Published online Nov 15, 2014. doi: 10.4291/wjgp.v5.i4.514
Revised: July 1, 2014
Accepted: September 6, 2014
Published online: November 15, 2014
Processing time: 179 Days and 4.7 Hours
Alcohol consumption is one of the leading causes of liver diseases and liver-related death worldwide. The gut is a habitat for billions of microorganisms which promotes metabolism and digestion in their symbiotic relationship with the host. Alterations of gut microbiome by alcohol consumption are referred to bacterial overgrowth, release of bacteria-derived products, and/or changed microbiota equilibrium. Alcohol consumption also perturbs the function of gastrointestinal mucosa and elicits a pathophysiological condition. These adverse effects caused by alcohol may ultimately result in a broad change of gastrointestinal luminal metabolites such as bile acids, short chain fatty acids, and branched chain amino acids. Gut microbiota alterations, metabolic changes produced in a dysbiotic intestinal environment, and the host factors are all critical contributors to the development and progression of alcoholic liver disease. This review summarizes recent findings of how alcohol-induced alterations of gut microbiota and metabolome, and discusses the mechanistic link between gastrointestinal dyshomeostasis and alcoholic liver injury.
Core tip: Excessive alcohol consumption causes alcoholic liver disease (ALD) with the mechanisms of pathogenesis largely unknown. Alterations of gut microbiota and metabolites are critical contributors to the development of ALD, which may lead to identification of therapeutic targets for ALD. This review summarizes recent findings of how alcohol-induced alterations of gut microbiota and metabolome, and discusses the mechanistic link between gastrointestinal dyshomeostasis and alcoholic liver injury.