PREVENTION AND REVERSAL DESPITE HYPERGLYCEMIA OF GLYCOGEN INFILTRATION (“HYDROPIC DEGENERATION”) IN THE PANCREAS IN ALLOXAN DIABETES IN THE RABBIT1

Abstract

18 rabbits, after periods of alloxan diabetes ranging from 8-48 weeks, presented in each case glycogen infiltration of the pancreatic islet, ductular and centro-acinar cells (i.e., what has previously been described as "hydropic degeneration" of these cells). Treatment of some of these alloxan-diabetic rabbits with large doses of insulin for periods of about 30 days restored normal structural appearance to the pancreatic islet, ductule and centro-acinar cells that had previously become infiltrated with glycogen. The restored islet cells had the cytological characteristics of beta type cells. Upon cessation of therapy, symptoms of diabetes reappeared rapidly and glycogen infiltration developed again in the pancreas. Treatment of other alloxan-diabetic rabbits with small doses of insulin for periods of several weeks restored glycogen-filled pancreatic cells to normal appearance; this result was attained despite the continuous persistence of marked hyperglycemia during therapy. Treatment of alloxan-diabetic rabbits with small doses of insulin for periods of several months beginning immediately after the injn. of alloxan prevented the development of glycogen infiltration in the pancreas. Prevention was attained even though hyperglycemia of marked degree persisted continuously during treatment. When therapy was discontinued, typical lesions developed more rapidly than was the case when no insulin was given following injn. of alloxan. Accelerated development of the lesion occurred regardless of whether or not there was further elevation of the blood sugar level.