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绿原酸对高脂乳诱导小鼠胰岛素抵抗形成的影响 被引量:23

Effects of chlorogenic acid on mouse insulin resistance development induced by high fat emulsion
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摘要 目的探讨绿原酸(Chlorogenic acid,CGA)是否具有缓减或抑制高脂乳剂诱导小鼠产生胰岛素抵抗(Insulin Re-sistance,IR)的作用及其机制。方法 SPF级雌性昆明小鼠随机分为3组:对照组(Control)、高脂乳剂组(high fat emul-sion,HFE)灌胃高脂乳剂、绿原酸干预组(CGA+HFE)同时灌胃高脂乳剂和绿原酸。用自动血糖仪检测口服糖耐量(OGTT)。用酶联免疫法(Elisa)测空腹血清胰岛素(FINS)水平,计算胰岛素敏感指数(ISI)和胰岛素抵抗指数(HOMA-IR)。用全自动生化仪和相应的试剂盒检测血清中的甘油三酯(TC)、总胆固醇(TG)、高密度胆固醇(HDL-C)、低密度胆固醇(LDL-C)的含量。用RT-PCR法检测各组小鼠肝脏组织6-磷酸葡萄糖酶基因(glucose-6-phosphatase,G-6-Pase)和骨骼肌中葡萄糖转运体4基因(Glucose transporter 4,GLUT-4)的mRNA表达水平。并用HE染色法观察肾脏和胰腺的组织形态变化,通过免疫组化分析β细胞在胰腺中的分布与数量变化。结果高脂乳剂组小鼠出现了明显的IR,绿原酸干预组小鼠糖耐量能力有明显的改善、ISI升高、HOMA-IR降低、血清中TG、TC、和LDL-C的含量降低、肝脏G-6-Pase mRNA水平下调、骨骼肌GLUT-4mRNA水平上调。在组织水平上,绿原酸减少了高脂乳剂对肾脏和胰腺的损伤。结论绿原酸具有降血糖和降血脂作用,有效缓解高脂乳诱导的小鼠形成IR。 Aim To investigate the effects and mechanisms of chlorogenic acid (CGA) against insulin resistance (IR) enduced by high-fat emulsion. Methods SPF grade female Kunming mice were randomly divided into 3 groups, 10 mice for each group. All groups were free to normal diet and water, besides, the control group received saline as placebo by gastric perfusion. Model group was given high-fat emulsion (HFE) by gastric perfusion, and the CGA interference group (CGA + HFE ) was given both high-fat emulsion and CGA (20 mg · kg-1 body weight) by gastric perfusion at the same time. Oral glucose tolerance (OGT) was tested with glucose meter, the serum content of fasting blood glucose (FBG) was detected by ELISA. Total cholesterol (TC), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL- C) and triglycerides (TG) were determined with automatic biochemical analyzer. The expression of G-6- Pase mRNA in the liver and GLUT4 mRNA in the skeletal muscle were detected by RT-PCR. Pathological changes of kidney and pancreas were observed by HE dying, and the distribution and quantities of 15-cell in the pancreas were analyzed by immunohistochemistry. Results The HFE group mice showed obvious IR, but CGA relieved these symptoms. The CGA interference group mice had better glucose tolerance, higher ISI and lower HOMA-IR index. And the contents of TG, TC and LDL-C in serum were decreased in the CGA interference group. Compared with HFE group, the expression of G-6-Pase mRNA was down-regulated and GLUT-4 transcript was up-regulated in the CGA interference group. At the tissue level, CGA reduced the lesion of kidney and pancreas by high-fat emulsion. Conclusion CGA has hypoglycemic and hypolipidemic function, and can relieve the mouse IR development significantly.
出处 《中国药理学通报》 CAS CSCD 北大核心 2013年第5期654-658,共5页 Chinese Pharmacological Bulletin
基金 国家自然科学基金资助项目(No 31071531)
关键词 绿原酸 胰岛素抵抗 高脂乳剂 降血脂 降血糖 小鼠 chlorogenic acid insulin resistance high fat emulsion hypolipidemic hypoglycemic mice
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  • 1胡秋芬,杨光宇,黄章杰,李海涛,尹家元.微柱高效液相色谱法测定金银花中的多酚类物质[J].分析化学,2005,33(1):69-72. 被引量:35
  • 2田爱平,郭赛珊,申竹芳.高脂饲料与胰岛素抵抗动物模型[J].中国药理学通报,2006,22(3):267-269. 被引量:52
  • 3Steppan C M,Bailey S T, Bhat S,et al. The hormone resistin links obesity to diabetes[ J ]. Nature ,2001,409:307 - 12.
  • 4Rajala M W, Obici S, Scherer P E, et al. Adipose-derived resistin and gut-derived resistin-like molecule-β selectively impair insulin action on glucose production[ J]. J Clin Invest,2003,111:225 - 30.
  • 5Muse E D, Obici S, Bhanot S, et al. Role of resistin in diet-induced hepatic insulin resistance [ J ]. J Clin Invest,2004,114:232 - 9.
  • 6Banerjee R R,Rangwala S M, Shapiro J S,et al. Regulation of fasted blood glucose by resistin[ J]. Science,2004,303 : 1195 - 8.
  • 7Rangwala S M, Rich A S, Rhoades B, et al. Abnormal glucose homeostasis due to chronic hyperresistinemia [ J ]. Diabetes, 2004,53 (8) :1937 -41.
  • 8Qi Y, Nie Z Y, Lee Y S, et al. Loss of resistin improves glucose homeostasis in leptin deficiency[ J]. Diatetes ,2006,55:3083 - 90.
  • 9Viollet B, Foretz M, Guigas B, et al. Activation of AMP-activated protein kinase in the liver: a new strategy for the management of metabolic hepatic disorders[ J]. J Physiol,2006,574 ( 1 ) :41 -53.
  • 10Foretz M, Ancellin N, Andreelli F, et al. Short-term overexpression of a constitutively active form of AMP-activated protein kinasc in the liver leads to mild hypoglycemia and fatty liver[ J]. Diabetes, 2005,54:1331 - 9.

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