期刊
CURRENT OPINION IN INFECTIOUS DISEASES
卷 34, 期 5, 页码 477-482出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/QCO.0000000000000759
关键词
dysbiosis; fecal microbiota transplantation; microbiome; nonalcoholic fatty liver disease; nonalcoholic steatohepatitis
资金
- Section of Gastroenterology and Hepatology at Baylor College of Medicine
Alterations in the intestinal microbiome have a strong influence on human health, including the progression of nonalcoholic fatty liver disease (NAFLD). Therapeutic interventions targeting the microbiome, such as antibiotics and probiotics, may help slow or prevent the progression of NAFLD. While evidence supporting dysbiosis-mediated NAFLD progression has been largely gathered from animal trials, more research is needed in humans to establish causality.
Purpose of review We have increasing evidence that alterations of the intestinal microbiome have a strong influence on human health. Previous work has demonstrated the association between changes in the microbiome and metabolic risk factors. One related area of interest is the relationship between dysbiosis and nonalcoholic fatty liver disease (NAFLD), as the global prevalence of NAFLD, and its resultant complications, increases. Recent findings In this review, we summarize the hypothesized pathophysiology of dysbiosis-mediated progression of NAFLD, including promotion of an inflammatory intestinal environment, increased intestinal permeability, endogenous ethanol production, short-chain fatty acid production, secondary bile acid metabolism, and choline depletion. We also review potential therapeutic interventions of the microbiome to slow or prevent NAFLD progression, including antibiotics, probiotics, prebiotics, fecal microbiota transplant, and farnesoid x receptor agonism. Much of the evidence supporting dysbiosis-mediated NAFLD progression has been gathered in high-quality animal trials. There remains a need for additional observational and randomized controlled trials in humans to establish causality between the suspected factors and pathogenesis of NAFLD.
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