Journal
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
Volume 295, Issue 1, Pages E10-E16Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpendo.00011.2008
Keywords
ethanol; cytokine; triglyceride; fatty acid oxidation; fatty acid synthesis; innate immunity; endotoxin; endoplasmic reticulum stress
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Funding
- NIAAA NIH HHS [R01 AA-15070-04, AA-07611-20] Funding Source: Medline
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Many new mechanisms for alcoholic steatosis have been suggested by work reported in the last five years. These include alterations of transcriptional controls of lipid metabolism, better understanding of the effects of abnormal methionine metabolism on the endoplasmic reticulum stress response, unraveling of the basis for sensitization of the Kupffer cell to lipopolysaccharide, a better understanding of the role of cytokines and adipokines in alcoholic liver disease, and implication of the innate immune and complement systems in responses to alcohol. Much of this work has been facilitated by work with knockout mice. Undoubtedly, there are interrelationships among these various pathogenic mechanisms that ultimately will provide a more cohesive picture of how heavy alcohol use deranges hepatic lipid metabolism.
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