Abstract
Non-alcoholic fatty liver disease (NAFLD) is the most common form of chronic liver disease in children and adolescents. Although obesity is the leading cause of NAFLD, the etiologies of NAFLD are multifactorial (e.g., high-fat diet, a lack of exercise, gender, maternal obesity, the antibiotic use), and each of these factors leads to dysbiosis of the gut microbiota community. The gut microbiota is a key player in the development and regulation of the gut mucosal immune system as well as the regulation of both NAFLD and obesity. Dysbiosis of the gut microbiota promotes the development of NAFLD via alteration of gut-liver homeostasis, including disruption of the gut barrier, portal transport of bacterial endotoxin (lipopolysaccharide) to the liver, altered bile acid profiles, and decreased concentrations of short-chain fatty acids. In terms of prevention and treatment, conventional approaches (e.g., dietary and exercise interventions) against obesity and NAFLD have been confirmed to recover the dysbiosis and dysbiosis-mediated altered metabolism. In addition, increased understanding of the importance of gut microbiota-mediated homeostasis in the prevention of NAFLD suggests the potential effectiveness of gut microbiota-targeted preventive and therapeutic strategies (e.g., probiotics and fecal transplantation) against NAFLD in children and adolescents. This review comprehensively summarizes our current knowledge of the gut microbiota, focusing on its interaction with NAFLD and its potential therapeutic role in obese children and adolescents with this disorder.
Highlights
At least 1014 diverse micro-organisms, dominated by anaerobic bacteria and representing 500–1,000 different species [1], populate the human gastrointestinal tract [2]
Endogenous ethanol reaches the liver via the portal vein and causes oxidative stress secondary to hepatic inflammation (Figure 3). These results indicate that inflammation of the intestinal mucosa, portal transport of LPS and ethanol derived from dysbiotic bacteria, LPS–TLR4 signaling, and ethanol-mediated hepatic inflammation are all involved in the pathogenesis of Non-alcoholic fatty liver disease (NAFLD)
Early maternal diet intervention by restricting high fat consumption effectively reduced the incidence of NAFLD in the pups [170]. Another murine study showed that short-term maternal treatment with a potent antioxidant, pyrroloquinoline quinone, prior to weaning attenuated disruptions in macrophage and microbiota function [134]; these findings suggest that early reshaping of the gut microbiota combined with macrophage reprogramming during early weaning may alleviate the sustained proinflammatory environment, preventing the rapid progression of non-alcoholic fatty liver to non-alcoholic steatohepatitis (NASH) in the offspring of obese mothers
Summary
At least 1014 diverse micro-organisms, dominated by anaerobic bacteria and representing 500–1,000 different species [1], populate the human gastrointestinal tract [2]. No age-associated gut microbiota profile consistently characterizes children from adolescents, a high prevalence of Bifidobacterium (within the phylum Actinobacteria) is a well-known signature of for children compared with adults [40] (Figure 2). The NAFLD-associated gut microbiota typically is described as showing decreased α-diversity (richness and evenness), significantly altered β-diversity, and significant differences in the abundance of bacteria at the phylum, class, family, or genus level, compared with the microbiota of appropriate control subjects. NAFLD is associated with lower bacterial diversity, increased abundance of the phylum Bacteroidetes, and decreased abundance of the phylum Firmicutes compared with non-NAFLD controls, according to a Taiwanese study [58]. Non-obese adult patients with NAFLD demonstrate gut dysbiosis, characterized as decreased diversity and phylum-level changes (reduced Firmicutes and increased Bacteroidetes) in gut microbiota composition [63].
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