Microbial function, especially related to bile acid metabolism, can modulate alcohol-associated injury even in the presence of cirrhosis and alcoholic hepatitis. Microbial culture studies detect only a small number of the species of intestinal bacteria.
Loomba R, Sanyal AJ. Specific alterations in the gut—liver—brain axis that are complicit in the interactions between the gut microbiota and alcohol addiction are also reviewed.
The bacteria obtain nutrients within the protected anoxic microenvironment of the human intestine. There are thus many concerns about the public health impact of childhood obesity and its clinical consequences [ 4 ]. Fecal microbiome and volatile organic compound metabolome in obese humans with nonalcoholic fatty liver disease.
It is therefore not surprising that recent literature emphasizes a potential role for gut dysbiosis in the pathophysiology of NAFLD. It encompasses a disease spectrum ranging from simple steatosis to nonalcoholic steatohepatitis NASHwhich is histologically characterized by hepatocyte injury, inflammation and variable degrees of fibrosis.
Bosscher D, Breynaert A, Pieters L, Hermans N Food-based strategies to modulate the composition of the intestinal microbiota and their associated health effects.
Recent evidence has introduced gut microbiota as a new crucial player in this complex story. Clin Liver Dis 18 1: Metagenomic analysis and 16S ribosomal RNA gene sequencing, which is specific for prokaryotic ribosomes, have shown that Firmicutes, Bacteroidetes, Actinobacteria and Proteobacteria are the predominant bacterial phyla among the intestinal bacteria in adults [ 1718 ].
J Appl Toxicol 34 6: These findings demonstrate that host genetic background, diet, and the gut microbiota interact to influence NAFLD pathogenesis in humans, as is now known to occur in rodent models.
PubMed Google Scholar Sookoian S, Pirola CJ. Sequencing gut microbiota before the diet identified two classes of bacteria that predicted choline-deficiency-induced fatty liver: Branched-chain fatty acids, which can be de novo synthetized by several gut bacterial species, have been associated with insulin resistance and metabolic disease development [ 14 ].
HFD-related increases in liver fibrosis were associated with gut dysbiosis, especially an increase in Proteobacteria. Other potential mechanisms are emerging rapidly.
Overall, the known contributing factors are limited in their ability to explain the rising prevalence of obesity [ 7 ]. CMAJ Open 3 3: J Lipid Res 48 9: Distinctly altered gut microbiota in the progression of liver disease. Allard states that there is no conflict of interest. S CrossRef Google Scholar The severity of nonalcoholic fatty liver disease is associated with gut dysbiosis and shift in the metabolic function of the gut microbiota.
Several genes contribute to weight gain by controlling feeding behavior, energy expenditure and metabolism, but can only partially account for the development of obesity.Changes in gut microbiota due to supplemented fatty acids in diet-induced obese mice - Volume Issue 4 - Jorge R.
Mujico, Gyselle C. Baccan, Alina Gheorghe, Ligia E. Díaz, Ascensión MarcosCited by: microbiota and thereby modulate its effects on human pathophysiology. This review provides an overview of the relationship between the gut microbiota and liver diseases in orderCited by: 2.
Nonalcoholic fatty liver disease (NAFLD) is a chronic liver disorder that is increasing in prevalence with the worldwide epidemic of obesity. NAFLD is the hepatic manifestation of the metabolic. · This Review focuses on clinical studies involving the gut microbiota in patients with alcoholic liver disease across the spectrum from alcoholic fatty liver to cirrhosis and alcoholic hepatitis Cited by: 1.
Despite evidence that the intestinal microbiota (IM) is involved in the pathogenesis of obesity, the IM composition of patients with nonalcoholic fatty liver disease (NAFLD) has not. Aron-Wisnewsky J, Gaborit B, Dutour A, Clement K () Gut microbiota and non-alcoholic fatty liver disease: new insights.
Clinical microbiology and infection: the official publication of the European Society of Clinical Microbiology and Infectious Diseases 19 (4)–Cited by: 2.