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Potent effects of dioscin against obesity in mice
Min Liu1, Lina Xu1, Lianhong Yin1
1College of Pharmacy, Dalian Medical University, Western 9 Lvshunnan Road, Dalian 116044, China.
Abstract:
The mechanisms of the natural product dioscin against non-alcoholic fatty liver disease (NAFLD) are unclear. Thus, the purpose of the present study was to further confirm its effects of prevention and then to elucidate the potential mechanisms underlying its activity in mice. High-fat diet (HFD)-induced C57BL/6J mice and ob/ob mice were used as the experimental models. Serum and hepatic biochemical parameters were determined, and the mRNA and protein expression levels were detected. The results indicated that dioscin alleviated body weight and liver lipid accumulation symptoms, increased oxygen consumption and energy expenditure, and improved the levels of serum and hepatic biochemical parameters. Further investigations revealed that dioscin significantly attenuated oxidative damage, suppressed inflammation, inhibited triglyceride and cholesterol synthesis, promoted fatty acid β-oxidation, down-regulated MAPK phosphorylation levels, and induced autophagy to alleviate fatty liver conditions. Dioscin prevents diet induced obesity and NAFLD by increasing energy expenditure. This agent should be developed as a new candidate for obesity and NAFLD prevention.
Insights
Dioscin effectively combats non-alcoholic fatty liver disease (NAFLD) and obesity in mice by boosting energy expenditure. This natural compound reduces liver fat and inflammation, showing promise for future treatments.
Area of Science:
- Pharmacology
- Hepatology
- Metabolic Diseases
Background:
- The natural product dioscin's role in non-alcoholic fatty liver disease (NAFLD) is not fully understood.
- Investigating dioscin's preventive effects and underlying mechanisms is crucial for potential therapeutic development.
Purpose of the Study:
- To confirm dioscin's preventive effects on NAFLD.
- To elucidate the molecular mechanisms by which dioscin acts against NAFLD in mouse models.
Main Methods:
- Utilized high-fat diet (HFD)-induced and ob/ob mouse models.
- Assessed serum and hepatic biochemical parameters.
- Analyzed mRNA and protein expression levels, including MAPK phosphorylation and autophagy markers.
Main Results:
- Dioscin treatment reduced body weight and liver lipid accumulation.
- It increased oxygen consumption and energy expenditure.
- Dioscin attenuated oxidative damage, suppressed inflammation, modulated lipid synthesis and fatty acid oxidation, and induced autophagy.
Conclusions:
- Dioscin demonstrates efficacy in preventing diet-induced obesity and NAFLD in mice.
- Its mechanism involves increasing energy expenditure and modulating key metabolic and inflammatory pathways.
- Dioscin is a potential candidate for the prevention and treatment of obesity and NAFLD.
