LIVER CYSTS IN STREPTOZOTOCIN-TREATED RATS

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Abstract
Finch and Morris [1977] implicate intraportally transplanted islets as a cause of bile cyst formation in rats surviving for more than 1 yr after amelioration of streptozotocin-induced diabetes. The etiology of the cysts cannot be decided on the basis of their experiments, although a simple experiment, intraportal transplantation of islets to normal rats not treated with streptozotocin would provide the answer. Observations make it seem likely that streptozotocin itself, and not intraportally transplanted islet tissue, was responsible for the bile duct proliferation and cyst formation in the rats studied by Finch and Morris. Streptozotocin, a N-nitrosomethylamide, is chemically related to N-nitrosodimethylamine (dimethylnitrosamine) and other nitrosamine compounds known to cause neoplastic changes or cancer of the liver in experimental animals. Virtually every hepatocarcinogen, including nitrosamines, induces ductal proliferation in the liver early in carcinogenesis. Streptozotocin, and not intraportally transplanted islet tissue, is the cause of the liver cysts. Finch and Morris were unable to make this distinction because they used only the intraportal route for islet transplantation and their control diabetic rats survived for no longer than 5 mo. Although all efforts should be made to minimize risks, the observations of Finch and Morris should not be a deterrent to clinical islet transplant trials.