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目的探讨高脂饮食所致肥胖导致胰岛素抵抗的物质基础。方法将30只雄性Wistar大鼠分为正常对照组、高脂组,正常对照组喂饲普通块料,高脂组喂饱和脂肪酸提供59%热卡的高脂饲料。各组共喂饲3月后测定体重,空腹血糖,糖负荷30、60、120min血糖,空腹胰岛素,胰岛素耐量,血脂,血清游离脂肪酸谱。结果与正常对照组比较,高脂组大鼠从第4周开始体重明显升高,空腹血糖和糖负荷30、60、120min血糖,糖耐量试验中葡萄糖曲线下面积,皮下注射胰岛素后40、90、120min血糖,胰岛素耐量试验中葡萄糖曲线下面积,血清胰岛素,胰岛素抵抗指数,血清瘦素,血清胆固醇和甘油三酯含量均明显升高。高脂组大鼠血清游离脂肪酸谱中饱和脂肪酸明显升高、不饱和脂肪酸明显下降。结论肥胖导致胰岛素抵抗的物质基础与脂肪代谢异常,特别是和饱和脂肪酸的升高、不饱和脂肪酸的下降有关。
Objective To investigate the material basis of obesity caused by high-fat diet leading to insulin resistance. Methods Thirty male Wistar rats were divided into normal control group, hyperlipidemic group and normal control group fed with normal block, and high fat group fed with high fat diet with 59% calories. Body weight, fasting blood glucose, glucose load 30, 60, 120min, blood sugar, fasting insulin, insulin resistance, blood lipid and serum free fatty acid were measured in all groups after 3 months of feeding. Results Compared with the normal control group, the body weight of rats in high fat group increased significantly from the 4th week, the fasting blood glucose and glucose load of 30, 60 and 120min, the area under the curve of glucose in glucose tolerance test, the subcutaneous injection of insulin 40, 90 , 120min blood glucose, insulin tolerance test area under the curve of glucose, serum insulin, insulin resistance index, serum leptin, serum cholesterol and triglyceride levels were significantly increased. The serum free fatty acid profiles of saturated fatty acids in hyperlipidemic rats were significantly increased, and unsaturated fatty acids decreased significantly. Conclusion The material basis of obesity leading to insulin resistance is related to abnormal lipid metabolism, especially with the increase of saturated fatty acids and the decline of unsaturated fatty acids.