There is a growing consensus that alcohol-related liver disease (ALD) should be considered a metabolic disorder under the influence of the gut-liver axis. Metabolome data have highlighted fatty acid-activated G protein-coupled receptors (GPCRs) as the main affected pathways, where the relationship of G-protein-coupled receptor 119 (GPR119) with ALD remains unexplored.
A recent publication in Science Advances has uncovered NMNAT1 as a promising therapeutic target for alcohol-associated liver disease (ALD). Early ALD can be reversible, but prolonged alcohol abuse may lead to progressive steatohepatitis, fibrosis and even cirrhosis or hepatocellular carcinoma.
Researchers have investigated the role of the voltage-dependent potassium channel Kv1.3 in vivo in a murine model of ethanol-exposed alcohol-related liver disease (ALD).
The ongoing European Association for the Study of the Liver 2024 congress in Milan opened yesterday with several presentations on cell plasticity and its role in liver function and regeneration in chronic liver disease situations.
Genome sequencing initiated to investigate how chronic liver disease leads on to hepatocellular carcinoma has instead uncovered mutations that impact fat metabolism and reduce the sensitivity of hepatocytes to insulin.
