Abstract
The Spontaneously Diabetic Torii (SDT) rat is a novel model for nonobese type 2 diabetes. In this study we investigated the glycolipid metabolic changes with phlorizin-treatment, which inhibits intestinal glucose uptake and renal glucose reabsorption, in male SDT rats. Phlorizin (100 mg/kg, b.i.d., s.c.) was administered for 4 weeks to SDT rats from 20 to 24 weeks of age. As a result, phlorizin reduced the development of hyperglycemia and decreased the hemoglobin A1c (HbA1c) levels. In the liver, phlorizin increased mRNA levels of glucokinase, the enzymes related with the glycogen cascade and the proteins associated with lipid metabolism. In conclusion, chronic administration of phlorizin in SDT rats produced a good glycemic control and an improvement in liver function.
Highlights
Type 2 diabetes is a polygenic disorder characterized by defects in insulin secretion and insulin sensitivity, which leads to glycolipid metabolic abnormalities [1]
Spontaneously Diabetic Torii (SDT) rats show a remarkable hyperglycemia after the onset of diabetes mellitus
Phlorizin treatment showed no change in the body weights in SDT rats (Figure 1(a))
Summary
Type 2 diabetes is a polygenic disorder characterized by defects in insulin secretion and insulin sensitivity, which leads to glycolipid metabolic abnormalities [1]. Male SDT rats develop diabetes mellitus from about 20 weeks of age and diabetic complications, such as ocular lesions and nephropathy, from about 40 weeks of age [8, 9]. SDT rats show glucose intolerance before the onset of diabetes. SDT rats show a remarkable hyperglycemia after the onset of diabetes mellitus. Correction of hyperglycemia with phlorizin, which shows a reduction of glucotoxicity, has been shown to normalize the abnormalities in the peripheral tissues and pancreas [16]. Phlorizin was administered to male SDT rats, and the effects of phlorizin on the metabolic abnormalities were investigated
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