Sexual dimorphism and regulation of resistin, adiponectin, and leptin expression in the mouse.
OBJECTIVE: To examine gender differences and hormonal regulation of resistin, adiponectin, and leptin. RESEARCH METHODS AND PROCEDURES: Plasma levels were measured, and mRNA expression in perigonadal fat was quantified by RNase protection assays. RESULTS: Plasma resistin declined with age despite an increase in adiposity in both genders. In male mice, plasma leptin increased, whereas adiponectin levels were constant. In females, both adiponectin and leptin levels increased with age. Resistin mRNA levels were significantly higher in female than male mice at all ages, whereas leptin and adiponectin mRNA levels were similar in fat from 6-week-old male and female mice, and sexual dimorphism was apparent only in the older mice, with higher levels apparent in females. Castration did not abolish gender differences in plasma levels or resistin, adiponectin, or leptin mRNAs. Castration of male mice did not significantly change adipokine mRNA levels or plasma levels of resistin or leptin; however, adiponectin was significantly increased. Dihydrotestosterone treatment had no effect on adipokine mRNA expression or resistin and adiponectin levels but increased leptin levels. In contrast, ovariectomy significantly increased resistin mRNA abundance and decreased leptin and adiponectin mRNAs. Plasma leptin levels were also increased by ovariectomy, whereas resistin and adiponectin levels were unchanged. Estrogen replacement significantly reduced resistin mRNA and increased leptin and adiponectin mRNA levels but had no effect on plasma adipokine levels. DISCUSSION: The gender differences in adipokine mRNA expression and plasma levels were not ablated by castration and seem to be dependent on other factors in addition to gonadal steroids.[1]References
- Sexual dimorphism and regulation of resistin, adiponectin, and leptin expression in the mouse. Gui, Y., Silha, J.V., Murphy, L.J. Obes. Res. (2004) [Pubmed]
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