Anti-obesity and anti-hepatosteatosis effects of dietary scopoletin in high-fat diet fed mice

• Published in: Journal of functional foods 2016-08, Vol.25, p.433-446
• Main Authors: Ham, Ju Ri, Lee, Hae-In, Choi, Ra-Yeong, Sim, Mi-Ok, Choi, Myung-Sook, Kwon, Eun-Young, Yun, Kyeong Won, Kim, Myung-Joo, Lee, Mi-Kyung
• Format: Article
• Language: English
• Subjects: High-fat; Non-alcoholic liver disease; Obesity; Scopoletin; Transcriptome
• ISSN: 1756-4646; 2214-9414
• DOI: 10.1016/j.jff.2016.06.026

•Scopoletin attenuates non-alcoholic fatty liver disease in high-fat diet fed mice.•Scopoletin identified 3 gene networks related to lipid metabolism and inflammation.•Target genes of lipid metabolism are Cidea, Apoa4, Cyp7a1 and Errfi1.•Target genes of inflammation are Col1a1, Mmp13, Cdkn1a and Saa1. The effects of scopoletin on non-alcoholic fatty liver in obese mice were investigated. Mice were fed high-fat diet (HF) with or without two doses of scopoletin (0.01 and 0.05%, w/w) for 16 weeks. Both doses of scopoletin led to similar reductions in body weight, visceral fat, serum levels of leptin, lipid, TNFα, IL-6, IFNγ and MCP-1, insulin resistance and hepatic lipid accumulation, whereas they increased serum adiponectin and faecal lipid levels. Ingenuity pathway analysis revealed that hepatic gene networks related to lipid concentrations, inflammation of organs, quantity of adipose tissue, proliferation of cell and necrosis were down-regulated in the scopoletin group. The top up- or down-regulated genes were Cidea, Apoa4, Cyp7a1, Errfi1, Col1a1, Mmp13, Cdkn1a, Gdf15 and Saa1, which emerged as associated genes related to hepatic steatosis and inflammation. These results indicate that scopoletin may ameliorate HF-induced hepatic dysfunction via regulation of lipid metabolic and inflammatory genes.