Abstract
Alcoholic liver disease (ALD) comprises a spectrum of liver pathology, including steatosis, steatohepatitis, and cirrhosis. Previous work from our group and others suggests that dietary fat, both the amount and composition, plays a pivotal role in ALD development and progression; however, the impact of specific dietary fatty acids on ALD pathogenesis is not fully elucidated. Preclinical rodent models of ALD revealed the deleterious effects of omega-6 polyunsaturated fatty acids (n-6 PUFAs), specifically linoleic acid (LA), and this may be partially attributed to the increased levels of pro-inflammatory oxidized LA metabolites. There is limited understanding regarding the role of omega-3 polyunsaturated fatty acids (n-3 PUFAs, such as alpha-linolenic acid, eicosapentaenoic acid, and docosahexaenoic acid), and bioactive n-3 PUFA-derived lipid molecules in ALD. Given that majority of n-6 and n-3 PUFAs-derived metabolites are potent endogenous signaling molecules, knowledge regarding the changes in these lipid mediators may shed new light on the mechanisms contributing to ALD pathogenesis and reveal novel therapeutic targets and biomarkers of this disease. The current review summarizes relevant scientific literature regarding the role of dietary fat, distinct fatty acids, and bioactive fatty acid metabolites in ALD, and highlights recent advances in the field.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
