 or 2 h. A similar tendency toward decreased gene expression was evident for acetyl CoA carboxylase. The expression of peroxisome proliferator‐activated receptor α (PPARα) and carnitine palmitoyl transferase I mRNA was dramatically enhanced subsequent to treatment with 10 or 100 µM DHEA for periods of time from 6 to 48 h, while there was a decrease in the expression of PPARα in the presence of 10 µM DHEA after 1 and 2 h of exposure, and in the presence of 100 µM DHEA after 2 h of exposure. Hepatocytes treated with 10 or 100 µM DHEA contained more mitochondria and mitochondria with a higher electron density than did untreated hepatocytes. Furthermore, cell survival was significantly inhibited by treatment with 100 µM DHEA at 24, 48 and 72 h. In contrast, 1 µM DHEA administration significantly increased cell survival after 72 h; however, 10 µM DHEA treatment had no pronounced effect on cell survival. Overall, the results reported here indicate that DHEA accelerates lipid catabolism by direct regulation of hepatic gene expression and by induction of changes in hepatocyte mitochondria.