Preclinical study reveals how alcohol promotes fat buildup in liver
Cedars-Sinai investigators have discovered a signaling interaction between two proteins in cells that controls fat accumulation in the livers of laboratory mice with alcohol-associated liver disease. The findings point to a potential method to reduce liver damage in patients with the condition.
Excessive fat in the liver is an early characteristic of alcohol-associated liver disease, which is the most frequent underlying cause of alcohol-associated deaths, according to the U.S. Centers for Disease Control and Prevention.
The new study found that a specific cellular signaling pathway, which helps maintain normal fat levels in the liver, was suppressed in alcohol-associated liver disease mice. The findings were published in the journal Signal Transduction and Targeted Therapy.
"Therapeutic approaches that control fat accumulation may be able to stop liver disease from progressing to a more advanced state," said Komal Ramani, Ph.D., associate professor of Medicine and Biomedical Sciences, member of the Karsh Division of Gastroenterology and Hepatology in the Department of Medicine at Cedars-Sinai and corresponding author of the study.
"Based on our research, one possible treatment could involve creating a drug to mimic the interaction that is integral to the signaling pathway, to normalize fat levels in the liver."
