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岩藻黄质对高脂饮食诱导的肥胖小鼠胰岛素抵抗的影响
引用本文:黄莉莉,黄小强,张小琴,刘剑,张怡评,赵海誉,黄鸣清.岩藻黄质对高脂饮食诱导的肥胖小鼠胰岛素抵抗的影响[J].中国中药杂志,2021(1):171-176.
作者姓名:黄莉莉  黄小强  张小琴  刘剑  张怡评  赵海誉  黄鸣清
作者单位:福建中医药大学药学院;黄河科技学院医学院;自然资源部第三海洋研究所海洋生物资源开发利用工程技术创新中心;中国中医科学院中药研究所
基金项目:国家自然科学基金项目(81373941,81973437);自然资源部第三海洋研究所基本科研业务费专项(2017007,2017026);福建省科技计划项目(2018N0014)。
摘    要:研究岩藻黄质对高脂饮食诱导的肥胖小鼠胰岛素抵抗的作用及其分子机制。将50只C57BL/6J雄性小鼠随机分为正常组(10只)、高脂组(40只),高脂组经高脂饲料喂养12周形成肥胖胰岛素抵抗模型,将其随机分为模型组、岩藻黄质0.2%剂量组、岩藻黄质0.4%剂量组和二甲双胍组,每组10只,连续喂养含有相应药物饲料6周后,测定各组小鼠体质量和附睾脂肪质量;检测血清中空腹血糖(FBG)、空腹胰岛素(FINS)、总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDLC)、高密度脂蛋白胆固醇(HDL-C)含量,并计算胰岛素抵抗指数(HOMA-IR);HE染色法观察各组小鼠肝脏病理变化;Western blot法检测肝脏组织中胰岛素受体底物1(IRS-1)/磷酸肌醇-3-激酶(PI3K)/苏氨酸蛋白激酶(Akt)和过氧化物酶体增殖剂激活受体-γ(PPARγ)/胆固醇调节元件结合蛋白-1(SREBP-1)/脂肪酸合成酶(FAS)通路相关蛋白的表达。结果显示,与模型组相比,各给药组小鼠的体质量、附睾脂肪质量以及FBG,FINS,TC,TG,LDL-C,HOMA-IR水平,肝组织中PPARγ,SREBP-1和FAS蛋白表达显著降低(P<0.05或P<0.01),同时HDL-C水平及肝组织中p-IRS-1,IRS-1,PI3K,p-Akt的蛋白表达显著升高(P<0.05或P<0.01),且肝组织病理形态明显改善。结果表明,岩藻黄质可明显减轻肥胖小鼠的肥胖及糖脂紊乱,并改善胰岛素抵抗,其作用可能与调控IRS-1/PI3K/Akt和PPARγ/SREBP-1/FAS通路有关。

关 键 词:岩藻黄质  肥胖  胰岛素抵抗  IRS-1/PI3K/Akt  PPARγ/SREBP-1/FAS

Effect of fucoxanthin on insulin resistance in obese mice induced by high fat diet
HUANG Li-li,HUANG Xiao-qiang,ZHANG Xiao-qin,LIU Jian,ZHANG Yi-ping,ZHAO Hai-yu,HUANG Ming-qing.Effect of fucoxanthin on insulin resistance in obese mice induced by high fat diet[J].China Journal of Chinese Materia Medica,2021(1):171-176.
Authors:HUANG Li-li  HUANG Xiao-qiang  ZHANG Xiao-qin  LIU Jian  ZHANG Yi-ping  ZHAO Hai-yu  HUANG Ming-qing
Institution:(College of Pharmacy,Fujian University of Traditional Chinese Medicine,Fuzhou 350108,China;Medical School,Huanghe Science&Technology College,Zhengzhou 450063,China;State Oceanic Administration Technical Innovation Center for Utilization of Marine Biological Resources,Third Institute of Oceanography,Xiamen 361005,China;Institute of Chinese Materia Medica,China Academy of Chinese Medical Sciences,Beijing 100700,China)
Abstract:The aim of this paper was to study the effect and mechanism of fucoxanthin on insulin resistance of obese mice induced by high-fat diet.Fifty C57BL/6J male mice were randomly divided into control group and high-fat diet group.The insulin resistance model was induced with high-fat diet for 12 weeks,and model mice were randomly divided into model group,fucoxanthin-0.2%group,fucoxanthin-0.4%group and metformin group.After dietary treatment for 6 weeks,the body weight and epididymal fat weight in each group were measured.Fasting blood glucose(FBG),fasting insulin(FINS),total cholesterol(TC),triglyceride(TG),lowdensity lipoprotein(LDL-C)and high-density lipoprotein(HDL-C)were measured,and insulin resistance index(HOMA-IR)was calcula-ted.The pathological morphology in liver was observed by hematoxylin eosin staining,and the expressions of some key proteins in insulin receptor substrate 1(IRS-1)/posphoinositide 3-kinase(PI3K)/serine-threonine kinase(Akt)and peroxisome proliferatorsactivated receptor-γ(PPARγ)/sterol regulatory element binding protein-1(SREBP-1)/fatty acid synthetase(FAS)pathways in liver were detected by Western blot.According to the findings,compared with the model group,levels of body weight,epididymal fat weight,FBG,FINS,TC,TG,LDL-C and HOMA-IR,as well as protein expressions of PPARγ,SREBP-1 and FAS in liver were significantly reduced(P<0.05 or P<0.01),while level of HDL-C and protein expressions of p-IRS-1,IRS-1,PI3K and p-Akt in liver were signi-ficantly increased after treatment with fucoxanthin(P<0.05 or P<0.01).And the pathological changes of liver tissue in fucoxanthin-treated mice were also improved obviously.The results showed that fucoxanthin could improve obesity,hyperglycemia and hyperlipidemia,and alleviate insulin resistance in obese mice,and its mechanism is possibly related to the regulation of IRS-1/PI3K/Akt and PPARγ/SREBP-1/FAS pathways.
Keywords:fucoxanthin  obesity  insulin resistance  IRS-1/PI3K/Akt  PPARγ/SREBP-1/FAS
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