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

Abstract

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.