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首页> 外文期刊>The Journal of Nutritional Biochemistry >Cocoa-rich diet ameliorates hepatic insulin resistance by modulating insulin signaling and glucose homeostasis in Zucker diabetic fatty rats
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Cocoa-rich diet ameliorates hepatic insulin resistance by modulating insulin signaling and glucose homeostasis in Zucker diabetic fatty rats

机译：富含可可的饮食可通过调节Zucker糖尿病脂肪大鼠的胰岛素信号传导和葡萄糖稳态来改善肝胰岛素抵抗

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摘要

Insulin resistance is the primary characteristic of type 2 diabetes and results from insulin signaling defects. Cocoa has been shown to exert anti-diabetic effects by lowering glucose levels. However, the molecular mechanisms responsible for this preventive activity and whether cocoa exerts potential beneficial effects on the insulin signaling pathway in the liver remain largely unknown. Thus, in this study, the potential anti-diabetic properties of cocoa on glucose homeostasis and insulin signaling were evaluated in type 2 diabetic Zucker diabetic fatty (ZDF) rats. Male ZDF rats were fed a control or cocoa-rich diet (10%), and Zucker lean animals received the control diet. ZDF rats supplemented with cocoa (ZDF-Co) showed a significant decrease in body weight gain, glucose and insulin levels, as well as an improved glucose tolerance and insulin resistance. Cocoa-rich diet further ameliorated the hepatic insulin resistance by abolishing the increased serine-phosphorylated levels of the insulin receptor substrate 1 and preventing the inactivation of the glycogen synthase kinase 3/glycogen synthase pathway in the liver of cocoa-fed ZDF rats. The anti-hyperglycemic effect of cocoa appeared to be at least mediated through the decreased levels of hepatic phosphoenolpyruvate carboxykinase and increased values of glucokinase and glucose transporter 2 in the liver of ZDF-Co rats. Moreover, cocoa-rich diet suppressed c-Jun N-terminal kinase and p38 activation caused by insulin resistance. These findings suggest that cocoa has the potential to alleviate both hyperglycemia and hepatic insulin resistance in type 2 diabetic ZDF rats. (C) 2015 Elsevier Inc. All rights reserved.
机译：胰岛素抵抗是2型糖尿病的主要特征，归因于胰岛素信号传导缺陷。已显示可可可通过降低葡萄糖水平发挥抗糖尿病作用。但是，造成这种预防活性的分子机制以及可可是否对肝脏中的胰岛素信号传导途径产生潜在的有益作用，目前尚不清楚。因此，在这项研究中，在2型糖尿病Zucker糖尿病性脂肪（ZDF）大鼠中评估了可可对葡萄糖稳态和胰岛素信号传导的潜在抗糖尿病特性。给雄性ZDF大鼠喂食对照或富含可可的饮食（10％），而Zucker瘦肉动物则接受对照饮食。补充了可可（ZDF-Co）的ZDF大鼠表现出体重增加，葡萄糖和胰岛素水平显着降低，以及改善的葡萄糖耐量和胰岛素抵抗。富含可可的饮食通过取消胰岛素受体底物1丝氨酸磷酸化水平的增加和防止可可喂养的ZDF大鼠肝脏中糖原合酶激酶3 /糖原合酶途径的失活，进一步改善了肝胰岛素抵抗。可可的抗高血糖作用似乎至少是通过ZDF-Co大鼠肝脏中肝磷酸烯醇丙酮酸羧化激酶水平的降低以及葡萄糖激酶和葡萄糖转运蛋白2值的增加介导的。此外，富含可可的饮食抑制了c-Jun N末端激酶和胰岛素抵抗引起的p38活化。这些发现表明可可具有缓解2型糖尿病ZDF大鼠高血糖和肝胰岛素抵抗的潜力。 （C）2015 Elsevier Inc.保留所有权利。

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