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电针通过AMPK/ACC信号通路减轻高脂饮食诱导的胰岛素抵抗相关的骨骼肌脂质代谢紊乱。

Electroacupuncture Mitigates Skeletal Muscular Lipid Metabolism Disorder Related to High-Fat-Diet Induced Insulin Resistance through the AMPK/ACC Signaling Pathway.

作者信息

Li Zhixing, Lan Danchun, Zhang Haihua, Zhang Hongtao, Chen Xiaozhuan, Sun Jian

机构信息

Department of Soft Tissue Traumatology, Fourth Affiliated Hospital of Guangzhou University of Chinese Medicine, Shenzhen 518033, China.

Department of Acu-Moxibustion, Foshan Hospital of Traditional Chinese Medicine, Foshan, Foshan 528000, China.

出版信息

Evid Based Complement Alternat Med. 2018 Nov 7;2018:7925842. doi: 10.1155/2018/7925842. eCollection 2018.

DOI:10.1155/2018/7925842
PMID:30524482
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6247435/
Abstract

The aim of this work is to investigate the effect of electroacupuncture (EA) on insulin sensitivity in high-fat diet (HFD) induced insulin resistance (IR) rats and to evaluate expression of AMPK/ACC signaling components. Thirty-two male Sprague-Dawley rats were randomized into control group, HFD group, HFD+Pi (oral gavage of pioglitazone) group, and HFD+EA group. Acupuncture was subcutaneously applied to Zusanli (ST40) and Sanyinjiao (SP6). For Zusanli (ST40) and Sanyinjiao (SP6), needles were connected to an electroacupuncture (EA) apparatus. Fasting plasma glucose was measured by glucose oxidase method. Plasma fasting insulin (FINS) and adiponectin (ADP) were determined by ELISA. Triglyceride (TG) and cholesterol (TC) were determined by Gpo-pap. Proteins of adiponectin receptor 1 (adipoR1), AMP-activated Protein Kinase (AMPK), and acetyl-CoA carboxylase (ACC) were determined by Western blot, respectively. Compared with the control group, HFD group exhibits increased levels of FPG, FINS, and homeostatic model assessment of insulin resistance (HOMA-IR) and decreased level of ADP and insulin sensitivity index (ISI). These changes were reversed by both EA and pioglitazone. Proteins of adipoR1 and AMPK were decreased, while ACC were increased in HFD group compared to control group. Proteins of these molecules were restored back to normal levels upon EA and pioglitazone. EA can improve the insulin sensitivity of insulin resistance rats; the positive regulation of the AMPK/ACC pathway in the skeletal muscle may be a possible mechanism of EA in the treatment of IR.

摘要

本研究旨在探讨电针(EA)对高脂饮食(HFD)诱导的胰岛素抵抗(IR)大鼠胰岛素敏感性的影响,并评估AMPK/ACC信号通路相关成分的表达。将32只雄性Sprague-Dawley大鼠随机分为对照组、HFD组、HFD+Pi(口服吡格列酮)组和HFD+EA组。针刺足三里(ST40)和三阴交(SP6)穴位。对于足三里(ST40)和三阴交(SP6),将针连接到电针仪上。采用葡萄糖氧化酶法测定空腹血糖。采用酶联免疫吸附测定法测定空腹血浆胰岛素(FINS)和脂联素(ADP)。采用甘油磷酸氧化酶-过氧化物酶法(Gpo-pap)测定甘油三酯(TG)和胆固醇(TC)。分别采用蛋白质免疫印迹法检测脂联素受体-1(adipoR1)、AMP活化蛋白激酶(AMPK)和乙酰辅酶A羧化酶(ACC)的蛋白表达。与对照组相比,HFD组空腹血糖(FPG)、FINS水平升高,胰岛素抵抗稳态模型评估(HOMA-IR)升高,ADP水平和胰岛素敏感指数(ISI)降低。电针和吡格列酮均可逆转这些变化。与对照组相比,HFD组adipoR1和AMPK蛋白表达降低,ACC蛋白表达升高。电针和吡格列酮可使这些分子的蛋白表达恢复至正常水平。电针可改善胰岛素抵抗大鼠的胰岛素敏感性;骨骼肌中AMPK/ACC信号通路的正向调节可能是电针治疗IR的潜在机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f557/6247435/53dea47b55e2/ECAM2018-7925842.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f557/6247435/6bad32369df7/ECAM2018-7925842.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f557/6247435/1cd70b9fecbd/ECAM2018-7925842.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f557/6247435/53dea47b55e2/ECAM2018-7925842.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f557/6247435/6bad32369df7/ECAM2018-7925842.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f557/6247435/1cd70b9fecbd/ECAM2018-7925842.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f557/6247435/53dea47b55e2/ECAM2018-7925842.003.jpg

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