4.7 Review

Insights into the Impact of Microbiota in the Treatment of NAFLD/NASH and Its Potential as a Biomarker for Prognosis and Diagnosis

Journal

BIOMEDICINES
Volume 9, Issue 2, Pages -

Publisher

MDPI
DOI: 10.3390/biomedicines9020145

Keywords

non-alcoholic steatohepatitis; intestinal permeability; microbiota; probiotics; physical exercise; fecal microbiota transplantation

Funding

  1. National Agency for Research and Development (ANID) BECAS Chile [72180543]
  2. Fundacion Ramon Areces, Madrid, Spain
  3. 'Fundacion Alfonso Martin Escudero' (Spain)

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Non-alcoholic fatty liver disease (NAFLD) is linked to obesity and metabolic disorders, leading to the more severe non-alcoholic steatohepatitis (NASH) which increases the risks of cirrhosis, liver failure, and hepatocellular carcinoma. Liver steatosis is associated with certain markers, but imaging methods are inaccurate, while changes in gut microbiota are related to NAFLD/NASH.
Non-alcoholic fatty liver disease (NAFLD) is an increasing cause of chronic liver illness associated with obesity and metabolic disorders, such as hypertension, dyslipidemia, or type 2 diabetes mellitus. A more severe type of NAFLD, non-alcoholic steatohepatitis (NASH), is considered an ongoing global health threat and dramatically increases the risks of cirrhosis, liver failure, and hepatocellular carcinoma. Several reports have demonstrated that liver steatosis is associated with the elevation of certain clinical and biochemical markers but with low predictive potential. In addition, current imaging methods are inaccurate and inadequate for quantification of liver steatosis and do not distinguish clearly between the microvesicular and the macrovesicular types. On the other hand, an unhealthy status usually presents an altered gut microbiota, associated with the loss of its functions. Indeed, NAFLD pathophysiology has been linked to lower microbial diversity and a weakened intestinal barrier, exposing the host to bacterial components and stimulating pathways of immune defense and inflammation via toll-like receptor signaling. Moreover, this activation of inflammation in hepatocytes induces progression from simple steatosis to NASH. In the present review, we aim to: (a) summarize studies on both human and animals addressed to determine the impact of alterations in gut microbiota in NASH; (b) evaluate the potential role of such alterations as biomarkers for prognosis and diagnosis of this disorder; and (c) discuss the involvement of microbiota in the current treatment for NAFLD/NASH (i.e., bariatric surgery, physical exercise and lifestyle, diet, probiotics and prebiotics, and fecal microbiota transplantation).

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