Effect of estradiol-17 beta on glucose and proline uptake in plasma membrane vesicles from the R3230AC rat mammary carcinoma.

Purified plasma membrane vesicles isolated from R3230AC rat mammary tumors displayed carrier-mediated and stereospecific uptake. Uptake was shown to be proportional to protein concentration, sensitive to increasing osmolarity, and inhibited only by substrates entering by the same carrier. Carrier-mediated glucose uptake was inhibited rapidly by estradiol-17 beta and phloretin in a dose-dependent manner, whereas proline uptake was not affected by estradiol-17 beta. The data suggest that the inhibition of glucose by estradiol and phloretin, originally observed in whole cells, occurs by an interaction of the steroid with a component on the plasma membrane. In contrast, the lack of effects of estradiol on proline transport into vesicles implies that intracellular components may have mediated the estrogen-induced effects observed in whole cells.