Abstract
Nonalcoholic fatty liver disease (NAFLD) is a serious liver disorder associated with the accumulation of fat and inflammation. The objective of this study was to determine the gut microbiota composition that might influence the progression of NAFLD. Germ-free mice were inoculated with feces from patients with nonalcoholic steatohepatitis (NASH) or from healthy persons (HL) and then fed a standard diet (STD) or high-fat diet (HFD). We found that the epididymal fat weight, hepatic steatosis, multifocal necrosis, and inflammatory cell infiltration significantly increased in the NASH-HFD group. These findings were consistent with markedly elevated serum levels of alanine transaminase, aspartate transaminase, endotoxin, interleukin 6 (IL-6), monocyte chemotactic protein 1 (Mcp1), and hepatic triglycerides. In addition, the mRNA expression levels of Toll-like receptor 2 (Tlr2), Toll-like receptor 4 (Tlr4), tumor necrosis factor alpha (Tnf-α), Mcp1, and peroxisome proliferator-activated receptor gamma (Ppar-γ) significantly increased. Only abundant lipid accumulation and a few inflammatory reactions were observed in group HL-HFD. Relative abundance of Bacteroidetes and Firmicutes shifted in the HFD-fed mice. Furthermore, the relative abundance of Streptococcaceae was the highest in group NASH-HFD. Nevertheless, obesity-related Lactobacillaceae were significantly upregulated in HL-HFD mice. Our results revealed that the gut microbiota from NASH Patients aggravated hepatic steatosis and inflammation. These findings might partially explain the NAFLD progress distinctly was related to different compositions of gut microbiota.
Highlights
Diet-induced nonalcoholic fatty liver disease (NAFLD) is one of the most common chronic liver disorders worldwide [1] due to the epidemic increase in the prevalence of obesity in affluent societies.The development and progression of NAFLD involve complex pathophysiological processes [2] and are influenced by host factors such as genetic polymorphisms, diet, and, as reported more recently, the composition of the gut microbiota
Our findings indicate that the colonization with fecal bacteria from healthy persons (HL) should have a greater relation with obesity or NAFLD induction
Our results indicate a higher abundance of the phylum Firmicutes and a lower abundance of the phylum Bacteroidetes, as well as Proteobacteria in the nonalcoholic steatohepatitis (NASH)-high-fat diet (HFD) group when compared with group HL-standard diet (STD)
Summary
Diet-induced nonalcoholic fatty liver disease (NAFLD) is one of the most common chronic liver disorders worldwide [1] due to the epidemic increase in the prevalence of obesity in affluent societies.The development and progression of NAFLD involve complex pathophysiological processes [2] and are influenced by host factors such as genetic polymorphisms, diet, and, as reported more recently, the composition of the gut microbiota. Diet-induced nonalcoholic fatty liver disease (NAFLD) is one of the most common chronic liver disorders worldwide [1] due to the epidemic increase in the prevalence of obesity in affluent societies. NAFLD includes a wide spectrum of hepatic pathological characteristics ranging from simple steatosis to nonalcoholic steatohepatitis (NASH) with or without fibrosis, cirrhosis, and hepatocellular carcinoma [3]. In a subset of the population (~10–20%), NAFLD progresses to NASH. This population has hepatic steatosis accompanied by inflammation and fibrosis. In the liver samples of patients with NAFLD, inflammasome components are significantly upregulated in the patients with NASH when compared to those with non-NASH
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