Katharina Brandl1, Bernd Schnabl. 1. aSkaggs School of Pharmacy and Pharmaceutical Sciences, University of California San Diego bDepartment of Medicine, University of California San Diego, La Jolla, California, USA cDepartment of Medicine, VA San Diego Healthcare System, San Diego, California, USA.
Abstract
PURPOSE OF REVIEW: Nonalcoholic fatty liver disease (NAFLD) is a liver disease with high prevalence in western countries. Progression from NAFLD to nonalcoholic steatohepatitis (NASH) occurs in 10-20%. NASH pathogenesis is multifactorial including genetic and environmental factors. The gut microbiota is involved in disease progression and its role is complex. RECENT FINDINGS: NASH is associated with changes in the intestinal microbiota, although findings in recent studies are inconsistent. Dysbiosis can trigger intestinal inflammation and impair the gut barrier. Microbial products can now reach the liver, induce hepatic inflammation and contribute to NAFLD and NASH progression. As the gut microbiota is also involved in the regulation of metabolic pathways, metabolomic approaches identified unique metabolomic profiles in patients with NASH. Altered metabolite patterns can serve as biomarkers, whereas specific metabolites (such as ethanol) have been linked with disease progression. Modifying metabolic profiles might serve as new therapeutic microbiome-based approaches. SUMMARY: In this review, we will highlight findings from the recent literature important to the gut-liver axis. We will predominantly focus on human studies with NASH.
PURPOSE OF REVIEW: Nonalcoholic fatty liver disease (NAFLD) is a liver disease with high prevalence in western countries. Progression from NAFLD to nonalcoholic steatohepatitis (NASH) occurs in 10-20%. NASH pathogenesis is multifactorial including genetic and environmental factors. The gut microbiota is involved in disease progression and its role is complex. RECENT FINDINGS: NASH is associated with changes in the intestinal microbiota, although findings in recent studies are inconsistent. Dysbiosis can trigger intestinal inflammation and impair the gut barrier. Microbial products can now reach the liver, induce hepatic inflammation and contribute to NAFLD and NASH progression. As the gut microbiota is also involved in the regulation of metabolic pathways, metabolomic approaches identified unique metabolomic profiles in patients with NASH. Altered metabolite patterns can serve as biomarkers, whereas specific metabolites (such as ethanol) have been linked with disease progression. Modifying metabolic profiles might serve as new therapeutic microbiome-based approaches. SUMMARY: In this review, we will highlight findings from the recent literature important to the gut-liver axis. We will predominantly focus on human studies with NASH.
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