摘要
目的：探讨高脂肪、蔗糖膳食的致肥胖作用机理。方法：应用高胰岛素血症的下丘脑腹内侧核损伤性肥胖大鼠和正常胰岛素水平的ＳＤ大鼠，饲以高脂肪、蔗糖和正常饲料，观察甘油三酯的代谢、胰岛素、脂蛋白脂酶活性的变化，分析胰岛素与甘油三酯生成、脂蛋白脂酶活性的相关关系。结果：高脂肪膳食具有明显的增加体重和脂肪的作用，但高蔗糖膳食仅有促进脂肪生成的作用；两者均可引起胰岛素水平的升高，升高的胰岛素水平提高脂蛋白酯酶的活性。高脂肪膳食引起外源性甘油三酯的升高，在脂蛋白脂酶的作用下，外源性甘油三酯进入脂肪细胞；高蔗糖膳食通过胰岛素的作用，促进内源性甘油三酯的分泌，在脂蛋白脂酶的作用下，内源性甘油三酯进入脂肪细胞。结论：高脂肪膳食和高蔗糖膳食导致肥胖的作用机理并不相同，不同之处是前者引起外源性甘油三酯的升高，后者促进内源性甘油三酯的产生。相同之处是两种膳食均引起胰岛素水平升高，升高的胰岛素水平提高脂蛋白酯酶活性，在脂蛋白酯酶的作用下，甘油三酯进入脂肪细胞。
Objective:To gain insight into mechanisms whereby high fat and sucrose diets affect triglyceride metabilism and induce obesity. Methods:Changes in fasting plasma triglyceride levels, hepatic triglyceride secretion and clearance rate, insulin and lipoprotein lipase were observed in VMH lesioned normal rats. Results: A high fat diet had a potency to increase body weight and body fat, but a high sucrose diet only had an effect in increasing body fat. Both diets could cause increase in plasma insulin concentration. Increased insulin level promoted enhancement in activity of lipoprotein lipase.A high fat diet led to increase in exogenous triglyceride in blood, which was rapidly transferred into adipocyte under action of lipoprotein lipase.A high sucrose diet caused increase in insulin concentration which was a stimulation factor for hepatic production of endogenous triglycerides.The endogenous triglycerides entered adipocyte under action of incereased lipoprotein lipase.Conclusion:Mechanisms by which high fat and sucrose diets lead to obesity are different.The difference is that a high fat diet induces increase in exogenous triglycerides, and a high sucrose diet induces overproduction of endogenous triglycerides.However,both diets have the same aspect,i.e.both diets cause hyperinsulinemia.Increased insulin level leads to enhancement of lipoprotein activity which promotes entrance of increased triglyceride into adipocyte.
出处
《营养学报》
CAS
CSCD
北大核心
1999年第1期42-47,共6页
Acta Nutrimenta Sinica
基金
日中医学协会提供课题
关键词
脂肪
蔗糖
甘油三酯
肥胖
dietary fat dietary sucrose triglyceride obesity
