Four weeks exercise training enhanced the hepatic insulin sensitivity in high fat- and high carbohydrate-diet fed hyperinsulinemic rats

四周的运动训练提高了高脂高碳水化合物饮食喂养的高胰岛素血症大鼠的肝脏胰岛素敏感性。

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Abstract

AIM: Hyperinsulinemia is considered the primary defect underlying the development of type 2 diabetes. The liver is essential for the regular glucose homeostasis. In this study, we examined the effect of physical training on the insulin signaling, oxidative stress enzymes and Glucose-6-phosphatase(G6Pase) activity in the liver of Wistar rats. METHODS: Adult male Wistar rats were divided into Control diet group(C), High carbohydrate diet(HCD), High fat diet(HFD), HCD and HFD with training(HCD Ex & HFD Ex). HFD Ex and HCD Ex were trained on a small animal treadmill running at 20 m/min for 30 min, 5 days/wk. The present work investigated the effect of training on hepatic insulin receptor(InsR) signaling events, oxidative stress marker expressions and G6Pase activity in hyperinsulinemic rats. RESULTS: High carbohydrate and fat feeding led to hyperinsulinemic status with increased hepatic G6Pase activity and impaired phosphorylation of insulin receptor substrate 1(IRS1) and reduced expression of antioxidant enzymes.Training significantly reduced hepatic G6Pase activity, upregulated phosphoinositide 3 kinase(PI3K) docking site phosphorylation and downregulated the negative IRS1 phosphorylations thereby increasing the glucose transporter(GLUT) expressions (aa(P < 0.001) when compared to HFD, b(P < 0.01),bb (P < 0.001 when compared to HCD). Anti oxidant enzymes like CAT, SOD, eNOS expression were increased with reduction in the expression of inflammatory enzymes like TNF-α and COX-2 (*(P < 0.05),**(P < 0.01),***(P < 0.001) when compared to control, †(P < 0.05),††(P < 0.01),†††(P < 0.001) when compared to HFD and HCD). CONCLUSION: Thus, our study shows that four weeks training enhanced the hepatic insulin sensitivity in high fat and high carbohydrate-diet fed hyperinsulinemic rats. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s40200-020-00694-y.

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