Evidence that the lipolytic defect induced by estradiol-treatment in hamster adipocytes is related to an estrogen receptor-mediated defect in the adenylate cyclase catalytic subunit but not in Ns.

This study demonstrates that estradiol-treatment (10 micrograms per day x 5 days) does not impair the level of Ns, the adenylate cyclase stimulatory regulatory protein, in hamster fat cell membranes. In addition, this report shows that the defective cyclic AMP response induced in intact adipocytes by the estradiol-treatment is either unaltered by the administration of alpha-bromocriptine or abolished by tamoxifen- or 4-hydroxytamoxifen-treatment. It can thus be concluded that the reduced lipolytic response found in hamster fat cells after estradiol-treatment is related only to an estradiol-receptor-mediated defect in adenylate cyclase catalytic subunit activity which is independent from increased prolactin secretion.