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目的探讨高脂膳食诱导肥胖的发生是否与小肠黏膜糖类消化及吸收功能的改变相关联。方法 46只雄性SD大鼠随机分为高脂组(n=31)与正常对照组(n=15),分别用高脂饲料和基础饲料饲养24周。24周后高脂饲料组大鼠根据体重分为肥胖组(n=16)及肥胖抵抗组(n=10)。测定大鼠的体重及腹腔脂肪湿重、空腹血糖水平、小肠黏膜麦芽糖酶及蔗糖酶活性。免疫组织化学法、RT-PCR法及蛋白质免疫印迹法检测大鼠小肠黏膜中Na+-依赖型葡萄糖转运蛋白(SGLT-1)的表达水平。结果肥胖组大鼠的体重、腹腔脂肪湿重、空腹血糖水平、小肠黏膜麦芽糖酶活性及SGLT-1蛋白表达量显著高于正常对照组及肥胖抵抗组(P<0.05)。3组大鼠小肠黏膜蔗糖酶活性无明显差异(P>0.05)。肥胖组大鼠小肠黏膜SGLT-1 mRNA的表达水平与正常对照组及肥胖抵抗组比较分别增加了12.5%和23%,但差异无显著性(P>0.05)。结论高脂膳食诱导的大鼠肥胖与小肠黏膜中麦芽糖酶活性增强及糖吸收的关键分子SGLT-1的表达增加相关联。
Objective To investigate whether the incidence of obesity induced by high-fat diet is associated with changes in intestinal mucosal carbohydrate digestion and absorption. Methods Forty-six male Sprague Dawley rats were randomly divided into high fat diet (n = 31) and normal control diet (n = 15), and were fed with high fat diet and basic diet for 24 weeks respectively. After 24 weeks, the rats in the high fat diet group were divided into obesity group (n = 16) and obesity resistance group (n = 10) according to body weight. The body weight, intraperitoneal fat wet weight, fasting blood glucose level, intestinal mucosal maltase and sucrase activity were measured. The expression of Na + -dependent glucose transporter (SGLT-1) in rat intestinal mucosa was detected by immunohistochemistry, RT-PCR and Western blot. Results Body weight, wet weight of abdominal fat, fasting blood glucose, intestinal mucosal maltase activity and SGLT-1 protein expression in obese group were significantly higher than those in normal control group and obesity resistant group (P <0.05). There was no significant difference in the activity of sucrase in the intestinal mucosa between the three groups (P> 0.05). The expression of SGLT-1 mRNA in intestinal mucosa of obese rats increased by 12.5% and 23% compared with that of normal control group and obesity resistant group, respectively, but the difference was not significant (P> 0.05). Conclusion The obesity induced by high-fat diet is related to the increase of the expression of SGLT-1, a key molecule that enhances the activity of maltase in intestinal mucosa and the absorption of glucose.