Abstract

In order to examine the effect of sex hormones on diabetic pathogenesis in female Spontaneously Diabetic Torii (SDT) rats, we performed oophorectomy on female SDT rats, administered female hormones after the oophorectomy, and measured body weight changes, plasma glucose concentration, and pancreatic histopathology. At 26 weeks of age, the body weight was significantly heavier in the oophorectomized group and significantly lighter in the estradiol benzoate (EB) administration group than in the sham-operated control group. Although glucose concentration did not significantly change in the oophorectomized group, it was significantly lower in the EB administration group than in both control and the oophorectomized group. Severe histopathological change was observed in the oophoretomized group but not in the EB administration group. Thus, EB blocked weight gain and pancreatic islet change that was induced by oophoretomy and it also lowered glucose concentration. These results suggest that estrogen plays a preventive role for diabetic pathogenesis in female SDT rats.

Highlights

  • The Spontaneously Diabetic Torii (SDT) rat serves as a new model for non-obese type 2 diabetes mellitus

  • It has been reported that male SDT rats begin showing pancreatic islet histopathology including hemorrhage in the pancreatic islets at 8-10 weeks of age, and inflammatory cell infiltration with fibroblasts infiltrating the pancreatic islets by 16 weeks of age [1, 2, 13]

  • In this study oophorectomies were performed on female SDT rats, followed by administration of female sex hormones, and subsequent effects were observed on diabetic pathogenesis factors such as body weight, plasma glucose concentration, and pancreatic histopathology

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Summary

Introduction

The Spontaneously Diabetic Torii (SDT) rat serves as a new model for non-obese type 2 diabetes mellitus. In this study oophorectomies were performed on female SDT rats, followed by administration of female sex hormones, and subsequent effects were observed on diabetic pathogenesis factors such as body weight, plasma glucose concentration, and pancreatic histopathology.

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Conclusion
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