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首页> 外文期刊>Life sciences >Increase in DPP-IV in the intestine, liver and kidney of the rat treated with high fat diet and streptozotocin.
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Increase in DPP-IV in the intestine, liver and kidney of the rat treated with high fat diet and streptozotocin.

机译：用高脂饮食和链脲佐菌素治疗的大鼠的肠，肝和肾中DPP-IV的增加。

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High fat diet or insulin deficiency is commonly seen in Type II diabetes, while the mechanism remains unclear. To test our hypothesis that DPP-IV contributes to Type II diabetes, we examined the expression and activity of DPP-IV in rats (n=8 to each group) treated for 12 weeks with 3 separate diets: a) normal control; b) a high fat diet; and c) a high fat diet plus streptozotocin, a chemical for induction of insulin-deficient diabetes. Compared to rats on the normal diet, the rats with a high fat diet significantly increased DPP-IV's expression and activity about 142-152% in the intestine (P<0.05) and 153-240% in kidneys (P<0.05), but there was no change in the liver. Administration of streptozotocin to the rats treated with the high fat diet showed an insufficient insulin secretion and higher blood glucose in response to glucose/insulin tolerance test, and an increase in expression of DPP-IV and activity by 188-242% in the intestine (P<0.01); 191-225% in liver (P<0.01); and 211-321% in the kidneys (P<0.01). Immunohistochemistry studies confirmed the above results, showing increased DPP-IV immunostaining localized primarily in intestinal epithelium, hepatocytes and renal tubular cells. This study, for the first time reports an increase in DPP-IV associated with a high fat diet, as well as in the combination of a high fat diet with an insulin deficiency. Since both high fat diet and insulin deficiency are closely linked with etiology of Type II diabetes, the evidence in this study suggests a role of DPP-IV in development of Type II diabetes.
机译：高脂饮食或胰岛素缺乏症常见于II型糖尿病，但机制尚不清楚。为了检验我们的假设DPP-IV促成II型糖尿病，我们检查了DPP-IV在大鼠中的表达和活性（每组n = 8），用3种不同的饮食治疗了12周。 b）高脂饮食; c）高脂饮食加链脲佐菌素，一种可诱导胰岛素缺乏的糖尿病的化学物质。与正常饮食的大鼠相比，高脂饮食的大鼠肠中DPP-IV的表达和活性显着增加约142-152％（P <0.05），肾脏中增加153-240％（P <0.05），但肝脏没有变化。对高脂饮食治疗的大鼠给予链脲佐菌素后，对葡萄糖/胰岛素耐受性试验的胰岛素分泌不足，血糖升高，肠内DPP-IV的表达和活性增加了188-242％（ P <0.01）;肝脏191-225％（P <0.01）;肾脏中有211-321％（P <0.01）。免疫组织化学研究证实了以上结果，表明DPP-IV免疫染色增加主要定位于肠上皮，肝细胞和肾小管细胞。这项研究首次报道了与高脂饮食相关的DPP-IV的增加，以及高脂饮食与胰岛素缺乏症的结合。由于高脂饮食和胰岛素缺乏症均与II型糖尿病的病因密切相关，因此本研究中的证据表明DPP-IV在II型糖尿病的发展中具有重要作用。

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