ISLET IMPLANTATION INTO DIABETIC MICE WITH PANCREATIC INSULITIS

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Abstract
Repeated injections of small doses of streptozotocin (s.z.) lead to a slowly‐developing hyperglycemia with a concomitant infiltration of lymphocytes into the pancreatic islets. Similarly, intrasplenically islet‐implanted but otherwise normal mice became diabetic when given the multi‐s.z.‐treatment, suggesting that the splenic location of the islets does not protect them from the toxic effects of s.z. or immunereactions. Intrasplenic, syngeneic islet implantation normalized the elevated blood sugars of multi‐s.z: treated mice, irrespective of whether the transplantation was performed 8 or 15 days after the first injection of s.z. These findings suggest that s.z. has to be present in order to trigger the auto‐immune process of this insulitis model. In support of this suggestion, we observed that hyperglycemic, multi‐s.z.‐treated mice cured by islet implantation reverted to a hyperglycemic state when treated repeatedly with small doses of s.z., suggesting the presence of a booster‐dose phenomenon.