Huang Li-Li, Huang Xiao-Qiang, Zhang Xiao-Qin, Liu Jian, Zhang Yi-Ping, Zhao Hai-Yu, Huang Ming-Qing
College of Pharmacy, Fujian University of Traditional Chinese Medicine Fuzhou 350108, China.
Medical School, Huanghe Science & Technology College Zhengzhou 450063, China.
Zhongguo Zhong Yao Za Zhi. 2021 Jan;46(1):171-176. doi: 10.19540/j.cnki.cjcmm.20200927.402.
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 C57 BL/6 J 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), low-density 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(PI3 K)/serine-threonine kinase(Akt) and peroxisome proliferators-activated 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, PI3 K 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/PI3 K/Akt and PPARγ/SREBP-1/FAS pathways.
本文旨在研究岩藻黄质对高脂饮食诱导的肥胖小鼠胰岛素抵抗的影响及其机制。将50只C57 BL/6 J雄性小鼠随机分为对照组和高脂饮食组。采用高脂饮食诱导胰岛素抵抗模型12周，将模型小鼠随机分为模型组、0.2%岩藻黄质组、0.4%岩藻黄质组和二甲双胍组。经6周饮食处理后，测量各组小鼠的体重和附睾脂肪重量。检测空腹血糖（FBG）、空腹胰岛素（FINS）、总胆固醇（TC）、甘油三酯（TG）、低密度脂蛋白（LDL-C）和高密度脂蛋白（HDL-C），并计算胰岛素抵抗指数（HOMA-IR）。采用苏木精-伊红染色观察肝脏病理形态，采用蛋白质免疫印迹法检测肝脏中胰岛素受体底物1（IRS-1）/磷脂酰肌醇3激酶（PI3 K）/丝氨酸-苏氨酸激酶（Akt）和过氧化物酶体增殖物激活受体γ（PPARγ）/固醇调节元件结合蛋白-1（SREBP-1）/脂肪酸合成酶（FAS）通路中一些关键蛋白的表达。结果显示，与模型组相比，岩藻黄质处理后小鼠的体重、附睾脂肪重量、FBG、FINS、TC、TG、LDL-C和HOMA-IR水平以及肝脏中PPARγ、SREBP-1和FAS的蛋白表达均显著降低（P<0.05或P<0.01），而HDL-C水平以及肝脏中p-IRS-1、IRS-1、PI3 K和p-Akt的蛋白表达显著升高（P<0.05或P<0.01）。岩藻黄质处理小鼠的肝组织病理变化也明显改善。结果表明，岩藻黄质可改善肥胖小鼠的肥胖、高血糖和高脂血症，减轻胰岛素抵抗，其机制可能与调节IRS-1/PI3 K/Akt和PPARγ/SREBP-1/FAS通路有关。
