α‑Mangostin Regulates Hepatic Steatosis and Obesity through SirT1-AMPK and PPARγ Pathways in High-Fat Diet-Induced Obese Mice

Previous studies have shown that α-mangostin (α-MG) suppresses intracellular fat accumulation and stimulation of lipolysis in in vitro systems. Together with the relatively high distribution of α-MG in liver and fat, these observations made it possible to propose a plausible hypothesis that an α-MG supplement may regulate hepatic steatosis and obesity. An α-MG supplement (50 mg/kg) reduced the body weight gain (13.8%) and epidymal and retroperitoneal fat mass accumulation (15.0 and 11.3%, respectively), as well as the biochemical serum profiles such as cholesterol [TC (26.9%), LDL-C (39.1%), and HDL-C (15.3%)], glucose (30.2%), triglyceride (29.7%), and fatty acid (30.3%) levels in high-fat fed mice compared with the high-fat diet-treated group, indicating that α-MG may regulate lipid metabolism. In addition, an α-MG supplement up-regulated hepatic AMPK, SirT1, and PPARγ levels compared with the high-fat diet states, suggesting that α-MG regulates hepatic steatosis and obesity through the SirT1-AMPK and PPARγ pathways in high-fat diet-induced obese mice.