The mechanism by which sex steroid hormones modulate the lipolytic process in fat cells is still not completely understood, particularly at the level of the membrane. As estrogens seem to have regional influence on adipose tissue, we have compared the effects of long term ovariectomy (3 weeks) on the membranous transducing system controlling lipolysis in two rat fat deposits, the femoral sc and the parametrial adipose tissue. These experiments demonstrate the following. 1) Compared to parametrial adipocytes, sc adipocytes have a reduced cAMP production and a decreased beta-adrenoceptor number associated with a reduced lipolytic activity. 2) In parametrial adipocytes, ovariectomy induces a decrease in cAMP production and in both the beta-agonist-stimulated response and the catalytic activity of adenylate cyclase in association with a decreased lipolysis. In contrast, these parameters are unaltered by ovariectomy in sc adipocytes. This study, which reveals site-related differences in the sensitivity of the fat cell adenylate cyclase system to ovarian status, suggests that these differences may explain some of the sex-related regional specificities of adipose tissue metabolism and distribution.
In the rat, castration induces a decreased weight of fat depots. One possible explanation for these alterations could be that the capacities of preadipocytes to proliferate and differentiate are reduced by castration. Considering the regional specification of adipose tissue metabolism, these capacities and their eventual modulation by the androgenic status were presently compared in cultured preadipocytes from rat subcutaneous (SC) and epididymal fat depots.In epididymal preadipocytes, castration induced an increase in their proliferative capacity and conversely, a decrease in their adipogenesis.In vivo treatment by testosterone reversed the proliferative alteration but not the defective adipogenesis caused by castration.In vitro, no direct effect of testosterone on the proliferative capacities of epididymal preadipocytes could be observed suggesting that testosterone acts indirectly or needs the presence of other cofactors, such as insulin, dexamethasone and growth hormone. Surprisingly, testosterone partly counteracted the inhibitory effect of growth hormone on preadipocyte differentiation.In contrast to these observations, SC preadipocytes were completely insensitive to the androgenic status in terms of proliferation and differentiation.This study showing site-specific effects of castration on preadipocyte proliferation and differentiation suggests that part of the decreased fatness induced by castration in the rat is related to the modulatory effect of androgenic status on adipogenesis in some deep fat depots.
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