Esculetin, a coumarin derivative, suppresses adipogenesis through modulation of the AMPK pathway in 3T3-L1 adipocytes

• Published in: Journal of functional foods Vol. 12; pp. 509 - 515
• Main Authors: Kim, Younghwa, Lee, Junsoo
• Format: Journal Article
• Language: English
• Published: Elsevier Ltd 01.01.2015; Elsevier
• Subjects: 3T3-L1 cells; Adipogenesis; AMPK; Esculetin; Obesity; 3T3-L1 cells; Obesity; AMPK; Esculetin; Adipogenesis
• ISSN: 1756-4646; 2214-9414
• DOI: 10.1016/j.jff.2014.12.004

•Esculetin inhibited lipid accumulation and the expression of adipogenic specific proteins.•Esculetin increased phosphorylation of AMPK and acetyl-CoA carboxylase.•Pretreatment with AMPK inhibitor abolished the inhibitory effects of esculetin on PPARγ expression.•Esculetin has anti-adipogenic effects through modulation of PPARγ and C/EBPα via the AMPK signaling pathway. Obesity is one of the most serious health problems in both Westernized and developing countries. AMP-activated protein kinase (AMPK) has emerged as a major regulator of appetite, body weight, and cellular energy balance. In this study, we investigated the effect of esculetin (ECT) on adipogenesis via activation of AMPK in 3T3-L1 cells. ECT markedly inhibited lipid accumulation and suppressed the expression of adipogenic specific proteins including peroxisome proliferator-activated receptors (PPARγ), CCAAT/enhancer binding protein a (C/EBPα), and adipocyte fatty acid binding protein (aP2). Moreover, ECT significantly increased phosphorylation of AMPK and acetyl-CoA carboxylase (ACC) and intracellular reactive oxygen species (ROS) production. However, pretreatment with compound C, a specific AMPK inhibitor, abolished the inhibitory effects of ECT on PPARγ and C/EBPα expression. Therefore, these results indicate that ECT has anti-adipogenic effects through modulation of PPARγ and C/EBPα via the AMPK signaling pathway.