岩藻黄质对高脂饮食诱导的肥胖小鼠胰岛素抵抗的影响

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...

Effect of fucoxanthin on insulin resistance in obese mice induced by high fat diet

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.