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Liver Update: Relationship between Obesity, fatty liver disease and intestinal microbiota

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eMediNexus    21 May 2021

Nonalcoholic fatty liver disease (NAFLD), a chronic liver disorder has increased prevalence with the global epidemic of obesity. It is the hepatic manifestation of the metabolic syndrome is defined as a spectrum of liver pathology ranges from simple steatosis to steatosis with inflammation nonalcoholic steatohepatitis and even cirrhosis. Various genetic and environmental factors play a major role in the development of obesity and NAFLD, however, the exact mechanisms are unknown. Intestinal ecosystem includes trillions of microorganisms such as bacteria, Archaea, yeasts and viruses and several studies substantiates the relationship between the intestinal microbial changes and obesity and also its complications, including insulin resistance and NAFLD. 

As the gut and liver are interrelated with the portal venous system, liver becomes more susceptible to translocation of bacteria, bacterial products, endotoxins or secreted cytokines. Altered intestinal microbiota or dysbiosis may trigger hepatic fat deposition through several mechanisms via modulation of gut permeability, aggravating low-grade inflammation, regulation of dietary choline metabolism, modulation of bile acid metabolism and generating endogenous ethanol. 

Nutrition is the most significant environmental factor; and plays a crucial role by inducing fat accumulation in the liver and may involve interactions with the microbiota. Several animal and human studies have evaluated the possible relationships between the intestinal microbiota and NAFLD. One of such study showed that microbiota stimulated monosaccharide absorption from the intestinal lumen, enhanced de novo fatty acid synthesis and triglyceride production, which can be substantiated by increased activity of acetyl-CoA carboxylase and fatty acid synthase.

Evidences suggest that western type fat- and energy-rich diet have the potential to alter intestinal microbiota. On contrary, altered microbiota also influence the host metabolism and leads to inflammation and increased fat deposition of the body. Various experimental models showed that gut microbiota can modify host energy homeostasis and adiposity via different mechanisms, including energy harvest from the diet, lipopolysaccharides (LPSs)-induced chronic inflammation, and modulation of tissue fatty acid composition, host gene expression and gut-derived peptide secretion. Thus, modulation of gut microbiota by diet modifications or by using probiotics, prebiotics and synbiotics as a treatment for obesity and fatty liver disease might be the issue of further investigations.

Source: Arslan N. Obesity, fatty liver disease and intestinal microbiota. World J Gastroenterol. 2014 Nov 28;20(44):16452-63. 

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