Abstract

The hypothesis that insulin itself participates in the pathogenesis of diabetic microangiopathy was tested in alloxan diabetic male rats by giving them daily injections of a commercial protamine zinc insulin for 3 months after 9 months of untreated diabetes. Insulin doses were adjusted so that the urine volumes and glucosuria were kept at low levels. When compared with untreated alloxan diabetic rats of the same diabetes duration (12 months), the insulin treated animals showed a significantly decreased incidence and quantity of mesangial IgG. There was also a tendency to less glomerular basement membrane thickness and mesangial area in the treated rats, but the differences between the two groups were not significant. The glomeruli of nondiabetic insulin treated animals did not differ from those of untreated controls. These results do not support the assumption that the presence of insulin contributes to the pathogenesis of diabetic glomerulosclerosis. The findings favour the concept that glomerular disease in diabetes is the result of insulin deficiency. Furthermore, deposition of glomerular IgG in alloxan diabetic rats is evidently a reversible phenomenon.

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