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目的研究尼古丁对大鼠胰岛素敏感性的影响及其与过氧化酶体增殖物激活受体(PPAR-γ)的关系。方法将10～11周龄的雄性SD大鼠随机分为生理盐水组和尼古丁组,两组又各分为3个亚组(1周、3周及6周组),分别给生理盐水(生理盐水组)或3mg·kg-1·d-1尼古丁(尼古丁组)1周、3周、6周。各组均为皮下注射给药,每天1次。每周记录大鼠体质量变化。给药3周、6周后进行胰岛素耐量试验;给药1周、3周和6周后检测血清生化指标;给药6周后对各部位脂肪称量,并通过蛋白质印迹方法检测PPAR-γ蛋白在内脏脂肪和皮下脂肪的表达情况。结果尼古丁给药后大鼠体质量增幅减缓;胰岛素耐量试验显示给药3周、6周后胰岛素敏感性增强(P<0.05);3周后血清三酰甘油明显下降(P<0.01);6周后血清胰岛素敏感性相关指数明显增加(P<0.05);给药6周后皮下脂肪、内脏脂肪的绝对质量和相对质量均下降(P<0.01),且内脏脂肪下降幅度大于皮下脂肪,而内脏脂肪和皮下脂肪PPAR-γ蛋白表达不改变。结论尼古丁可增强大鼠胰岛素敏感性,该作用部分与尼古丁减少脂肪组织,尤其是内脏脂肪组织量及减少血清三酰甘油水平有关,而与脂肪组织中PPAR-γ表达无关。
Objective To investigate the effect of nicotine on insulin sensitivity in rats and its relationship with peroxisome proliferator activated receptor (PPAR-γ). Methods Male Sprague-Dawley rats aged 10-11 weeks were randomly divided into normal saline group and nicotine group. The two groups were divided into 3 subgroups (1 week, 3 weeks and 6 weeks) Saline group) or nicotine 3 mg · kg-1 · d-1 (nicotine group) for 1 week, 3 weeks and 6 weeks. Each group were subcutaneously administered once a day. Weekly changes in body weight were recorded. After 3 weeks and 6 weeks, insulin resistance test was performed. Serum biochemical indexes were measured at 1 week, 3 weeks and 6 weeks after administration. The fat of each part was weighed 6 weeks after the administration, and PPAR-γ was detected by Western blotting Protein expression in visceral fat and subcutaneous fat. Results After the administration of nicotine, the increase of body weight in rats was slowed down. Insulin tolerance test showed that insulin sensitivity increased after 3 weeks and 6 weeks (P <0.05), but decreased significantly after 3 weeks (P <0.01). After 6 weeks, the absolute and relative mass of subcutaneous fat and visceral fat decreased (P <0.01), and the visceral fat decreased more than that of subcutaneous fat, while the serum insulin sensitivity correlated significantly (P <0.05) The visceral fat and subcutaneous fat PPAR-γ protein expression did not change. Conclusions Nicotine can increase insulin sensitivity in rats, which is partly related to the reduction of adipose tissue, especially visceral fat mass and serum triglyceride level, but not to the expression of PPAR-γ in adipose tissue.