Alterations of Pancreas During Cortisone Diabetes in Rabbits.

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Abstract
Intramuscular injection of cortisone acetate causes glycosuria which regresses to become reestablished if the dosage of cortisone is increased. Morphologically, the most prominent lesion observed was ductular and centroacinar proliferation and the formation of irregularly shaped and "Mulberry" islets. In addition, numerous mitotic beta cells were observed up to 10 days after starting cortisone treatment. Similarly, degranulation of the beta cells was most prominent at early stages. Glycogen infiltration seemed to appear first in the ductular tissue and required a greater degree and duration of diabetes before affecting the beta cells. Degranulation and increased mitotic activity of beta cells are thought to be a response to hyperglycemia as is the glycogen infiltration of ducts and beta cells. Proliferative activity on the other hand is considered to represent a more direct action of cortisone on the pancreas.