摘要
目的:探讨酮替芬对高糖高脂饮食诱导的大鼠肥胖模型的减肥作用及其机制。方法:SD大鼠随机分成肥胖模型组、酮替芬干预组和正常对照组,肥胖模型组和酮替芬干预组以高糖高脂饲料饲喂,正常对照组以基础饲料饲喂,酮替芬干预组每天灌胃给予酮替芬0.09mg/kg,持续12周。称重,计算Lee's指数,检测空腹血糖(FBG)、空腹胰岛素(FINS)、瘦素(LEP)、游离脂肪酸(FFA)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)、白介素-6(IL-6)、肿瘤坏死因子-α(TNF-α);检测白色脂肪解偶联蛋白2(UCP2)mRNA的表达。结果:酮替芬明显降低肥胖模型大鼠的体质量及Lee's指数(P<0.05),降低FBG、FINS和LEP水平(P<0.05),降低FFA、TG和LDL-C水平(P<0.05)和IL-6、TNF-α水平(P<0.05),而增加UCP2mRNA的表达水平(P<0.05)。结论:酮替芬能够降低肥胖模型大鼠炎症介质和游离脂肪酸水平,减轻高胰岛素血症和高瘦素血症,促进脂肪组织能量代谢,实现减肥作用。
AIM. To investigate the antiobe- sity effect and mechanism of ketotifen in high- carbon hydrate-fat diet induced obese rats. METHODS. Male SD rats were randomly divided into three groups, obese group, ketotifen group and normal control group. Rats of obese group and ketotifen group were fed with high-carbon hydrate-fat diet, while the rats of normal control group were fed with basal feed. Rats of ketotifen group were daily given a gavage of ketotifen 0.09 mg/kg for 12 weeks. The body weights were tested and then the Lee＇s indexes were cal- culated,The fasting blood glucose（FBG）,fasting insulin（FINS） and leptin（LEP）, free fatty acid （FFA）, riglyceride（TG） and low density lipo- protein cholesterin （LDL-C）, interleukin -6 （IL- 6） and tumor nectosis factor-alpha（TNF-α） were analyzed, UCP2 mRNA in white adipose weremeasured. RESULTS： Ketotifen reduced body weight and Lee＇s indexes obviously in obese rats （P〈0.05）, lowered FBG,FINS and LEP levels and reduced FFA, TG and LDL-C levels signifi- cantly（P〈0.05）. Furthermore, ketotifen could decrease IL-6 and TNF-α levels and increase the UCP2 mRNA expression obviously（P〈0.05）. CONCLUSION： Ketotifen has antiobesity effects on high-carbon hydrate-fat diet induced obese rats by reduction of inflammation medium and free fatty acid leves,alleviation of hyperinsuline- mia and hyperleptindemia and promotion of adi- pose tissue energy metabolism.
出处
《中国临床药理学与治疗学》
CAS
CSCD
2014年第1期23-28,共6页
Chinese Journal of Clinical Pharmacology and Therapeutics
基金
浙江省自然科学基金(LQ12H07003)
温州市科技局基金资助(Y20100063)
