Glucose-stimulated Insulin Production Research Articles

Effect of progestins on glucose and lipid metabolism.

Gestamimetic amounts of progesterone enhance basal and glucose-stimulated insulin production. Contraceptive doses of synthetic progestins cause a moderate increase or no change in glucose-stimulated insulin production, depending on route of administration and species tested. Estrogens potentiate the insulinotropic effects of progesterone and the synthetic progestins. Basal serum triglyceride concentrations are generally unaffected by progesterone or 17 alpha-acetoxyprogesterone treatment but may decrease during 19-nortestosterone administration. Glucose tolerance does not change during treatment with gestamimetic doses of progesterone alone but may improve in rats and monkeys during concurrent estrogen administration. By contrast, deterioration of glucose tolerance is observed in women treated concurrently with synthetic estrogen plus 19-nortestosterone derivatives and, occasionally, with 19-nortestosterone derivatives alone. No consistent changes in glucose metabolism have been observed after treatment with 17 alpha-acetoxyprogesterone derivatives alone. The cause of the species-related differences in glucose metabolism during 19-nortestosterone treatment is obscure.

The role of human chorionic somatomammotropin (HCS) and gonadal steroids in gestational diabetes.

Maternal carbohydrate tolerance during gestation appears to be altered by at least two mechanisms: 1) decreased sensitivity of insulin-sensitive tissues to the hypoglycemic action of insulin, and 2) alterations in the sensitivity of the islets of Langerhans to the insulinogenic stimulus of glucose. The effect of physiologic amounts of unconjugated estriol and estradiol on these parameters is as yet unknown. Decreased sensitivity to insulin can be produced experimentally in female Rhesus monkeys by human chorionic somatomammotropin (HCS) and by progesterone administration. Progesterone administration enhances glucose-stimulated insulin production in both monkeys and man. By contrast, HCS administration reverses the progesterone-enhanced serum insulin response to glucose in monkeys and actually retards insulin production in response to glucose in subclinical diabetic women. The latter pattern of insulin response is similar to, but not identical with, that seen in women with gestational diabetes. Whether progesterone and/or the estrogens elaborated by the conceptus alter the effect of HCS on insulin production or sensitivity to insulin in normal or subclinical diabetic women remains to be determined.