This Article Order Full text via Infotrieve Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Mandel, T. E. Articles by Carter, W. M. Search for Related Content PubMed PubMed Citation Articles by Mandel, T. E. Articles by Carter, W. M.

American Journal of Pathology, Vol 104, 227-236, Copyright © 1981 by American Society for Investigative Pathology

REGULAR ARTICLES

Long-term isografts of cultured fetal mouse pancreatic islets. The oncogenic effects of streptozotocin and the prevention of diabetic renal complications

TE Mandel, L Hoffman and WM Carter

Female CBA mice made diabetic with a single intravenous dose of streptozotocin (STZ) were either grafted with cultured fetal mouse pancreatic islets onto the splenic capsule, treated with insulin, or left untreated. An age- and sex-matched group of nondiabetic mice served as normal controls. All islets-grafted and most insulin-treated mice survived and had normal fasting blood glucose levels. By contrast, of the untreated diabetic mice, one died and the survivors showed poor weight gain. Light-microscopic examination of the islet isografts showed a progressive increase in graft size and beta-cell granulation over the 9-month study period. Quantitative electron-microscopic examination of the kidney showed that, whereas the islet-grafted and nondiabetic control mice had similar glomerular capillary basement membrane (GCBM) thickness, the untreated diabetic and insulin-treated mice had markedly thickened GCBM. All STZ-treated mice develop diffuse hepatic dysplasia and, at later time points, some showed biliary hyperplasia, intrahepatic cysts, and occasionally nodular dysplasia. With increasing time after STZ, most mice developed renal adenomas. One untreated diabetic mouse also developed a solitary functional pancreatic beta-cell adenoma. STZ effects were not affected by treatment of diabetes.