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Lipid accumulation in the liver due to chronic alcohol consumption (CAC) is crucial in the development of alcohol liver disease (ALD). It is promoted by the NADH/NAD ratio increase via alcohol dehydrogenase (ADH)-dependent alcohol metabolism and lipogenesis increase via peroxisome proliferator-activated receptor γ (PPARγ) in the liver. The transcriptional activity of PPARγ on lipogenic genes is inhibited by S-nitrosylation but activated by denitrosylation via S-nitrosoglutathione reductase (GSNOR), an enzyme identical to ADH3. Besides ADH1, ADH3 also participates in alcohol metabolism. Therefore, we investigated the specific contribution of ADH3 to ALD onset. ADH3-knockout () and wild-type (WT) mice were administered a 10% ethanol solution for 12 months. exhibited no significant pathological changes in the liver, whereas WT exhibited marked hepatic lipid accumulation ( < 0.005) with increased serum transaminase levels. exhibited no death during CAC, whereas WT exhibited a 40% death. Liver mRNA levels were elevated by CAC in WT ( < 0.01). The alcohol elimination rate measured after injecting 4 g/kg ethanol was not significantly different between two strains, although the rate was increased in both strains by CAC. Thus, ADH3 plays a key role in the ALD onset, likely by acting as GSNOR.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10419236 | PMC |
| http://dx.doi.org/10.3390/ijms241512102 | DOI Listing |
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