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Department of Molecular Medicine (N.S., E.R.-B., X.W., L.C., A.F.-M., G.N., P.T.-E.), and Atherosclerosis Research Unit, King Gustaf V Research Institute (R.M.F.), Karolinska Hospital, Karolinska Institute, SE-171 76 Stockholm, Sweden; and Department of Laboratory Medicine, Division of Clinical Pharmacology, Huddinge University Hospital, Karolinska Institute (G.T.), SE-141 86 Stockholm, Sweden
Address all correspondence and requests for reprints to: Dr. Nina Ståhlberg, Karolinska Institute, Department of Molecular Medicine, CMM L8:01, Karolinska Hospital, 171 76 Stockholm, Sweden. E-mail: nina.stahlberg{at}cmm.ki.se.
The aim of this study was to identify genes for hepatic fuel metabolism with a gender-differentiated expression and to determine which of these that might be regulated by the female-specific secretion of GH. Effects of gender and continuous infusion of GH to male rats were studied in the liver using cDNA microarrays representing 3200 genes. Sixty-nine transcripts displayed higher expression levels in females, and 177 displayed higher expression in males. The portion of GH-regulated genes was the same (30%) within the two groups of gender-specific genes. The male liver had a higher expression of genes involved in fuel metabolism, indicating that male rats might have a greater capacity for high metabolic turnover, compared with females. Most notable among the female-predominant transcripts was fatty acid translocase/CD36, with 18-fold higher mRNA levels in the female liver and 4-fold higher mRNA levels in males treated with GH, compared with untreated males. This gender-differentiated expression was confirmed at mRNA and protein levels in the rat and at the mRNA level in human livers. Although purely speculative, it is possible that higher levels of fatty acid translocase/CD36 in human female liver might contribute to the sexually dimorphic development of diseases resulting from or characterized by disturbances in lipid metabolism, such as arteriosclerosis, hyperlipidemia, and insulin resistance.
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