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首页> 外文期刊>International Journal of Experimental Diabetes Research: Experimental Diabesity Research >Hyperinsulinemia Induced Altered Insulin Signaling Pathway in Muscle of High Fat- and Carbohydrate-Fed Rats: Effect of Exercise
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Hyperinsulinemia Induced Altered Insulin Signaling Pathway in Muscle of High Fat- and Carbohydrate-Fed Rats: Effect of Exercise

机译：高胰岛素血症诱导高脂肪和碳水化合物喂养大鼠肌肉中的胰岛素信号通路改变：运动效果

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Insulin resistance is a state of impaired responsiveness to insulin action. This condition not only results in deficient glucose uptake but increases the risk for cardiovascular diseases (CVD), stroke, and obesity. The present work investigates the molecular mechanisms of high carbohydrate and fat diet in inducing prediabetic hyperinsulinemia and effect of exercise on InsR signaling events, muscular AChE, and lactate dehydrogenase activity. Adult male Wistar rats were divided into the control (C) diet group, high-carbohydrate diet (HCD) group, high-fat diet (HFD) group, and HCD and HFD groups with exercise (HCD Ex and HFD Ex, respectively). Acetyl choline esterase activity, lactate dehydrogenase activity, total lactate levels, IRS1 phosphorylations, and Glut4 expression patterns were studied in the muscle tissue among these groups. High carbohydrate and fat feeding led to hyperinsulinemic status with reduced acetylcholine esterase (AChE) activity and impaired phosphorylation of IRS1 along with increased lactate concentrations in the muscle. Exercise significantly upregulated phosphoinositide 3 kinase (PI3K) docking site phosphorylation and downregulated the negative IRS1 phosphorylations thereby increasing the glucose transporter (GLUT) expressions and reducing the lactate accumulation. Also, the levels of second messengers like IP3 and cAMP were increased with exercise. Increased second messenger levels induce calcium release thereby activating the downstream pathway promoting the translocation of GLUT4 to the plasma membrane. Our results showed that the metabolic and signaling pathway dysregulations seen during diet-induced hyperinsulinemia, a metabolic condition seen during the early stages in the development of prediabetes, were improved with vigorous physical exercise. Thus, exercise can be considered as an excellent management approach over drug therapy for diabetes and its complications.
机译：胰岛素抵抗是对胰岛素作用的反应性受损的状态。这种情况不仅导致葡萄糖摄取的缺陷，而且增加了心血管疾病（CVD），中风和肥胖的风险。目前的作品研究了高碳水化合物和脂肪饮食的分子机制在诱导前脂质胰蛋白症，运动对INSR信号传导事件，肌肉疼痛和乳酸脱氢酶活性的影响。成年雄性Wistar大鼠分为对照（c）饮食组，高碳水化合物饮食（HCD）组，高脂饮食（HFD）组和HCD和HFD组分别分别进行运动（HCD EX和HFD EX）。在这些组中的肌肉组织中研究了乙酰胆碱酯酶活性，乳酸脱氢酶活性，总乳酸水平，IRS1磷酸化和Glut4表达模式。高碳水化合物和脂肪饲料导致高胰岛素血症状态，具有降低的乙酰胆碱酯酶（ACHE）活性和IRS1的磷酸化效果，以及肌肉中的增加的乳酸浓度。锻炼显着上调磷酸膦酸3激酶（PI3K）对接部位磷酸化，下调负IRS1磷酸化，从而增加葡萄糖转运蛋白（凝乳）表达并降低乳酸积累。此外，IP3和营地等第二信使的水平随身携带。增加的第二信使水平诱导钙释放，从而激活促进促进Glut4的易位到质膜的下游途径。我们的研究结果表明，在饮食诱导的高胰岛素血症期间看到的代谢和信号通路呼吸缺乏率，在剧烈的体育锻炼中提高了预先发生的早期阶段期间的代谢病症。因此，可以认为锻炼是对糖尿病药物治疗的优秀管理方法及其并发症。

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