饮食诱导代谢综合征小鼠模型的建立

目的建立以高脂纯化饲料诱导的、遗传背景和环境因素共同起作用的C57BL/6J小鼠代谢综合征（MS）模型,为研究营养因素与代谢综合征的关系提供周期较短、稳定性好、可重复性、与人类发病可比性高的动物模型。方法雄性3周龄C57BL/6J小鼠30只适应性喂养10d后随机分为2组,其中一组（10只）给予普通生长饲料（对照组）,另一组（20只）给予高脂纯化饲料（模型组）。喂养期间对空腹血糖（FBG）、体重进行连续监测,同时监测体重指数（BMI）、血清胰岛素（FINS）、血清甘油三脂（TG）、总胆固醇（TC）、高密度脂蛋白（HDL-C）、低密度脂蛋白（LDL-C）,实验期10周。实验结束时取内脏脂肪和肝脏称重,取肝胰做病理分析。结果分组喂养1周时,模型组小鼠体重出现显著性升高（P〈0.001）,并表现为中心型肥胖。4周时FBG显著性升高（P〈0.05）,5周时FINS开始升高但无显著性差异。8周时血清TC、HDL-C显著性升高（P〈0.001）,10周时TG、TC、HDL-C、LDL-C均升高（P〈0.01）。HE染色显示肝脏中度脂肪变,胰岛细胞无明显改变。结论单纯施以高脂饲料10周即可建立MS小鼠模型。并且该模型造模方法简单易行、周期较短、稳定性好、可重复性高,与人类MS自然发病过程类似,是MS较理想的动物模型。

Establishment of Diet-induced Metabolic Syndrome Mouse Model

Objective To establish C57BL/6J metabolic syndrome（MS） mouse model induced with high-fat purified ingredient diets, which may reflect the interaction of genetic background and environmental challenges such as high-fat/high-calorie diets that predispose to the development of human metabolic syndrome and provide stable perlod-briefly and highly repetitious animal model for studying the interplay between nutritional factors and MS. Methods After adaptation for 10 days, 30 males aged 3 weeks were randomly divided into two groups. One of them（ 10 mice） was fed on conventional chow diet served as controls, the other group（20 mice） were fed high-fat purified ingredient diets （model group） for 10 weeks. The body weight （BW） and fasting blood glucose （FBG） were serially measured. The body weight index （BMI）, fasting serum insulin （FINS）, fasting serum triglyceride （TG）, total cholesterol （TC）, high-density lipoprotein-eholesterol （HDL-C）, and low-density lipoprotein-eholesterol （LDL-C） were also determined. After sacrificed, mouse visceral fat and liver were excavated for weight measurement, and the liver and pancreas for HE stain analysis. Results Compared with the controls, the mice in model group show significantly higher body weight and demonstrated central obesity after 1-week high-fat diet（ P 〈 0.001 ）. After 4 weeks, HF group began to show hyperglycemia （P 〈 0.05 ）. After 5 weeks, it appeared hyperinsulinemia but with no significant difference between model and control groups. The model group showed higher serum TG and HDL-C after 8 weeks （ P 〈 0.001）. After 10 weeks, the TC and LDL-C in model group reached higher level （ P 〈 0.01 ）. HE dyeing illustrated moderate hepatic steatosis in model group. Conclusion Just fed on high fat diet for 10 weeks, C57BL/6J mouse mimicked human MS progression and appeared MS phenotypes. With reproducible, simple and period-brief, this mouse model is a very useful animal model in human MS research.