Testosterone (T) and dehydroepiandrosterone (DHEA) are fat-reducing hormone
s, even though they exert this effect by different mechanisms. In particula
r, T inhibits lipid uptake and lipoprotein-lipase (LDL) activity in adipocy
tes, and stimulates lipolysis by increasing the number of lipolytic B-adren
ergic receptors. An indirect sign of these effects is the decrease of adipo
cyte leptin production. Lastly, T inhibits differentiation of adipocyte pre
cursor cells, Concerning DHEA, this hormone does not seen to have any of T
effects; however, DHEA stimulates resting metabolic rate (RMR) and lipid ox
idation, and enhances glucose disposal, by increasing the expression of GLU
T-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, th
us, to an increase of the molar ratio between lipolytic hormones and insuli
n. Noteworthy, the fat-reducing effect of both T and DHEA seems to be more
evident at the level of visceral adipose tissue.