Abstract
Summary
1. Cortisone acetate administered intramuscularly to rabbits caused the gradual appearance of glycosuria which reached a maximum at the 5th to 9th days and then declined. Increased dosage reestablished the glycosuria but it again regressed. 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. 2. The degranulation and increased mitotic activity of the beta cells are thought to be a response to hyperglycemia as is the glycogen infiltration of ducts and beta cells. The proliferative activity on the other hand is considered to represent a more direct action of cortisone on the pancreas.
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