Abstract
Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease worldwide as a result of the increasing prevalence of obesity, starting from early life stages. It is characterized by a spectrum of liver diseases ranging from simple fatty liver (NAFL) to steatohepatitis (NASH), with a possible progression to fibrosis, thus increasing liver-related morbidity and mortality. NAFLD development is driven by the co-action of several risk factors, including obesity and metabolic syndrome, which may be both genetically induced and diet-related. Recently, particular attention has been paid to the gut-liver axis, which may play a physio-pathological role in the onset and progression of the disease. The gut microbiota is intended to act as a bioreactor that can guarantee autonomous metabolic and immunological functions and that can drive functional strategies within the environment of the body in response to external stimuli. The complexity of the gut microbiota suggests that it behaves as an organ. Therefore, the concept of the gut-liver axis must be complemented with the gut-microbiota-liver network due to the high intricacy of the microbiota components and metabolic activities; these activities form the active diet-driven power plant of the host. Such complexity can only be revealed using systems biology, which can integrate clinical phenomics and gut microbiota data.
Highlights
In the past decade, the incidence of non-alcoholic fatty liver disease (NAFLD) has reached epidemic proportions, and Non-alcoholic fatty liver disease (NAFLD) has become one of the most frequent causes of chronic liver disease worldwide [1,2]
This paper provides an overview of current evidence for the role of the gut microbiome in NAFLD pathogenesis and discusses a “deciphering” code to reveal the role of the gut microbiota within the gut-microbiota-liver axis using an approach with multiple levels of complexity: (i) a description of the gut microbial communities by exploiting both genomics- and metagenomics-based strategies; (ii) elucidation of the gut microbial metabolic activities and evaluation of how microbial networks alter the entire metabolism using metabolomics approaches; and (iii) metabonomic analyses of the contribution of diet, which is intended to be an external stimulus, to the microbial and host metabolic network and to the gut homeostasis
The results showed that the expression of inflammatory cytokines, such as tumor necrosis factor (TNF), IL-1β, and TLR-2, Toll-like receptor-4 (TLR-4), TLR-5, and TLR-9, was increased in the liver but was decreased in the small intestine of the HFD-fed mice, while the expression of TLRs in the primary hepatocytes and Kupffer cells (KCs) was increased by treatment with palmitic acid (PA)
Summary
The incidence of non-alcoholic fatty liver disease (NAFLD) has reached epidemic proportions, and NAFLD has become one of the most frequent causes of chronic liver disease worldwide [1,2]. Among the new strategies recently proposed, the use of prebiotics and probiotics should be considered; these compounds play a role in modulating diet-altered and inflammatory gut microbiota Their potential effects on the NAFLD condition have recently been investigated in animal models and in some human studies, additional randomized controlled clinical trials are needed to demonstrate the efficacy of these dietary components in the treatment of NAFLD [39]. It is reasonable to assume that a combined pharmacological approach that targets lifestyle habits and both novel and old patho-mechanisms (e.g., insulin resistance, oxidative stress, gut-liver axis, and apoptosis) could be the best option for NAFLD therapy [40,41] These components form the entire combined host and gut microbial metabolome. The physicochemical modifications of the “bioreactor” intestine can suggest targeted strategies for NAFLD intervention that are directed towards controlling and modifying the function of gut microbiota; this control may be achieved through diet-linked solutions
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