Glycine attenuates high fructose-induced liver injury in adolescent mice by modulating lipid metabolism and gut microbiota

Abstract

Glycine is a functional amino acid and its beneficial effects have been widely reported. However, it is unclear whether glycine has preventive effects on fructose-induced adverse metabolic consequences. Therefore, in this study, we explored the preventive effects and potential mechanisms of glycine against high fructose exposure-induced hepatic steatosis and metabolic disorders in adolescent mice. The results showed that high fructose exposure induced a significant increase in triglyceride levels as well as lipid droplet accumulation in the liver of adolescent mice, and glycine supplementation reversed these adverse changes. In addition, glycine supplementation alleviated fructose-induced liver inflammation, apoptosis, and oxidative stress. Further results revealed that the antioxidant function of glycine may be related to its role in enhancing hepatic antioxidant enzymes activity and promoting glutathione synthesis. Furthermore, we found that glycine supplementation significantly increased the expression of genes and proteins related to fatty acid β-oxidation, which is a key pathway in the regulation of hepatic lipid content. Importantly, our results showed that glycine supplementation inhibited the activation of MAPK cascade proteins induced by fructose. Finally, the results of 16S rRNA analysis of cecal contents revealed that glycine supplementation ameliorated fructose-induced disturbances in the composition and structure of the gut microbiota. In conclusion, our study showed that glycine has preventive activity on high fructose exposure-induced hepatic steatosis and injury in adolescent mice.