Inbred Lewis rats were made diabetic by streptozotocin. Six to 10 mth after the induction of diabetes, each rat underwent a renal biopsy and received an intraperitoneal transplat of isologous neonatal pancreatic islet tissue. Serial blood glucose determinations were performed to confirm amelioration of the diabetes. In 7 rats, renal biopsy specimens were obtained weekly for 3 wk and then every other week for up to 9 wk following islet transplantation. Biopsies were also done on age matched normal control and untreated diabetic animals. All biopsy specimens were examined by light microscopy and by immunofluorescent microscopy with staining for IgG, IgM, and B1C. The glomerular lesions secondary to diabetes mellitus in the rat can be arrested or reversed when a return to the normal metabolic state is effected by pancreatic islet transplantation. Most likely, glomerular mesangial function is deranged when exposed to the diabetic milieu, and macromolecules, which are normally cleared in the mesangium, and accumulate in noxious quantities. Cure of the diabetic condition restores normal mesangial function. Human and rat diabetic glomerular lesions are similar. These observations provide a rational basis for attempting to halt the progression of diabetic lesions in man by pancreas or islet transplantation.
|Original language||English (US)|
|Number of pages||3|
|State||Published - 1974|