Glycine accelerates recovery from alcohol-induced liver injury

J Pharmacol Exp Ther. 1998 Aug;286(2):1014-9.


Glycine prevents hepatic damage caused by hypoxia-reoxygenation, diminishes mortality due to endotoxin and minimizes alcoholic liver injury by decreasing blood ethanol. Our purpose was to investigate the effect of dietary glycine during recovery from early alcohol-induced injury, using a model that mimics the clinical presentation and histopathology with alcoholics. Male Wistar rats were exposed to ethanol continuously for 6 wk via intragastric feeding that resulted in typical histology of alcoholic liver injury, including steatosis, inflammation, necrosis and increased serum levels of aspartate aminotransferase and alanine aminotransferase. After cessation of ethanol, one group of rats received a control diet, the other a glycine-containing diet for 2 wk. During this period, all parameters studied tended to return to baseline values. However, serum aspartate aminotransferase and alanine aminotransferase recovered about 30% more rapidly in rats fed glycine. Further, the hepatic pathology score was also significantly lower in the glycine group than in controls (0.5 vs. 2.6). After 1 wk, steatosis was reduced significantly more in the glycine group (5. 6%) than in controls (8.9%). Glycine also diminished numbers of infiltrating leukocytes and necrotic cells significantly more than in controls. This beneficial effect of glycine may be partly explained by the fact that glycine increased influx of chloride into Kupffer cells leading to diminished tumor necrosis factor-alpha production. These results indicate that a glycine containing diet expedites the process of recovery from ethanol-induced liver injury and may lead to its clinical application in alcoholic hepatitis.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Alanine Transaminase / blood
  • Animals
  • Aspartate Aminotransferases / blood
  • Central Nervous System Depressants / toxicity*
  • Central Nervous System Depressants / urine
  • Chemical and Drug Induced Liver Injury / drug therapy*
  • Chemical and Drug Induced Liver Injury / pathology
  • Chlorides / metabolism
  • Diet
  • Ethanol / toxicity*
  • Ethanol / urine
  • Glycine / therapeutic use*
  • Image Processing, Computer-Assisted
  • Kupffer Cells / drug effects
  • Kupffer Cells / metabolism
  • Leukocyte Count / drug effects
  • Liver / pathology
  • Male
  • Rats
  • Rats, Wistar
  • Tumor Necrosis Factor-alpha / biosynthesis


  • Central Nervous System Depressants
  • Chlorides
  • Tumor Necrosis Factor-alpha
  • Ethanol
  • Aspartate Aminotransferases
  • Alanine Transaminase
  • Glycine