Glycine Stabilize the Tissue Fatty Acid Composition in an Experimental Model of Alcohol-Induced Hepatotoxicity

Abstract

Background and Aim: The aim of the present study was to investigate the effect of the administration of glycine, a non-essential amino acid on tissue fatty acid composition in experimental rats.Methods: Liver cell damage was induced by the administration of ethanol (7.9 g/kg b.w.) for 30 days by intragastric intubation. Control rats were given isocaloric glucose solution. Glycine was subsequently administered at a dose of 0.6 g/kg bodyweight every day by intragastric intubation for the next 30 days.Results: Feeding alcohol significantly elevated the activities of serum aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatases (ALP) and gamma-glutamyl transpeptidase (GGT) and altered the liver and brain fatty acid composition compared with control rats. Subsequently, glycine supplementation to alcohol-fed rats significantly lowered the activities of serum AST, ALT, ALP, GGT and normalized the liver fatty acid composition compared with untreated alcohol-fed rats.Conclusion: The present study demonstrates that oral administration of glycine confers a significant protective effect against alcohol-induced hepatotoxicity by virtue of its ability to optimize the activities of serum AST, ALT, ALP and GGT, as well as the tissue fatty acid composition. Background and Aim: The aim of the present study was to investigate the effect of the administration of glycine, a non-essential amino acid on tissue fatty acid composition in experimental rats. Methods: Liver cell damage was induced by the administration of ethanol (7.9 g/kg b.w.) for 30 days by intragastric intubation. Control rats were given isocaloric glucose solution. Glycine was subsequently administered at a dose of 0.6 g/kg bodyweight every day by intragastric intubation for the next 30 days. Results: Feeding alcohol significantly elevated the activities of serum aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatases (ALP) and gamma-glutamyl transpeptidase (GGT) and altered the liver and brain fatty acid composition compared with control rats. Subsequently, glycine supplementation to alcohol-fed rats significantly lowered the activities of serum AST, ALT, ALP, GGT and normalized the liver fatty acid composition compared with untreated alcohol-fed rats. Conclusion: The present study demonstrates that oral administration of glycine confers a significant protective effect against alcohol-induced hepatotoxicity by virtue of its ability to optimize the activities of serum AST, ALT, ALP and GGT, as well as the tissue fatty acid composition.