Abstract
Following the administration of alloxan at a dose of 300 mg/kg body weight to non-diabetic adult Chinese hamsters the blood glucose level showed an initial triphasic tendency and a transient second hyperglycemic phase with return to the normal level after approximately 8–9 days. After the hyperglycemic period the glucose tolerance was impaired in most animals. This impairment diminished gradually and the glucose tolerance became normal approximately 4–5 weeks after alloxan injection. Histological examination showed early selective necrosis of the pancreatic islet β-cells and subsequent signs of regeneration of the islet tissue. Tubular structures and cells without obvious cytoplasmic granulation (“clear cells”; “agranular cells”) supposedly formed the basis of this regeneration. It is proposed that this regeneration of islet tissue is responsible for the transitory nature of the alloxan-induced hyperglycemia and the impaired glucose tolerance. In a few animals there were histological changes in the liver and kidneys.
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