Abstract

The effect of streptozotocin-induced diabetes (100mg/kg) on lactogenic binding sites, measured by iodinated ovine prolactin (PRL) binding, has been studied in liver microsomal membranes from male and female rats. In females, specific binding was reduced in diabetes from 13% to 4.5% of total tracer, while in males specific binding increased from 0.5% to 2.5%. Similar results were obtained using iodinated human growth hormone as tracer, though overall binding was higher. Scatchard plots of binding curves in females showed that changes in binding were due to changes in receptor concentration, while affinity remained unchanged at 2 × 10 9 M −1. In diabetes, serum PRL and estradiol levels fell by 60% in males but showed no significant change in females, and could therefore not account for receptor changes. In contrast, mean testosterone levels fell in diabetic males from 9.0 to 3.9 nM, and rose in diabetic females from 2.1 to 5.8 nM. Estrogen treatment of male rats caused a marked induction of binding in nondiabetic animals, and a change from the male to the female response to diabetes. Testosterone treatment of nondiabetic females suppressed binding, although not to male levels, and diabetes caused further suppression. These results are consistent with a role for testosterone in regulating PRL receptors in experimental diabetes, but suggest that other hormonal influences are also involved.

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