DISSOCIATION OF GLUCOCORTICOID INHIBITION OF GLUCOSE-TRANSPORT AND METABOLISM BY INCREASE IN ADIPOCYTE AGE AND-OR SIZE

The hypothesis that 17β-estradiol suppresses dopamine secretion into hypophysial portal blood was tested. Portal plasma concentrations of dopamine were significantly lower in proestrous rats (1.0 ± 0.1 ng/ml; mean ± SE) than in estrous rats (1.9 ± 0.38 ng/ml). To deplete the animal of endogenous steroid hormones, proestrous rats were adrenalectomized (Adx) and ovariectomized (Ovx). Twenty-four hours later, hypophysial portal blood was collected for 60 min, and the plasma from this blood was analyzed for dopamine. Arterial plasma from these rats was assayed for 17β-estradiol and progesterone. The concentrations of dopamine in the portal plasma of sham-operated rats and bilaterally Adx-Ovx rats were similar to those in estrous animals. The concentration of dopamine in portal plasma of Adx-Ovx rats injected 24 h earlier with 50 μg 17β-estradiol was 1.0 ± 0.31 ng/ml, which was comparabExposure of adipocytes from young rats (2–3 months old) to dexamethasone in vitro results in 40–50% inhibition of glucose transport and metabolism. Comparable experiments with older rats reveal that the hormonal effect on glucose metabolism is progressively reduced to about 20% in 12- to 13- month-old animals and about 5% in 24- to 26-month-old animals. However, no effect of dexamethasone on the glucose transport system can be detected in either of the older age groups when three different sugars are used to measure transport activity. The ability of dexamethasone to inhibit glucose phosphorylation seems to be closely related to inhibition of overall glucose oxidation in both young and old adipocytes. That the membrane may be generally more resistant to control of glucose transport is suggested by failure or reduced ability of insulin, vitamin K5, and hydrogen peroxide to stimulate this function in older cells. © 1979 by The Endocrine Society.