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

• Main Authors: Hai Yan Quan, Do Yeon Kim, Sung Hyun Chung
• Format: Article
• Language: English
• Published: Korean Society for Biochemistry and Molecular Biology 2013-04-01
• Series: BMB Reports
• Subjects: AMP-activated protein kinase; Caffeine; HepG2 cells; Lipid accumulation; Sterol regulatory element-binding protein
• Online Access: http://bmbreports.org/jbmb/pdf.php?data=MTMwOTI3MTBAcGRmX3JhaW50cmFjZV9sZWV5c0AlNUI0Ni00JTVEMTMwNDI2MjAzMl8lMjgyMDctMjEyJTI5Qk1CXzEyLTE1My5wZGY=

The main purpose of this study is to examine the effect ofcaffeine on lipid accumulation in human hepatoma HepG2cells. Significant decreases in the accumulation of hepaticlipids, such as triglyceride (TG), and cholesterol were observedwhen HepG2 cells were treated with caffeine as indicated.Caffeine decreased the mRNA level of lipogenesis-associatedgenes (SREBP1c, SREBP2, FAS, SCD1, HMGR and LDLR). Incontrast, mRNA level of CD36, which is responsible for lipiduptake and catabolism, was increased. Next, the effect ofcaffeine on AMP-activated protein kinase (AMPK) signalingpathway was examined. Phosphorylation of AMPK andacetyl-CoA carboxylase were evidently increased when thecells were treated with caffeine as indicated for 24 h. Theseeffects were all reversed in the presence of compound C, anAMPK inhibitor. In summary, these data indicate that caffeineeffectively depleted TG and cholesterol levels by inhibition oflipogenesis and stimulation of lipolysis through modulatingAMPK-SREBP signaling pathways. [BMB Reports 2013; 46(4):207-212]