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This version published online on December 18, 2003
Endocrinology, doi:10.1210/en.2003-0874
A more recent version of this article appeared on April 1, 2004
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Submitted on July 14, 2003
Accepted on December 9, 2003

Female-predominant expression of fatty acid translocase/CD36 in rat and human liver

Nina Ståhlberg1*, Elizabeth Rico-Bautista1, Rachel M Fisher1, Xuxia Wu1, Louisa Cheung1, Amilcar Flores-Morales1, Gunnel Tybring1, Gunnar Norstedt1, and Petra Tollet-Egnell1

1 Karolinska Institutet, Department of Molecular Medicine, Karolinska Hospital, SE-171 76 Stockholm; Karolinska Institutet, Atherosclerosis Research Unit, King Gustaf V Research Institute, Karolinska Hospital, SE-171 76 Stockholm; Karolinska Institutet, Department of Laboratory Medicine, Division of Clinical Pharmacology, Huddinge University Hospital, SE-141 86 Stockholm

* To whom correspondence should be addressed. 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 growth hormone (GH). Effects of gender and continuous infusion of GH to male rats were studied in the liver using cDNA microarrays representing 3200 genes. 69 transcripts displayed higher expression levels in females and 177 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 FAT/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 FAT/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.
Key words: Sex-differentiation • gene expression • fuel metabolism • fatty acid translocase/CD36 • liver




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