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Targeting the gut barrier for the treatment of alcoholic liver disease.
Liver Res 2017; 1(4):197-207LR

Abstract

Alcohol consumption remains one of the predominant causes of liver disease and liver-related death worldwide. Intriguingly, dysregulation of the gut barrier is a key factor promoting the pathogenesis of alcoholic liver disease (ALD). A functional gut barrier, which consists of a mucus layer, an intact epithelial monolayer and mucosal immune cells, supports nutrient absorption and prevents bacterial penetration. Compromised gut barrier function is associated with the progression of ALD. Indeed, alcohol consumption disrupts the gut barrier, increases gut permeability, and induces bacterial translocation both in ALD patients and in experimental models with ALD. Moreover, alcohol consumption also causes enteric dysbiosis with both numerical and proportional perturbations. Here, we review and discuss mechanisms of alcohol-induced gut barrier dysfunction to better understand the contribution of the gut-liver axis to the pathogenesis of ALD. Unfortunately, there is no effectual Food and Drug Administration-approved treatment for any stage of ALD. Therefore, we conclude with a discussion of potential strategies aimed at restoring the gut barrier in ALD. The principle behind antibiotics, prebiotics, probiotics and fecal microbiota transplants is to restore microbial symbiosis and subsequently gut barrier function. Nutrient-based treatments, such as dietary supplementation with zinc, niacin or fatty acids, have been shown to regulate tight junction expression, reduce intestinal inflammation, and prevent endotoxemia as well as liver injury caused by alcohol in experimental settings. Interestingly, saturated fatty acids may also directly control the gut microbiome. In summary, clinical and experimental studies highlight the significance and efficacy of the gut barrier in treating ALD.

Authors+Show Affiliations

Center for Translational Biomedical Research, School of Health and Human Sciences, University of North Carolina at Greensboro, Kannapolis, NC, USA. Department of Nutrition, School of Health and Human Sciences, University of North Carolina at Greensboro, Greensboro, NC, USA.Center for Translational Biomedical Research, School of Health and Human Sciences, University of North Carolina at Greensboro, Kannapolis, NC, USA.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

30034913

Citation

Zhou, Zhanxiang, and Wei Zhong. "Targeting the Gut Barrier for the Treatment of Alcoholic Liver Disease." Liver Research, vol. 1, no. 4, 2017, pp. 197-207.
Zhou Z, Zhong W. Targeting the gut barrier for the treatment of alcoholic liver disease. Liver Res. 2017;1(4):197-207.
Zhou, Z., & Zhong, W. (2017). Targeting the gut barrier for the treatment of alcoholic liver disease. Liver Research, 1(4), pp. 197-207. doi:10.1016/j.livres.2017.12.004.
Zhou Z, Zhong W. Targeting the Gut Barrier for the Treatment of Alcoholic Liver Disease. Liver Res. 2017;1(4):197-207. PubMed PMID: 30034913.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Targeting the gut barrier for the treatment of alcoholic liver disease. AU - Zhou,Zhanxiang, AU - Zhong,Wei, PY - 2018/7/24/entrez PY - 2018/7/24/pubmed PY - 2018/7/24/medline KW - Alcoholic liver disease (ALD) KW - Dietary intervention KW - Gut barrier KW - Gut hyperpermeability KW - Microbiota treatment SP - 197 EP - 207 JF - Liver research JO - Liver Res VL - 1 IS - 4 N2 - Alcohol consumption remains one of the predominant causes of liver disease and liver-related death worldwide. Intriguingly, dysregulation of the gut barrier is a key factor promoting the pathogenesis of alcoholic liver disease (ALD). A functional gut barrier, which consists of a mucus layer, an intact epithelial monolayer and mucosal immune cells, supports nutrient absorption and prevents bacterial penetration. Compromised gut barrier function is associated with the progression of ALD. Indeed, alcohol consumption disrupts the gut barrier, increases gut permeability, and induces bacterial translocation both in ALD patients and in experimental models with ALD. Moreover, alcohol consumption also causes enteric dysbiosis with both numerical and proportional perturbations. Here, we review and discuss mechanisms of alcohol-induced gut barrier dysfunction to better understand the contribution of the gut-liver axis to the pathogenesis of ALD. Unfortunately, there is no effectual Food and Drug Administration-approved treatment for any stage of ALD. Therefore, we conclude with a discussion of potential strategies aimed at restoring the gut barrier in ALD. The principle behind antibiotics, prebiotics, probiotics and fecal microbiota transplants is to restore microbial symbiosis and subsequently gut barrier function. Nutrient-based treatments, such as dietary supplementation with zinc, niacin or fatty acids, have been shown to regulate tight junction expression, reduce intestinal inflammation, and prevent endotoxemia as well as liver injury caused by alcohol in experimental settings. Interestingly, saturated fatty acids may also directly control the gut microbiome. In summary, clinical and experimental studies highlight the significance and efficacy of the gut barrier in treating ALD. SN - 2096-2878 UR - https://www.unboundmedicine.com/medline/citation/30034913/Targeting_the_gut_barrier_for_the_treatment_of_alcoholic_liver_disease_ L2 - https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/30034913/ DB - PRIME DP - Unbound Medicine ER -