Caffeine attenuates lipid accumulation via activation of AMP-activated protein kinase signaling pathway in HepG2 cells

• Published in: BMB reports Vol. 46; no. 4; pp. 207 - 212
• Main Authors: Quan, Hai Yan, Kim, Do Yeon, Chung, Sung Hyun
• Format: Journal Article
• Language: Korean
• Published: 생화학분자생물학회 30.04.2013
• Subjects: AMP-activated protein kinase; Caffeine; HepG2 cells; Lipid accumulation; Sterol regulatory element-binding protein; Lipid accumulation; HepG2 cells; AMP-activated protein kinase; Sterol regulatory element-binding protein; Caffeine
• ISSN: 1976-6696; 1976-670X

The main purpose of this study is to examine the effect of caffeine on lipid accumulation in human hepatoma HepG2 cells. Significant decreases in the accumulation of hepatic lipids, such as triglyceride (TG), and cholesterol were observed when HepG2 cells were treated with caffeine as indicated. Caffeine decreased the mRNA level of lipogenesis-associated genes (SREBP1c, SREBP2, FAS, SCD1, HMGR and LDLR). In contrast, mRNA level of CD36, which is responsible for lipid uptake and catabolism, was increased. Next, the effect of caffeine on AMP-activated protein kinase (AMPK) signaling pathway was examined. Phosphorylation of AMPK and acetyl-CoA carboxylase were evidently increased when the cells were treated with caffeine as indicated for 24 h. These effects were all reversed in the presence of compound C, an AMPK inhibitor. In summary, these data indicate that caffeine effectively depleted TG and cholesterol levels by inhibition of lipogenesis and stimulation of lipolysis through modulating AMPK-SREBP signaling pathways.