Korean Medicinal Herbs Research Team, National Development Institute of Korean Medicine, Jangheung-gun, 59338, Republic of Korea.
Korean Medicinal Herbs Research Team, National Development Institute of Korean Medicine, Jangheung-gun, 59338, Republic of Korea.
Chem Biol Interact. 2019 Sep 25;311:108755. doi: 10.1016/j.cbi.2019.108755. Epub 2019 Jul 15.
Effective control of white adipose tissue accumulation would provide a therapeutic strategy for obesity, which poses a growing global problem. The plant chemical mangiferin stimulates adenosine monophosphate-activated protein kinase (AMPK), which inhibits adipogenesis and has therefore been considered a therapeutic target for obesity and related diseases. We previously reported the anti-inflammatory properties of 6'-O-acetyl mangiferin (OAM). In this study, we evaluated the potential of OAM as an AMPK activator in vitro in 3T3-L1 preadipocytes. OAM inhibited adipogenesis as indicated by lower intracellular lipid and triglyceride accumulation as well as reduced adipogenic gene and protein expression upon treatment. OAM-treated 3T3-L1 cells excreted more glycerol, indicating increased lipolysis, which was supported by increased expression of lipolysis-related genes, including adipose triglyceride lipase and hormone-sensitive lipase. We determined that OAM upregulates lipolysis via phosphorylation-dependent activation of AMPK. Further, OAM upregulated the β-oxidation pathway as indicated by enhanced expression of phosphorylated acetyl-CoA-carboxylase and long-chain acyl-CoA synthetase 1. In conclusion, OAM markedly decreased intracellular lipid accumulation by enhancing lipolysis via AMPK activation and by upregulating β-oxidation. Thus, OAM has potential as a drug for the prevention and/or improvement of obesity and related diseases and deserves further study.
有效控制白色脂肪组织积累将为肥胖症提供一种治疗策略，肥胖症是一个日益严重的全球性问题。植物化学芒果苷刺激一磷酸腺苷激活蛋白激酶 (AMPK)，抑制脂肪生成，因此被认为是肥胖症和相关疾病的治疗靶点。我们之前报道了 6'-O-乙酰基芒果苷 (OAM) 的抗炎特性。在这项研究中，我们评估了 OAM 作为 3T3-L1 前脂肪细胞中体外 AMPK 激活剂的潜力。OAM 通过降低细胞内脂质和甘油三酯积累以及减少脂肪生成基因和蛋白表达来抑制脂肪生成。用 OAM 处理的 3T3-L1 细胞分泌出更多的甘油，表明脂肪分解增加，这得到了脂肪分解相关基因（包括脂肪甘油三酯脂肪酶和激素敏感脂肪酶）表达增加的支持。我们确定 OAM 通过依赖磷酸化的 AMPK 激活来上调脂肪分解。此外，OAM 通过增强磷酸化乙酰辅酶 A 羧化酶和长链酰基辅酶 A 合成酶 1 的表达来上调β-氧化途径。总之，OAM 通过 AMPK 激活增强脂肪分解和上调β-氧化显著减少细胞内脂质积累。因此，OAM 具有作为预防和/或改善肥胖症和相关疾病的药物的潜力，值得进一步研究。
