Sulforaphane Regulates Glucose and Lipid Metabolisms in Obese Mice by Restraining JNK and Activating Insulin and FGF21 Signal Pathways

Abstract

The most common complications of obesity are metabolic disorders such as nonalcoholic fatty liver disease (NAFLD), hyperglycemia, and low-grade inflammation. Sulforaphane (SFN) is a hydrolysate of glucosinolate (GLS) that is found in large quantities in cruciferous vegetables. The objective of this research was to evaluate the mechanism by which SFN relieves obesity complications in obese mice. C57BL/6J mice were fed a high-fat diet to induce obesity and treated daily with 10 mg/(kg body weight (bw)) SFN for 8 weeks, while a positive control group was treated daily with 300 mg/(kg bw) metformin. Our results indicated that SFN attenuated NAFLD, inflammation, oxidative stress, adipose tissue hypertrophy, and insulin resistance, as well as regulated glucose and lipid metabolism. SFN regulated glucose and lipid metabolism by deactivating c-Jun N-terminal kinase (JNK) and blocking the inhibitory effect of the insulin signaling pathway. SFN also regulated glucose metabolism by alleviating fibroblast growth factor 21 (FGF21) resistance. Our research provides an empirical basis for clinical treatment with SFN in obesity.