Diabetes in pregnancy: growth of the fetal pancreatic B cells in the rat.

The development of the pancreatic B cells in the offspring of normal (N), subdiabetic (SD), manifest diabetic (MD) and insulin-treated diabetic (MDI) rats was studied with the aid of immunocytochemical staining for insulin. Morphometric evaluation of the B-cell volume density and weight was made by point sampling. The offspring were studied on gestational days 20 and 22 and in the newborn state. In the N offspring the weight of the B-cell parenchyma doubled during the last 2 days of gestation. This rapid increase may be ascribed not only to high mitotic activity but also to differentiation of putative percursor cells to B cells. The mild glucose intolerance of the SD mothers had no major effects on the fetal B-cell development. In the MD group both the volume density and the weight of the B cells were considerably lower than in the N and SD groups at all ages studied. Despite prolonged gestation, the weight of the fetal B cells in the MD newborns was not greater than that in the 20-day-old fetuses of the N group. Insulin treatment of the MD mothers restored the fetal B-cell development towards normal. This study indicates that manifest maternal diabetes in the rat retards the development of the fetal B cells. This is in obvious contrast to the corresponding situation in human diabetic pregnancy, in which hyperinsulinism represents a striking feature of diabetic fetopathy. It is suggested that a milder form of maternal glucose intolerance together with the relatively longer gestational period in man, compared with the rat, may create conditions that favour fetal B-cell hyperplasia.