ANIMAL MODELS OF DISEASE: Classification and etiology of diabetes in dogs and cats

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   Figure 1

   Pancreatic histology. Severe infiltrations with T lymphocytes within a pancreatic islet in an 18-year-old DSH cat with diabetes mellitus. This is a rare finding, usually only few or no lymphocytes are found in islets of diabetic cats. Immunohistochemistry for CD3, HE counterstain (×40).
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   Figure 2

   Mean serum glucose (A) and insulin (B) concentrations (±s.e.m.) in 12 cats after i.v. administration of 0.5 g glucose/kg of body weight at entry into the study (baseline), after 9±2 months of weight gain, after a voluntary fast of 5–6 weeks (weight loss), and 5 weeks after the end of fasting (recovery). a–c: points with a different letter are significantly different (P<0.05) among periods. Note the development of impaired glucose tolerance despite increased insulin secretion with weight gain and improvement in glucose tolerance and the exaggerated insulin secretory response with weight loss. Reproduced, with permission, from Biourge et al. (1997).
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   Figure 3

   Pancreatic histology. Islet amyloidosis in a 16-year-old female spayed DSH cat with diabetes mellitus (H & E,×40).
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   Figure 4

   Pancreatic islets of healthy cats after receiving 0.9% NaCl, i.v. glucose infusion, and intravenous lipids for 10 days. No lesions were observed in the control cat and in the cat that received lipids. In the glucose-infused cat, a large area of the islet appeared devoid of nuclei and included several vacuoles, suggesting hydropic degeneration. Hydropic degeneration of islet cells indicates the accumulation of glycogen. The remaining islet nuclei appear larger than that in the control cat. (H & E,×40). Reproduced from Zini et al. (2009), with kind permission from Springer Science and Business Media.

• © 2014 Society for Endocrinology