Diet, Gut Microbiota and Non-Alcoholic Fatty Liver Disease: Three Parts of the Same Axis

Abstract

Non-Alcoholic Fatty Liver Disease (NAFLD) is the most common liver disease in the world. NAFLD is principally characterized by an excessive fat accumulation in the hepatocytes. Diet is considered as one of the main drivers to modulate the composition of gut microbiota, which participate in different processes, affecting human metabolism. A disruption in the homeostasis of gut microbiota may lead to dysbiosis, which is commonly reflected by a reduction of the beneficial species and an increment in pathogenic microbiota. Gut and liver are in close relation due to the anatomical and functional interactions led by the portal vein, thus altered intestinal microbiota might affect liver functions, promoting inflammation, insulin resistance and steatosis, which is translated into NAFLD. This review will highlight the association between diet, gut microbiota and liver, and how this axis may promote the development of NAFLD progression, discussing potential mechanisms and alterations due to the dysbiosis of gut microbiota. Finally, it will revise the variations in gut microbiota composition in NAFLD, and it will focus in specific species, which directly affect NAFLD progression.

Detection of Early Disease Risk Factors Associated with Metabolic Syndrome: A New Era with the NMR Metabolomics Assessment

“…Dysbiosis of the gut microbiota, which is an alteration of the bacterial intestinal composition, reflexed a decreasing number of species related to an increased intestinal barrier permeability, thus allowing the bacterial translocation and causing endotoxemia [211], which is an important risk factor for obesity development and related metabolic diseases, as it is confirmed in different studies [212]. The constant flow in the composition of the gut microbiota is due to changes in diet, environmental factors and lifestyle [213]. As an intrinsic factor, the immune system health may cause changes in gut microbiota composition that may promote the proliferation of specific bacterial species which could be harmful due to the immune deficiency or hyperimmunity [214].…”

Diet‐induced rodent models of obesity‐related metabolic disorders—A guide to a translational perspective

“…Overall, oxidative imbalance, low-grade inflammation, plasmatic and/or hepatic dyslipidaemia, impaired incretin effect, gut microbiota changes, endoplasmic reticulum stress and/or mitochondrial dysfunction are common cellular denominators of obesity-related metabolic diseases. [28][29][30][31] Similar to that in humans, chronic consumption of diets rich in fat and sugar leads to deleterious metabolic effects in rodents, despite differing responsiveness among species and strains. Thus, paradigms of longstanding free access to palatable calorie-dense food are widely used in preclinical research to model the progression of obesity and related comorbidities.…”

Liver-specific knockdown of ANGPTL8 alters the structure of the gut microbiota in mice

“…In the present study, the results illustrated that ANGP TL8 is a possible mediator of the crosstalk between the liver and the gut. There are multiple intestinal factors that act on the liver through the portal circulation, such as LPS and SCFAs, whereas bile acids are the only well-established hepatogenic molecules that are able to regulate the gut microbiota from the liver (Quesada-Vazquez et al 2020). ANGPTL8 is a novel hepatokine that exists in the circulatory system and is regarded as a hormone that is directly associated with the endocrine system.…”

“…However, previous studies have shown that the liver tissue influences the structure of the gut microbiota through secreting bile acids. Abnormal secretion of bile acids plays an important role in the dysbiosis of gut microbiota (Quesada-Vazquez et al 2020).…”