齐墩果酸通过TGR5调节肥胖小鼠体内糖脂代谢的实验研究  

Effect of OA on glucose and lipid metabolism in obese mice by its receptor TGR5

作　　者：陈小松[1] 闫柳[1] 郭志辉[1] 李铭[1] 黄楚珊[1] 

机构地区：[1]福建医科大学附属协和医院整形外科,福建福州350001

出　　处：《中国美容医学》2015年第21期27-32,共6页Chinese Journal of Aesthetic Medicine

基　　金：国家自然科学基金;NO.81372092;福建省科技计划重点项目;NO.2011Y0029;福建省卫生厅中青年骨干人才项目;NO.2103-ZQN-ZD-15

摘　　要：目的:本研究通过建立肥胖小鼠的动物模型,探索天然植物药齐墩果酸OA是否通过褐色脂肪中高表达的TGR5受体调节能量代谢,消耗能量达到减肥效果及其作用的机制。方法:取8~10周龄野生型与TGR5^(-/-)两组小鼠分别给予普通或高脂饮食。8周后,高脂饮食小鼠随机分为两组,一组继续喂饲高脂饮食,另一组改以HFD+OA继续喂养8周。共喂养16周后进行糖耐量实验,并取肝脏脂肪组织做病理学观察,RT-PCR检测肝脏糖代谢相关基因的表达。喂养过程中监测小鼠体重。结果:TGR5激活可调节OA诱导的减肥效应,并增强肥胖小鼠胰岛素敏感性、降低血糖,减少肝脏组织脂质沉积,下调肝脏糖异生代谢酶相关基因的表达。结论:OA可明显减少后天性肥胖小鼠体内脂质堆积,减轻肥胖小鼠体重,调节糖代谢,其作用是通过激活胆汁酸膜受体TGR5实现的。Objective To explore the effect of the natural compound OA on regulating glucose and lipid metabolism by its receptor TGR5 in BAT in diet-induced obesity animal models. Methods Wild- type and TGR5-/- mice（n=5/group）between 8 and 10 weeks old were fed with HFD or the control regular chow diet for 8 weeks.Then mice fed with HFD were randomly divided into two groups.One group were kept feeding with HFD.The other group was switched to HFD＋OA for additional 8 weeks. Glucose tolerance test was detected after 16 weeks.Hematoxylin and eosin staining was performed for standard histological examination in liver tissues.Expression of genes related to glucose metabolism in liver was measured by Rael-time PCR.Mouse body weights were monitored during the entire process. Results TGR5 is required to mediate the effect of OA on obesity and glucose regulation.TGR5 activation enhanced insulin sensitivity in TGR5-/- mice. Activities on TGR5 induced lipid deposition and down-regulated the mRNA levels of G6pc in liver. Conclusion The effect of OA on body weight control and anti-hyperglycemia in obese mice is achieved by its receptor TGR5.

关 键 词：TGR5 齐墩果酸 肥胖 糖脂代谢 TGR5-/-鼠 

分 类 号：Q591.5[生物学—生物化学]