Serum insulin and plasma glucagon in human pregnancy — On the pathogenesis of gestational diabetes. A review

Summary The possibility that the deterioration of glucose tolerance during pregnancy might be due to a change in the functional condition of the endocrine pancreas has been examined in normal pregnant women and in non-obese gestational diabetics. Three test-situations were applied to elucidate the problem: 1) an overnight fast; 2) a glucose tolerance test (OGTT); and 3) a protein-rich meal. After the overnight fast, hyperinsulinemia and hyperglucagonemia were found in late pregnancy in both groups. However, on a molar basis, basal insulin increased more than basal glucagon and the molar insulin: glucagon ratio was therefore increased. After oral administration of glucose, the insulin response was enhanced in the late stages of pregnancy both in normal women and in those with gestational diabetes while the depression of glucagon below fasting levels was exaggerated and sustained in both groups. In response to a protein-rich meal in normal late pregnancy, the glucagon response was significantly lower than post partum in the same subjects, whereas that of insulin was unchanged. Finally, in both groups the diminished glucose tolerance in pregnancy was not associated with an abnormally elevated proportion of total insulin immunoreactivity represented by the biologically almost inactive proinsulin. Based upon these findings and those reported in the literature, it is concluded that there is no evidence in support of the idea that the diabetogenicity of pregnancy can be explained by changes in the function of the endocrine pancreas in these patients.