Changes in the rate of carrier-mediated glucose transport by mouse mammary epithelial cells during ontogeny: hormone dependence delineated in vitro.

Abstract

Epithelial cells were isolated from mammary glands of mice in various physiological states, and the rate of carrier-mediated glucose transport was determined with 3-O-methylglucose. The basal rate (in the absence of exogenous insulin) increases about 40-fold as the animal of origin progresses from the virgin to the midlactating state and declines precipitously during involution. Insulin does not acutely stimulate carrier-mediated transport by cells isolated from virgin or lactating mice and evokes only about a 50% enhancement of this transport rate in the cells derived from pregnant and early postlactational animals. However, culture of mammary explants from pregnant mice in the presence of insulin, cortisol, and PRL before isolation of the epithelial cells results in a 400% increase in the basal rate of carrier-mediated glucose transport in the absence of exogenous hormones; this effect requires 3 days of incubation. The enhanced rate is equivalent to that in cells freshly isolated from animals in early lactation. Insulin-like growth factor I can mimic the chronic effect of insulin, but multiplication-stimulating activity, epidermal growth factor, and 20% fetal calf serum do not supplant insulin in this system. The maximum velocity, but not the Km, of 3-O-methylglucose transport is markedly increased during ontogeny; this is compatible with an increase in the number of functional transporters during development. The results suggest that insulin and/or insulin like growth factor I are implicated in development of the high basal rate of carrier-mediated glucose transport in mammary cells from lactating mice.