Alcohol and the Intestine
- PMID: 26501334
- PMCID: PMC4693248
- DOI: 10.3390/biom5042573
Alcohol and the Intestine
Abstract
Alcohol abuse is a significant contributor to the global burden of disease and can lead to tissue damage and organ dysfunction in a subset of alcoholics. However, a subset of alcoholics without any of these predisposing factors can develop alcohol-mediated organ injury. The gastrointestinal tract (GI) could be an important source of inflammation in alcohol-mediated organ damage. The purpose of review was to evaluate mechanisms of alcohol-induced endotoxemia (including dysbiosis and gut leakiness), and highlight the predisposing factors for alcohol-induced dysbiosis and gut leakiness to endotoxins. Barriers, including immunologic, physical, and biochemical can regulate the passage of toxins into the portal and systemic circulation. In addition, a host of environmental interactions including those influenced by circadian rhythms can impact alcohol-induced organ pathology. There appears to be a role for therapeutic measures to mitigate alcohol-induced organ damage by normalizing intestinal dysbiosis and/or improving intestinal barrier integrity. Ultimately, the inflammatory process that drives progression into organ damage from alcohol appears to be multifactorial. Understanding the role of the intestine in the pathogenesis of alcoholic liver disease can pose further avenues for pathogenic and treatment approaches.
Keywords: alcohol; dysbiosis; endotoxemia; gut leakiness.
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- K23 AA019966/AA/NIAAA NIH HHS/United States
- AA023417/AA/NIAAA NIH HHS/United States
- AA018729/AA/NIAAA NIH HHS/United States
- AA020216/AA/NIAAA NIH HHS/United States
- AA013745/AA/NIAAA NIH HHS/United States
- R01 AA013745/AA/NIAAA NIH HHS/United States
- RC2 AA019405/AA/NIAAA NIH HHS/United States
- AA019936/AA/NIAAA NIH HHS/United States
- R01 AA023417/AA/NIAAA NIH HHS/United States
- RC2AA019405/AA/NIAAA NIH HHS/United States
- R21 AA018729/AA/NIAAA NIH HHS/United States
- R01 AA020216/AA/NIAAA NIH HHS/United States
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