Regression of glycogen nephrosis in experimental diabetes after pancreatic islet transplantation.
Glycogen nephrosis, i.e. the Armanni-Ebstein lesion which manifests itself by intracellular accumulation of beta-glycogen has been studied in two groups of streptozotocin diabetic rats and compared to controls. One diabetic group was left untreated and the other diabetic group received pancreatic islet transplantation after 4 weeks duration of diabetes. The kidneys were studied after another 4 week period with normoglycemia. In the non-transplanted diabetic animals glycogen containing tubules comprised 43% of the distal tubule length in the cortex but in the transplanted animals no abnormal, glycogen containing cells could be recovered at the light microscope level. Measurements of the total distal tubule length in the non-transplanted diabetic animals showed that the distal tubules increased in length by 24%. In the transplanted diabetic animals distal tubule length remained the same as in the non-transplanted diabetic animals in spite of normalization of the tubular morphology. This finding could possibly be responsible for the incomplete normalization of kidney weight after treatment.
D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D001835:Body Weight; D003921:Diabetes Mellitus, Experimental / Q000150:complications* / Q000601:surgery; D005260:Female; D006003:Glycogen / Q000378:metabolism; D016381:Islets of Langerhans Transplantation; D007668:Kidney / Q000473:pathology*; D007684:Kidney Tubules / Q000473:pathology; D009401:Nephrosis / Q000209:etiology / Q000473:pathology / Q000628:therapy*; D009929:Organ Size; D051381:Rats; D011917:Rats, Inbred Lew
D001786:Blood Glucose; D006003:Glycogen