Male and female virgin rats having no arteriosclerosis and male and female breeder rats having established, naturally-occurring arteriosclerosis and relatively mild diabetes were given a single injection of alloxan which induced severe ketosis, hyperglycemia and hyperlipidemia. Animals were sacrificed one, two, three, four, five, six, and seven days, four and eight weeks after the onset of severe diabetes. Their livers showed prompt severe fatty metamorphosis and their islet beta cells total degranulation. After one week of untreated severe diabetes, the fatty infiltration of the liver became somewhat reduced as did the ketosis, hyperglycemia and hyperlipidemia. Concomitantly, the islets of Langerhans were greatly hypertrophied, the beta cells remaining degranulated. Male rats exhibited testicular atrophy and calcification; female rats manifested marked ovarian hypertrophy and corpora lutea formation. Many animals developed extensive areas of renal medullary necrosis. Approximately half of the animals of each group became emaciated with depleted islet beta cells; the remaining half had partially regranulated beta cells and were obese. The formerly nonarteriosclerotic virgin rats had developed microscopic arterial lesions, the emaciated and formerly arteriosclerotic breeder rats had developed extremely severe, calcific arteriosclerosis, but the obese, formerly arteriosclerotic breeder rats manifested very little evidence of arteriosclerosis indicating regression of arterial disease. It is concluded that partial restoration of insulin ameliorated while severe insulin deficiency caused acceleration and worsening of the arteriosclerosis in both the virgin and breeder rats and that the increased arteriosclerosis was due to the abnormal levels of glucose and lipid and to the effects of insulin deficiency on aortic metabolism per se.

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