Abstract
Non-alcoholic fatty liver disease (NAFLD) is a multifactorial disease in which environmental and genetic factors are involved. Although the molecular mechanisms involved in NAFLD onset and progression are not completely understood, the gut microbiome (GM) is thought to play a key role in the process, influencing multiple physiological functions. GM alterations in diversity and composition directly impact disease states with an inflammatory course, such as non-alcoholic steatohepatitis (NASH). However, how the GM influences liver disease susceptibility is largely unknown. Similarly, the impact of strategies targeting the GM for the treatment of NASH remains to be evaluated. This review provides a broad insight into the role of gut microbiota in NASH pathogenesis, as a diagnostic tool, and as a therapeutic target in this liver disease. We highlight the idea that the balance in metabolic fermentations can be key in maintaining liver homeostasis. We propose that an overabundance of alcohol-fermentation pathways in the GM may outcompete healthier, acid-producing members of the microbiota. In this way, GM ecology may precipitate a self-sustaining vicious cycle, boosting liver disease progression.
Highlights
Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease worldwide
NAFLD includes a spectrum of pathological situations, ranging from simple steatosis to non-alcoholic steatohepatitis (NASH), fibrosis and cirrhosis
It is widely accepted that changes to the composition and function of the gut microbiome (GM) are associated with NAFLD
Summary
Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease worldwide. Restricting the analysis to changes in diversity indices or comparisons at the phylum and other high-rank taxonomic levels is unlikely to yield insight into the molecular mechanisms involved For these reasons, we are in need of approaches able to infer causal links, rather than mere statistical associations between specific bacterial species and liver conditions. This effect is probably mediated clinical trial demonstrated that patients with type 2 diabetes under a high-fiber diet showed significant improvement in hemoglobin A1c (HbA1c) levels This effect is probably mediated by an increase in acetate- and butyrate-producing gut bacterial strains, accompanied by increased GLP-1 production [69]. Higher fecal SCFA concentrations were found in genetically obese mice, and were associated with increased gut permeability, excess adiposity and cardiometabolic risk factors [7,70]
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