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作 者:梁颖[1] 李焱[1] 蒋妍[1] 刘珊英[1] 黎锋[1] 肖辉盛[1] 刘丹[1] 严励[1] 傅祖植[1]
机构地区:[1]中山大学附属第二医院内分泌科,广州510120
出 处:《中国药学杂志》2011年第3期189-193,共5页Chinese Pharmaceutical Journal
基 金:2003年教育部回国人员启动基金;2006年广东省自然科学基金(6021329)
摘 要:目的探讨特异性阻断血管紧张素Ⅱ受体是否抑制高脂饮食诱导的肥胖,以及改善血脂紊乱。方法 40只雄性SD大鼠随机分为高脂治疗组、高脂组、对照治疗组和对照组。高脂组给予高脂饲料,对照组给予标准大鼠饲料,高脂治疗组给予高脂饲料+替米沙坦10 mg.kg-1.d-1灌胃,对照治疗组给予标准大鼠饲料+替米沙坦10 mg.kg-1.d-1灌胃。共饲养10周,每周称重(g)。10周后经大鼠上腔静脉取血,测血脂、FFAs及胰岛素水平。应用RT-PCR检测内脏脂肪的脂联素、TNF-α、IL-6、CD68和MCP-1的mRNA表达水平。结果 4组大鼠体重随时间变化的趋势的差别有统计学意义(P=0.002),喂养10周后高脂治疗组大鼠平均体重增加低于高脂组(P=0.012),高脂治疗组大鼠平均血TG水平显著低于高脂组(P=0.002);高脂治疗组平均血HDL-C水平显著高于高脂组(P=0.023);高脂治疗组和高脂组大鼠血TC水平无显著差异(P=0.054);高脂治疗组和高脂组大鼠血LDL-C水平无显著差异(P=0.842);高脂饮食减少大鼠脂肪组织中脂联素mRNA表达水平(P=0.014),替米沙坦对大鼠脂肪组织中脂联素mRNA表达水平无影响(P=0.063);高脂饮食和替米沙坦对TNF-α、IL-6、CD68和MCP-1的mRNA表达水平均无影响(P>0.05)。结论阻断RAS系统抑制饮食诱导的体重和内脏脂肪的增加,并改善高脂饮食引起的血脂异常。OBJECTIVE To investigate influence of RAS on the development of obesity induced with high-fat diet and its possible mechanism. METHODS 40 SD rats were randomly divided into four groups (n = 10 per group) as following: Group A was fed with standard diet( control group), group B was fed with telmisartan and standard diet( control treated group), group C was fed with high-fat diet (high-fat diet group), group D was fed with telmisartan and high-fat diet( highfat diet treated group). Body weight was measured before and after the treatment. At 10th week, lipids, FFA and insulin were measured. The expression of adipokines (TNF- a, IL-6, adiponectin , MCP-1 and CD68) in adipose tissue was determined by semi-quantitative RT-PCR. RESULTS There were significant differences among the four groups in body weight ( P = 0. 002 ). The increase of body weight was significantly higher in group C than group D(P =0.012). The level of TG was significantly higher in group C than group D(P =0.002). The level of HDL-C was significantly lower in the in group C than group D( P = 0. 023 ). High-fat diet had significant effect on the expression level of adiponectin mRNA(P =0. 014) and no significant effect on the expression levels of TNF-a, IL-6, adiponectin, MCP-1 and CD68 mRNA(P = 0.305 ;P = 0.390 ;P=0.063;P=0. 552;P = 0. 321, respectively). Telmisartan had no significant effect on the expression levels of TNF-a, IL-6, adiponectin, MCP-1 and CD68 mRNA ( P = 0.305 ;P = 0. 390 ;P = 0. 063 ;P = 0.552 ; P = 0. 321, respectively). CONCLUSION Telmisartan treatment for 10 weeks inhibited the increase of body weight induced by high-fat diet, suggesting that Aug II is involved in the development of obesity and improved dyslipidemia.
关 键 词:肾素-血管紧张素系统 肾素血管紧张素Ⅱ受体拮抗剂 替米沙坦 高脂饮食
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