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 beta-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.