姜黄素缓解小鼠高脂饲料喂养诱导肥胖的相关机制研究

The mechanism of the curcumin relieving high-fat diet-induced obesity in mice

目的 研究姜黄素缓解高脂诱导肥胖的作用及其相关机制.方法 选用8周龄C57BL/6雄性小鼠24只,随机分为3组,分别饲喂低脂日粮（对照组）、高脂日粮（模型组）和高脂日粮并灌服姜黄素（姜黄素组）.试验期为8周.结果 与模型组小鼠相比,姜黄素组小鼠体重、肝脏和附睾脂肪组织重量降低了13.8％、26.2％和61.0％（P＜0.05）;与模型组小鼠相比,姜黄素组小鼠棕榈酰基转移酶（cpt1）、酰基辅酶A脱氢酶（acdam）和过氧化物酶增值体激活受体γ辅激动子1α （pgc1α）表达提高了 950％、1752％和642％,P＜0.05）,而叉头蛋白O1（FOXO1）表达降低了83.6％（P＜0.05）.结论 姜黄素通过抑制FOXO1途经,促进脂肪酸氧化和提高线粒体功能,从而抑制肥胖的发生.

Objective The present study was conducted to investigate the effects of curcumin on high-fat induced obesity and its related mechanism. Methods 24 male C57BL/6 mice at 9 weeks old were randomly as- signed to three treatments： mice fed low-fat diet（Control group）, mice fed high-fat diet（Model group）, and mice fed high-fat diet and supplemented with eurcumin （Curcumin group）. The experiment lasted for 8 weeks. Results The results showed that when compared with micefedhigh-fat, weight gain, liver and epididymal fat weight in mice fed curcumin significantly decreased by 13.8%, 26.2% and 61%（P〈0.05）. Compared with mice fed high-fat, ex- pression of mitochondrial genes[peroxisome proliferator-activated receptor gamma coactivator 1 alpha（pgc1α） and fatty acid oxidation related genes （ carnitinepalmitoyltransferase 1A （ cpt 1 a ） and acyl-Coenzyme A dehydrogenase （ a- cadre）]were significantly increased by 642%, 950% and 1752%（P〈0.05）, while forkhead box protein O1 （FOX- O1 ）was significantly decreased by 83.6%（P〈0.05 ）. Conclusion Our results suggested that curcumin may attenu- ate high-fat induced obesity through decreasing lipogenesis and improving mitoehondrial function via FOXO1 path- way in liver.