PO-159游泳通过NF-κB信号通路调节胰岛素敏感性和单糖转运蛋白活性,改善代谢综合征

Sen Li, Jianya Huang
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摘要

目的糖尿病是一种以胰岛素分泌缺陷或(或)生物功能损害为主要表现的以高血糖和代谢综合征为特征的代谢性疾病。有证据表明,运动在糖尿病的发展过程中起着至关重要的作用,并影响胰岛素抵抗和单糖转运蛋白活性。本研究旨在通过胰岛素敏感性和单糖转运蛋白活性研究运动与糖尿病的关系。方法采用-ІІ型糖尿病小鼠db/db模型,分析游泳对葡萄糖和胰岛素代谢过程的影响。研究了实验小鼠的体重、葡萄糖代谢和血清胰岛素水平。分析实验小鼠血清中炎性因子IL-1、IL-17、TGF-β、VEGF的表达水平。观察生命中sirtuin-1和NF-κB信号通路的表达水平。组织学分析了游泳对-ІІ型糖尿病小鼠的治疗作用。结果游泳可上调葡萄糖和胰岛素的代谢。游泳运动促进了糖尿病小鼠脂肪和脂肪酸的消耗。此外,游泳可下调糖尿病小鼠血清中炎症因子IL-1、IL-17、TGF-β、VEGF的表达水平。实验小鼠游泳后肝脏中toll样受体4 (TLR4)和sirtuin-1表达水平上调。此外,我们观察到游泳可以改善实验小鼠游泳后肝脏的胰岛素敏感性和单糖转运蛋白(MTP)活性。组织学分析显示,游泳后的小鼠体内TTLR4和sirtuin-1的积累明显减少。游泳后小鼠NF-κB活性及p65、IKK-β、i -κB α表达水平上调。综上所述,游泳有利于-ІІ型糖尿病小鼠的葡萄糖和胰岛素代谢,并通过NF-κB信号通路调节胰岛素敏感性和单糖转运蛋白活性,进一步改善代谢综合征。
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PO-159 Swimming improves metabolic syndrome by regulation insulin sensitivity and monosaccharide transporter proteins activity via NF-κB signaling pathway
Objective Diabetes is one kind of metabolic diseases characterized by hyperglycemia and metabolic syndrome due to insulin secretion defects or/and biological function damage. Evidences have suggested that sports plays essential role in the progression of diabetes and affects insulin resistance and monosaccharide transporter proteins activity. The purpose of this study was to investigate relationship between sports and diabetes by evaluation the insulin sensitivity and monosaccharide transporter proteins activity. Methods A db/db mice model of type-ІІ diabetes mellitus was used to analyze the efficacy of swimming in the processes of glucose and insulin. Body weight, glucose metabolism and insulin serum levels were studied in experimental mice. Expression levels of inflammatory factors of IL-1, IL-17, TGF-β and VEGF in the serum was analyzed in the experimental mice. Expression levels of sirtuin-1 and NF-κB signaling pathway was investigate in the lives. Histological analysis was studied the therapeutic effects of swimming on mice with type-ІІ diabetes. Results Our results indicated that swimming up-regulated metabolism of glucose and insulin. Sport of swimming enhanced the consumption of fat and fatty acid in the mice with diabetes. In addition, expression levels of inflammatory factors of IL-1, IL-17, TGF-β and VEGF in the serum were down-regulated by swimming in the mice with diabetes. Toll-like receptor 4 (TLR4) and sirtuin-1 expression levels were up-regulated in the liver in the experimental mice after receive swimming. Furthermore, we observed that swimming improved insulin sensitivity and monosaccharide transporter proteins (MTP) activity in liver in the experimental mice after receive swimming. Histological analysis showed that TTLR4 and sirtuin-1 accumulation were significantly decreased in the live in mice treated by swimming. NF-κB activity and expression levels of p65,IKK-β and IκBα were up-regulated in the mice receiving swimming. Conclusions  In conclusion, these results indicate that swimming is beneficial for glucose and insulin metabolism for type-ІІ diabetes mice, which further improves metabolic syndrome by regulation insulin sensitivity and monosaccharide transporter proteins activity via NF-κB signaling pathway.
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