Fetal hyperinsulinemia is assumed to play a key role in the pathogenesis of diabetic fetopathy. To investigate the role of enhanced fetal B-cell mass as one cause of fetal hyperinsulinemia during diabetic pregnancy, we studied human fetal pancreatic slices from diabetic women (FDW) with poor metabolic control and nondiabetic women (FNDW) between 11 and 26 wk of pregnancy, morphometrically and by in vitro incubation experiments. Abortions had been performed due to different medical indications. We found a good correlation between the calculated B-cell mass and the gestational age in both FDW and FNDW, but the increase in FDW was much more pronounced. Such a correlation was also found in vitro regarding the insulin response to glucose and IBMX. The FDW had significantly higher values than FNDW of the same age range. In contrast to this, we found in two diabetic patients with tight metabolic control during the whole pregnancy results similar to those in FNDW. Therefore, we assume that it could be possible to prevent fetal hyperinsulinemia and perhaps even diabetic fetopathy in diabetic women by tight metabolic control during the whole pregnancy, but further investigations are necessary.

The in vitro insulin secretion of pancreatic slices between the 11th and 15th week of pregnancy of fetuses from non diabetic ( FNDW ) and diabetic women ( FDW ) after incubation in media supplemented with different secretagogues was investigated in order to study the development of diabetic fetopathy during human pregnancy in diabetic women. There was a stimulatory effect on the insulin secretion in FNDW even if glucose alone was used, which became more pronounced if IBMX was added to the incubation medium. The insulin secretion was significantly enhanced in FDW compared to FNDW . This incubation model using fetal pancreatic slices seems to be appropriate for studying the ontogenesis of the human fetal pancreas.