Evidence for a regional-specific control of rat preadipocyte proliferation and differentiation by the androgenic status.

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.