Potent effects of dioscin against obesity in mice.

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.

• Authors: Min Liu, Lina Xu, Lianhong Yin, Yan Qi, Youwei Xu, Xu Han, Yanyan Zhao, Huijun Sun, Jihong Yao, Yuan Lin, Kexin Liu, Jinyong Peng
• Journal: Scientific reports (Sci Rep) Vol. 5 Pg. 7973 (Jan 22 2015) ISSN: 2045-2322 [Electronic] England
• PMID: 25609476 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Blood Glucose
• Fatty Acids
• Triglycerides
• dioscin
• Cholesterol
• Diosgenin

Topics

• Animals
• Autophagy (drug effects)
• Blood Glucose (metabolism)
• Body Weight (drug effects)
• Cholesterol (biosynthesis)
• Diet, High-Fat
• Diosgenin (analogs & derivatives, pharmacology, therapeutic use)
• Energy Metabolism
• Fatty Acids (biosynthesis)
• Glucose Tolerance Test
• Inflammation (genetics, pathology)
• Liver (drug effects, pathology)
• MAP Kinase Signaling System (drug effects)
• Male
• Mice, Inbred C57BL
• Mice, Obese
• Obesity (blood, drug therapy)
• Oxidative Stress (drug effects)
• Phosphorylation (drug effects)
• Signal Transduction (drug effects)
• Triglycerides (biosynthesis)