1Department of Health Sciences, University "Magna Græcia", 88100 Catanzaro, Italy.
2Internal Medicine Residency Program, Università Politecnica delle Marche, 60121 Ancona, Italy.
3Clinical Nutrition Unit, Fondazione Policlinico A. Gemelli IRCCS, 00168 Rome, Italy.
4Department of Translational Medicine and Surgery, Università Cattolica del Sacro Cuore, 00168 Rome, Italy.
5T.A.R.G.I.D., Gasthuisberg University Hospital, KU Leuven, Herestraat 49, 3000 Leuven, Belgium.
6Clinical Nutrition and Internal Medicine Unit, "Madonna del Soccorso" General Hospital, 63074 San Benedetto del Tronto, Italy.
7Hepatology and Internal Medicine Unit, "Madonna del Soccorso" General Hospital, 63074 San Benedetto del Tronto, Italy.
8Healthcare Genetics and Genomics Doctoral Program, School of Nursing, College of Behavioral, Social and Health Sciences, Clemson University, 105 Sikes Hall, Clemson, SC 29631, USA.
Introduction: Gut microbiota is not only a taxonomic biologic ecosystem but is also involved in human intestinal and extra-intestinal functions such as immune system modulation, nutrient absorption and digestion, as well as metabolism regulation. The latter is strictly linked to non-alcoholic fatty liver disease (NAFLD) pathophysiology. Materials and methods: We reviewed the literature on the definition of gut microbiota, the concepts of "dysbiosis" and "eubiosis", their role in NAFLD pathogenesis, and the data on fecal microbiota transplantation (FMT) in these patients. We consulted the main medical databases using the following keywords, acronyms, and their associations: gut microbiota, eubiosis, dysbiosis, bile acids, NAFLD, and FMT. Results: Gut microbiota qualitative and quantitative composition is different in healthy subjects vs. NALFD patients. This dysbiosis is associated with and involved in NAFLD pathogenesis and evolution to non-acoholic steatohepatitis (NASH), liver cirrhosis, and hepatocellular carcinoma (HCC). In detail, microbial-driven metabolism of bile acids (BAs) and interaction with hepatic and intestinal farnesoid nuclear X receptor (FXR) have shown a determinant role in liver fat deposition and the development of fibrosis. Over the use of pre- or probiotics, FMT has shown preclinical and initial clinical promising results in NAFLD treatment through re-modulation of microbial dysbiosis. Conclusions: Promising clinical data support a larger investigation of gut microbiota dysbiosis reversion through FMT in NAFLD using randomized clinical trials to design precision-medicine treatments for these patients at different disease stages.