Sulforaphane attenuates obesity by inhibiting adipogenesis and activating the AMPK pathway in obese mice

• Published in: The Journal of nutritional biochemistry Vol. 25; no. 2; pp. 201 - 207
• Main Authors: Choi, Kyeong-Mi, Lee, Youn-Sun, Kim, Wonkyun, Kim, Seung Jung, Shin, Kyong-Oh, Yu, Ji-Yeon, Lee, Mi Kyeong, Lee, Yong-Moon, Hong, Jin Tae, Yun, Yeo-Pyo, Yoo, Hwan-Soo
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.02.2014
• Subjects: Adenylate Kinase - metabolism; Adipogenesis; Adipogenesis - drug effects; AMPK; Animals; Body Weight - drug effects; Cholesterol - blood; Enzyme Activation; Isothiocyanates - pharmacology; Isothiocyanates - therapeutic use; Leptin; Lipogenesis; Mice; Obesity; Obesity - drug therapy; Obesity - enzymology; Organ Size - drug effects; Sulforaphane; Obesity; AMPK; Lipogenesis; Sulforaphane; Leptin; Adipogenesis
• ISSN: 0955-2863; 1873-4847
• DOI: 10.1016/j.jnutbio.2013.10.007

Obesity is associated with metabolic disorders. Sulforaphane, an isothiocyanate, inhibits adipogenesis and the occurrence of cardiovascular disease. In this study, we investigated whether sulforaphane could prevent high-fat diet (HFD)-induced obesity in C57BL/6N mice. Mice were fed a normal diet (ND), HFD or HFD plus 0.1% sulforaphane (SFN) for 6 weeks. Food efficiency ratios and body weight were lower in HFD-SFN-fed mice than in HFD-fed mice. SFN attenuated HFD-induced visceral adiposity, adipocyte hypertrophy and fat accumulation in the liver. Serum total cholesterol and leptin, and liver triglyceride levels were lower in HFD-SFN-fed mice than in HFD-fed mice. SFN decreased the expression of peroxisome proliferator-activated receptor γ (PPARγ), CCAAT/enhancer-binding protein α (C/EBPα) and leptin in the adipose tissue of HFD-SFN mice and increased adiponectin expression. Phosphorylation of AMP-activated protein kinase α (AMPKα) and acetyl-CoA carboxylase in the adipose tissue of HFD-SFN-fed mice was elevated, and HMG-CoA reductase expression was decreased compared with HFD-fed mice. Thus, these results suggest that SFN may induce antiobesity activity by inhibiting adipogenesis through down-regulation of PPARγ and C/EBPα and by suppressing lipogenesis through activation of the AMPK pathway.