Endocrine pancreatic function in women with gestational diabetes.
Glucose tolerance deteriorates in normal human pregnancy but 99% of all pregnant women retain normal glucose tolerance whereas the remaining 1% develop abnormal glucose tolerance and are designated gestational diabetics. The possibility that glucose tolerance deteriorates in pregnancy because of diabetes-like changes in the secretory function of the endocrine pancreas has been investigated in gestational diabetics and healthy controls. Even though the insulin responses to oral glucose and mixed meals are equally large in gestational diabetics and normal pregnant women, the insulin responses of the gestational diabetics differ in two pertinent ways from those of the normals. First, a delayed insulin response is frequently seen, and second, the insulin response per unit of glycaemic stimulus (the 'insulinogenic index') is normally significantly lower than that of the normal pregnant women. Diabetes-like changes in the secretion of glucagon are not seen in neither group. Insulin degradation is unaffected by pregnancy and the proinsulin share of the total plasma insulin immunoreactivity does not increase in pregnancy. It is therefore likely that the main reason for the diabetogenicity of pregnancy is insulin resistance. Most pregnant women are able to increase their insulin secretion and thus overcome the resistance. Some pregnant women do, however, seem to have a more limited insulin secretory capacity which eventually may lead to the development of gestational diabetes.
D001786:Blood Glucose / Q000032:analysis; D005260:Female; D005934:Glucagon / Q000097:blood; D006801:Humans; D007328:Insulin / Q000097:blood; D007515:Islets of Langerhans / Q000503:physiopathology*; D011247:Pregnancy; D011254:Pregnancy in Diabetics / Q000503:physiopathology*; D011384:Proinsulin / Q000097:blood
D001786:Blood Glucose; D007328:Insulin; D005934:Glucagon; D011384:Proinsulin