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

Area of Science:

• Nutritional Science
• Metabolic Disorders
• Obesity Research

Background:

• Obesity is linked to metabolic disorders and cardiovascular disease.
• Sulforaphane (SFN), an isothiocyanate, shows potential in inhibiting adipogenesis and cardiovascular disease.
• Investigating SFN's efficacy against high-fat diet (HFD)-induced obesity is crucial.

Purpose of the Study:

• To determine if sulforaphane (SFN) can prevent high-fat diet (HFD)-induced obesity in C57BL/6N mice.
• To elucidate the molecular mechanisms underlying SFN's anti-obesity effects.

Main Methods:

• Mice were fed a normal diet (ND), HFD, or HFD plus 0.1% SFN for 6 weeks.
• Evaluated body weight, food efficiency, visceral adiposity, liver fat accumulation, and serum lipid profiles.
• Analyzed gene and protein expression related to adipogenesis (PPARγ, C/EBPα, leptin, adiponectin) and lipogenesis (AMPK pathway, HMG-CoA reductase) in adipose tissue.

Main Results:

• HFD-SFN mice exhibited lower body weight and food efficiency compared to HFD mice.
• SFN attenuated visceral adiposity, adipocyte hypertrophy, and hepatic fat accumulation.
• SFN reduced serum total cholesterol, leptin, and liver triglycerides.
• SFN downregulated PPARγ, C/EBPα, and leptin, while upregulating adiponectin in adipose tissue.
• SFN increased adipose tissue AMPKα and acetyl-CoA carboxylase phosphorylation and decreased HMG-CoA reductase expression.

Conclusions:

• SFN demonstrates significant anti-obesity activity against HFD-induced obesity in mice.
• SFN inhibits adipogenesis by downregulating PPARγ and C/EBPα expression.
• SFN suppresses lipogenesis via activation of the AMPK pathway.
• SFN holds potential as a therapeutic agent for managing obesity and related metabolic disorders.