scholarly journals FATTY LIVER AND GUT MICROBIOTA: A NEW MULTI-DIMENSIONAL APPROACH FOR PERSONALIZED PREVENTIVE MEDICINE

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
F. Bonino ◽  
M. Pane ◽  
A. Amoruso ◽  
M.R. Brunetto

Cardiovascular, degenerative, hepato-digestive, metabolic and neoplastic diseases are major causes of death; all of them are beckoned years before by fatty liver that can quantify by non-invasive ultrasound methods. Such a measure is sensitive and reproducible and qualifies as mirror of general health to monitor the efficacy of preventive care in pre-symptomatic subjects. One major determinant of alimentary and general health is the gut microbiota that regulates hepatic gene expression, lipid metabolism and contributes to hepatic inflammation and obesity. The microbiota can be dynamically modified by probiotic/ prebiotic supplementation, however a direct gut microbiota profiling by stool metagenomics is limited by sampling error. The study of blood and/or saliva metabolites (metabolomics) and circulating antimicrobial antibodies provide an indirect microbiota profiling. Studies need to be performed to test whether variation of metabolomics and antimicrobial antibody levels correlate with the in vivo bacteria dynamics. The non-invasive measure of fatty liver in combination with of the gut microbiota characterization by metagenomics, metabolomics and anti-microbial enzyme immune assays will provide an innovative technological approach to stratify individuals with fatty liver for both prevention, outcome prediction and personalized treatment and to identify new aetiologies, diagnostic and prognostic biomarkers and therapeutic targets

2019 ◽  
Vol 12 (5) ◽  
pp. dmm039206 ◽  
Author(s):  
Sara Carbajo-Pescador ◽  
David Porras ◽  
María Victoria García-Mediavilla ◽  
Susana Martínez-Flórez ◽  
María Juarez-Fernández ◽  
...  

Nutrients ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 2837 ◽  
Author(s):  
Chencheng Xie ◽  
Dina Halegoua-DeMarzio

Non-alcoholic fatty liver disease (NAFLD) is the hepatic consequence of metabolic syndrome, which often also includes obesity, diabetes, and dyslipidemia. The connection between gut microbiota (GM) and NAFLD has attracted significant attention in recent years. Data has shown that GM affects hepatic lipid metabolism and influences the balance between pro/anti-inflammatory effectors in the liver. Although studies reveal the association between GM dysbiosis and NAFLD, decoding the mechanisms of gut dysbiosis resulting in NAFLD remains challenging. The potential pathophysiology that links GM dysbiosis to NAFLD can be summarized as: (1) disrupting the balance between energy harvest and expenditure, (2) promoting hepatic inflammation (impairing intestinal integrity, facilitating endotoxemia, and initiating inflammatory cascades with cytokines releasing), and (3) altered biochemistry metabolism and GM-related metabolites (i.e., bile acid, short-chain fatty acids, aromatic amino acid derivatives, branched-chain amino acids, choline, ethanol). Due to the hypothesis that probiotics/synbiotics could normalize GM and reverse dysbiosis, there have been efforts to investigate the therapeutic effect of probiotics/synbiotics in patients with NAFLD. Recent randomized clinical trials suggest that probiotics/synbiotics could improve transaminases, hepatic steatosis, and reduce hepatic inflammation. Despite these promising results, future studies are necessary to understand the full role GM plays in NAFLD development and progression. Additionally, further data is needed to unravel probiotics/synbiotics efficacy, safety, and sustainability as a novel pharmacologic approaches to NAFLD.


2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Gemma Aragonès ◽  
Sergio González-García ◽  
Carmen Aguilar ◽  
Cristóbal Richart ◽  
Teresa Auguet

Nonalcoholic fatty liver disease (NAFLD) is a common, multifactorial, and poorly understood liver disease whose incidence is globally rising. During the past decade, several lines of evidence suggest that dysbiosis of intestinal microbiome represents an important factor contributing to NAFLD occurrence and its progression into NASH. The mechanisms that associate dysbiosis with NAFLD include changes in microbiota-derived mediators, deregulation of the gut endothelial barrier, translocation of mediators of dysbiosis, and hepatic inflammation. Changes in short chain fatty acids, bile acids, bacterial components, choline, and ethanol are the result of altered intestinal microbiota. We perform a narrative review of the previously published evidence and discuss the use of gut microbiota-derived mediators as potential markers in NAFLD.


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