Zheng Guodong, Qiu Yangyang, Zhang Qing-Feng, Li Dongming
Jiangxi Key Laboratory of Natural Product and Functional Food, College of Food Science and Engineering, Jiangxi Agricultural University,Nanchang330045,People's Republic of China.
Br J Nutr. 2014 Sep 28;112(6):1034-40. doi: 10.1017/S0007114514001652.
Obesity has become a public health concern due to its positive association with the incidence of many diseases, and coffee components including chlorogenic acid (CGA) and caffeine have been demonstrated to play roles in the suppression of fat accumulation. To investigate the mechanism by which CGA and caffeine regulate lipid metabolism, in the present study, forty mice were randomly assigned to four groups and fed diets containing no CGA or caffeine, CGA, caffeine, or CGA+caffeine for 24 weeks. Body weight, intraperitoneal adipose tissue (IPAT) weight, and serum biochemical parameters were measured, and the activities and mRNA and protein expression of lipid metabolism-related enzymes were analysed. There was a decrease in the body weight and IPAT weight of mice fed the CGA+caffeine diet. There was a significant decrease in the serum and hepatic concentrations of total cholesterol, TAG and leptin of mice fed the CGA+caffeine diet. The activities of carnitine acyltransferase (CAT) and acyl-CoA oxidase (ACO) were increased in mice fed the caffeine and CGA+caffeine diets, while the activity of fatty acid synthase (FAS) was suppressed in those fed the CGA+caffeine diet. The mRNA expression levels of AMP-activated protein kinase (AMPK), CAT and ACO were considerably up-regulated in mice fed the CGA+caffeine diet, while those of PPARγ2 were down-regulated. The protein expression levels of AMPK were increased and those of FAS were decreased in mice fed the CGA+caffeine diet. These results indicate that CGA+caffeine suppresses fat accumulation and body weight gain by regulating the activities and mRNA and protein expression levels of hepatic lipid metabolism-related enzymes and that these effects are stronger than those exerted by CGA and caffeine individually.
肥胖因其与多种疾病的发病率呈正相关而成为一个公共卫生问题，并且咖啡成分包括绿原酸（CGA）和咖啡因已被证明在抑制脂肪积累中发挥作用。为了研究CGA和咖啡因调节脂质代谢的机制，在本研究中，将40只小鼠随机分为四组，并给予不含CGA或咖啡因、CGA、咖啡因或CGA +咖啡因的饮食24周。测量体重、腹膜内脂肪组织（IPAT）重量和血清生化参数，并分析脂质代谢相关酶的活性以及mRNA和蛋白质表达。喂食CGA +咖啡因饮食的小鼠体重和IPAT重量有所下降。喂食CGA +咖啡因饮食的小鼠血清和肝脏中的总胆固醇、甘油三酯（TAG）和瘦素浓度显著降低。喂食咖啡因和CGA +咖啡因饮食的小鼠中肉碱酰基转移酶（CAT）和酰基辅酶A氧化酶（ACO）的活性增加，而喂食CGA +咖啡因饮食的小鼠中脂肪酸合酶（FAS）的活性受到抑制。喂食CGA +咖啡因饮食的小鼠中，AMP激活的蛋白激酶（AMPK）、CAT和ACO的mRNA表达水平显著上调，而过氧化物酶体增殖物激活受体γ2（PPARγ2）的mRNA表达水平下调。喂食CGA +咖啡因饮食的小鼠中，AMPK的蛋白表达水平增加，FAS的蛋白表达水平降低。这些结果表明，CGA +咖啡因通过调节肝脏脂质代谢相关酶的活性以及mRNA和蛋白质表达水平来抑制脂肪积累和体重增加，并且这些作用比CGA和咖啡因单独发挥的作用更强。
