Jiangxi Key Laboratory of Natural Product and Functional Food, School of Food Science and Engineering, Jiangxi Agricultural University, Nanchang, P.R. China.
J Food Biochem. 2021 Jul;45(7):e13795. doi: 10.1111/jfbc.13795. Epub 2021 May 25.
Obesity is a complex disease spreading in the world. In our previous studies, chlorogenic acid (CGA) and caffeine had ever been reported to reduce the body weight gain and fat accumulation in mice. This study investigated the anti-obesity effect of CGA and caffeine on 3T3-L1 cells. According to triglyceride (TG) assay and Oil-Red O staining, 40 μg/ml CGA and 160 μg/ml caffeine reduced TG content. Moreover, CGA + caffeine inhibited the mRNA expression of major adipogenic markers, PPAR-γ2, and C/EBPα in the metaphase and anaphase stages of differentiation induction (Day 2 and 4). CGA + caffeine improved P-AMPK/AMPK accompanied by decreasing the expression of GPDH and FAS to depress the lipid synthesis, increasing the mRNA expression of ACO and CAT to promote fatty acid oxidation and up-regulated the expression of hydrolysis-related enzyme adipose TG lipase (ATGL) and P-HSL/HSL. Furthermore, CGA + caffeine improved the expression of Glut4 which promoted the glucose transport. Taken together, these data demonstrated CGA + caffeine inhibited 3T3-L1 cells differentiation in the middle and late stages and reduced the fat accumulation through AMPK pathway by regulating the fat metabolism-related enzyme in 3T3-L1 cells to attenuates adipogenesis. PRACTICAL APPLICATIONS: The aim of this study was to elucidate the potential role of chlorogenic acid and caffeine in the treatment of obesity.
肥胖是一种在世界范围内蔓延的复杂疾病。在我们之前的研究中,曾报道绿原酸(CGA)和咖啡因可以减少小鼠的体重增加和脂肪积累。本研究旨在探讨 CGA 和咖啡因对 3T3-L1 细胞的抗肥胖作用。根据甘油三酯(TG)测定和油红 O 染色,40μg/ml 的 CGA 和 160μg/ml 的咖啡因可降低 TG 含量。此外,CGA+咖啡因在分化诱导的中期和后期(第 2 天和第 4 天)抑制主要脂肪生成标记物 PPAR-γ2 和 C/EBPα 的 mRNA 表达。CGA+咖啡因可改善 P-AMPK/AMPK,同时降低 GPDH 和 FAS 的表达以抑制脂质合成,增加 ACO 和 CAT 的 mRNA 表达以促进脂肪酸氧化,并上调水解相关酶脂肪 TG 脂肪酶(ATGL)和 P-HSL/HSL 的表达。此外,CGA+咖啡因可改善 Glut4 的表达,促进葡萄糖转运。综上所述,这些数据表明 CGA+咖啡因通过调节 3T3-L1 细胞中的脂肪代谢相关酶,抑制 3T3-L1 细胞在中期和后期的分化,减少脂肪积累,从而通过 AMPK 通路抑制脂肪生成。实际应用:本研究旨在阐明绿原酸和咖啡因在肥胖治疗中的潜在作用。