Role Of Methionine Metabolism Abnormity In Pathogenic Mechanism Of Progression Of Alcoholic Fatty Liver Diseases

Objective To explore the mechanism of methionine metabolism disturbances in the pathogenesis of AFL. Methods To establish an animal model of AFL, and measured the amino acids related with methionine metabolism in AFL rats, then investigated the prevention and treatment of Nutrients intervention on AFL rats, finally explored mechanism of SAM and Hcy in the pathogenesis of AFL. Results The amino acids related with methionine metabolism in serum and liver have greatly changed in AFL rats. The nutrients correcting methionine metabolism abnormity could prevent and treate AFL, and ameliorated symptom of AFL markedly. Hcy increased the expressions of SREBP-1 mRNA and MTT value, and decrease of hepatic SAM aggravated liver oxidation injury. Conclusion The possible mechanism of methionine metabolism abnormity was that Hcy increased the expressions of SREBP-1 mRNA, which regulated TG and FFA synthesis, in turn, to a fatty liver. In addition, Hcy self aggravated liver damage. Decrease of hepatic SAM aggravated liver oxidation injury, and SAM possibly protected against liver damage because of antioxidation.