Sulforaphane Regulates Glucose and Lipid Metabolisms in Obese Mice by Restraining JNK and Activating Insulin and FGF21 Signal Pathways
Sulforaphane
FGF21
Carbohydrate Metabolism
Cruciferous vegetables
DOI:
10.1021/acs.jafc.1c04933
Publication Date:
2021-10-28T05:13:30Z
AUTHORS (6)
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 glucosinolate (GLS) that found in large quantities cruciferous vegetables. objective this research was to evaluate the mechanism by which SFN relieves obese mice. C57BL/6J mice were fed high-fat diet induce treated daily with 10 mg/(kg body weight (bw)) for 8 weeks, while positive control group 300 bw) metformin. Our results indicated attenuated NAFLD, inflammation, oxidative stress, adipose tissue hypertrophy, insulin resistance, well regulated glucose lipid metabolism. metabolism deactivating c-Jun N-terminal kinase (JNK) blocking inhibitory effect signaling pathway. also alleviating fibroblast growth factor 21 (FGF21) resistance. provides an empirical basis clinical treatment obesity.
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