title: Effect of inborn pancreatic islet deficit in the Munich Wister Frömter rat.
abstract: 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 Frömter (MWF) rat, beside a reduction in the number of nephrons, there are also alterations in the number of pancreatic islets and of β 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 β 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 β 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 β cell mass of about 60% is responsible for altered glucose metabolism and could favor the development of diabetes.
authors.affiliation: Department of Biomedical Engineering, Mario Negri Institute for Pharmacological Research, Bergamo, Italy. marina.figliuzzi@marionegri.it
authors.forename: Marina
authors.initials: M
authors.lastname: Figliuzzi
authors.forename: Barbara
authors.initials: B
authors.lastname: Bonandrini
authors.forename: Irene
authors.initials: I
authors.lastname: Cattaneo
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Remuzzi
authors.forename: Andrea
authors.initials: A
authors.lastname: Remuzzi
mesh_terms: D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D001835:Body Weight; D002452:Cell Count; D005260:Female; D005947:Glucose / Q000378:metabolism*; D018149:Glucose Intolerance / Q000209:etiology; D005951:Glucose Tolerance Test; D007328:Insulin / Q000378:metabolism; D050417:Insulin-Secreting Cells / Q000378:metabolism; D007515:Islets of Langerhans / Q000002:abnormalities*; D009929:Organ Size; D010179:Pancreas / Q000473:pathology / Q000503:physiopathology; D051381:Rats; D011919:Rats, Inbred Strains
chemical_list: D001786:Blood Glucose; D007328:Insulin; D005947:Glucose