The adipose tissue metabolism: role of testosterone and dehydroepiandrosterone

Abstract

Testosterone (T) and dehydroepiandrosterone (DHEA) are fat-reducing hormones, even though they exert this effect by different mechanisms. In particular, T inhibits lipid uptake and lipoprotein-lipase (LDL) activity in adipocytes, and stimulates lipolysis by increasing the number of lipolytic b b-adrenergic receptors. An indirect sign of these effects is the decrease of adipocyte leptin production. Lastly, T inhibits differentiation of adipocyte precursor cells. Concerning DHEA, this hormone does not seen to have any of T effects; however, DHEA stimulates resting metabolic rate (RMR) and lipid oxidation, and enhances glucose disposal, by increasing the expression of GLUT-1 and GLUT-4 on fat cell plasma membrane. The insulin-like effect of DHEA would be associated to a decrease of plasma insulin concentrations and, thus, to an increase of the molar ratio between lipolytic hormones and insulin. Noteworthy, the fat-reducing effect of both T and DHEA seems to be more evident at the level of visceral adipose tissue. International Journal of Obesity (2000) 24, Suppl 2, S59±S63Keywords: adipose tissue; androgens; testosterone; dehydroepiandrosterone TestosteroneExperiments performed in a whole cell assay system demonstrated that mature adipocytes derived from male rat fat pad adipose precursor cells have speci®c receptors for androgens. 1 Unlike most hormones, fat cell exposure to testosterone, but not to dihydrotestosterone, induces an increase in the number of androgen receptors in a dose-dependent way. 1 This effect is mediated by protein synthesis, suggesting the formation of new receptors by testosterone. 1 Hypogonadism is associated with a signi®cant decrease of lipolytic response to catecholamines, while testosterone treatment normalizes this response and increases triglyceride turnover. 2 The lipolytic effect of testosterone is mediated by an increase in the b-adrenoceptors number, and of adenylate cyclase, protein-kinase A and hormone-sensitive lipase activity. 3 ± 6 An indirect proof of the lipolytic effect of testosterone is represented by the experimental ®nding that the treatment of male rats with an anti-androgen (cyproterone acetate) decreases the ratio between triglyceride degradation and FFA re-esteri®cation in the adipose tissue, 7 a metabolic short-circuit producing heat and, possibly, regulating body weight. In particular, cyproterone acetate administration induces a decrease of catecholamine-stimulated lipolysis, but it does not modify the activity of the fatty acidesterifying enzymes. 7 It is interesting to note that the density of abdominal subcutaneous adipocyte a 2 -adrenoceptors is higher in men than in women: 8 therefore, although the main effect of androgens is lipolytic, these hormones may also increase the number of antilipolytic adrenergic receptors. This hypothesis is con®rmed by experiments performed on adipose tissue obtained from male hamsters. 9 Lipoprotein lipase (LPL) supplies the adipocytes with free fatty acids for intracellular esteri®cation by hydrolyzing triglyceride-rich l...

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