高脂饮食诱导代谢综合征模型建立

Study on a rat model of metabolic syndrome induced by high-fat diet

目的通过高脂饮食喂养建立代谢综合征(MS)大鼠动物模型。方法 30只健康雄性W istar大鼠随机分为健康对照组和造模组,造模组给予高脂饮食喂养,通过血糖、胰岛素和高胰岛素一正常血糖嵌夹试验法判断胰岛素抵抗情况,并比较两组动物的体质量、血脂、收缩压及相关内脏病理变化。结果造模组大鼠体质量和收缩压明显大于健康对照组(476±39 vs 425±21g;122±3.5mm Hg vs 109±1.1mm Hg,P<0.05);空腹血糖及空腹胰岛素浓度均明显升高[(7.2±0.6)vs(4.8±0.1)mmol/L;(66.3±24.2)vs(36.3±19.8)mmol/L,P<0.01];胰岛素敏感性明显降低[(8.1±1.1)vs(18.2±2.1)mg.kg-1.m in-1,P<0.01];血清总胆固醇、三酰甘油、低密度脂蛋白浓度亦明显高于健康对照组(P<0.05)。同时,造模组大鼠肝细胞大量脂肪变,伴明显胞浆疏松化,末端回肠出现程度不等的坏死性肠炎表现。结论高脂饮食能诱导建立MS大鼠模型,并能产生与MS相关的内脏损伤。

Objective To establish a rat model of metabolic syndrome（MS）induced by high-fat diet.Methods 30 healthy male Wistar rats were randomly divided into normal control group and experimental group.The rats in experimental group were fed with high-fat diet.MS were determined through the metabolic parameters,such as blood glucose,insulin,glucose infusion rate（GIR）,weight,sysbolic blood pressure,and serum lipids.Pathological changes of liver and ileum were also investigated.Results The weights and sysbolic blood pressure of experimental rats were increased much more than the normal control group（476±39 vs 425±21g;122±3.5 vs 109±1.1;P0.05）.Comparing with the normal control group,the levels of fasting plasma glucose（FPG）and fasting insulin（FIN）in experimental group were extremely significantly increased（7.2±0.6 vs 4.8±0.1 mmol/L;66.3±24.2 vs 36.3±19.8 mmol/L,P0.01）;the insulin sensitivity were significantly lower（8.1±1.1 vs 18.2±2.1 mg·kg-1·min-1,P0.01）;And serum total cholesterol,triglycerides,low density lipoprotein concentrations were also significantly higher than the normal group（P0.05）.Meanwhile,hepatic steatosis and cytoplasm of osteoporosis appeared in the experimental group,as well as necrotizing enterocolitis of terminal ileum.Conclusion MS rat model can be induced by high-fat diet and the visceral injury related with MS can occur.