Effect of inborn pancreatic islet deficit in the Munich Wister Frömter rat

The total mass of pancreatic islet cells is a critical factor in glucose metabolic control. The aim of the present study was to investigate whether in the Munich Wistar Fromter (MWF) rat, beside a reduction in the number of nephrons, there are also alterations in the number of pancreatic islets and of beta-cell mass. We also examined glucose metabolism, both in normal conditions and following intravenous glucose injection. The number of islets per pancreas, estimated by morphometrical analysis, was significantly lower in MWF rats than in Wistar rats (3,501 +/- 1,285 vs. 7,259 +/- 2,330 islet/rat, respectively). Also the mean number of islets per gram of body weight was significantly lower in MWF rats than in Wistar rats (18 +/- 7 in MWF rats vs. 28 +/- 10 islets/g bw in Wistar rats). Morphometric analysis of beta-cell mass showed an average of 77.1 +/- 7% islet cells staining for insulin in MWF rats and 83.9 +/- 2.1% in the control Wistar rats. Despite the lower number of islets and beta-cells, MWF and Wistar rats had comparable fasting blood glucose levels but significant differences in blood glucose following an intraperitoneal glucose tolerance test. In summary, pancreatic islets of MWF and Wistar rats showed a marked difference in morphometrical characteristics. While this difference is not associated with blood glucose levels, glucose metabolism after IPGTT between MWF and Wistar rats is significantly different. These data suggest that an inborn deficit in beta-cell mass of about 60% is responsible for altered glucose metabolism and could favor the development of diabetes.