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Clinical trials of weak androgen androstenedione (AD) administered at a high concentration, showed an increase in muscle mass in men like strong androgens testosterone (T) and dihydro- testosterone (DHT), but did not show any inhibitory effect on fat mass unlike strong androgens. This observation prompted us to check the in-vitro effect of AD on adipogenesis using mouse me- senchymal multipotent cells (C3H10T1/2), which can differentiate into both myoblasts and adi- pocytes. Results indicated that AD inhibited adipogenesis at 10 nM, 100 nM and 1 μM concentra- tions, but not at 10 μM concentration. AD did not inhibit adipogenesis at 10 μM concentration and also did not inhibitmyogenesis at 10 μM concentration. Addition of bicalutamide, an androgen re- ceptor (AR) antagonist decreased myogenesis and increased adipogenesis, indicating that the ef- fect of AD was mediated through AR. Another weak androgen dehydroepiandrosterone (DHEA) also showed the same pattern of adipogenesis in 10T1/2 cells. AD also showed a similar pattern of adipogenesis in 3T3-L1 preadipocyte cells. Thus, the in-vitro results of AD on adipogenesis corre- lated with the in-vivo results of AD on fat-mass from clinical trials and suggested a possible differ- ence in biological action between weak androgens (AD, DHEA) and strong androgens (T, DHT) on adipogenesis. Since the biological action of AD was mediated through AR, this physiological dif- ference onadipogenesis could be due to the nature (partial agonist/antagonist) of AD binding to AR.

Effect of Androstenedione on Adipogenesis in Murine C3H10T1/2 Mesenchymal Cells