ArticleJournal of clinical biochemistry and nutrition2011
p59fyn is associated with the development of hepatic steatosis due to chronic ethanol consumption.
Article in Journal of clinical biochemistry and nutrition, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 6 citations in OpenAlex.
- Fyn Kinase: A Potential Target in Glucolipid Metabolism and Diabetes Mellitus.Current issues in molecular biology · 2025Review
- The Src family kinase Fyn mediates hyperosmolarity-induced Mrp2 and Bsep retrieval from canalicular membrane.The Journal of biological chemistry · 2011Article
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7 authors at 1 institution in 1 country.
Funding
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Abstract
p59fyn, a protein tyrosine kinase belonging to the src-family, is involved in the regulatory mechanism of acute response to ethanol in the central nervous system. A previous report showed an association between src-family kinase activity and fatty acid oxidation, and it also reported that hepatic free fatty acid levels were low in Fyn-/- mice. We examined, using Fyn-/- mice whether Fyn is also involved in fatty acid metabolism and the development of pathological changes in the liver in response to chronic ethanol consumption. C57BL/6J Fyn-/- and Fyn+/+ mice were fed for 8 weeks with either a liquid diet comprising ethanol or one in which the calories from ethanol were replaced with carbohydrates. Chronic ethanol consumption for 8 weeks resulted in remarkable hepatic steatosis in Fyn+/+ mice but not in Fyn-/- mice. Chronic ethanol consumption induced a significant decrease in hepatic FFA and triglyceride levels in Fyn-/- mice. Levels of interleukin-6, which is associated with the enhancement of fatty acid oxidation, was also increased significantly in the livers of ethanol-fed Fyn-/- mice. The results suggest that Fyn is involved in the enhancement of fatty acid oxidation and the development of hepatic steatosis caused by chronic ethanol consumption.
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