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Nutrients 2017, 9(11), 1220; doi:10.3390/nu9111220

Nonalcoholic Fatty Liver Disease Is Exacerbated in High-Fat Diet-Fed Gnotobiotic Mice by Colonization with the Gut Microbiota from Patients with Nonalcoholic Steatohepatitis

1
Animal Technology Laboratories, Agricultural Technology Research Institute, Miaoli 350, Taiwan
2
Department of Molecular Biology and Human Genetics, Tzu Chi University, Hualien 970, Taiwan
3
Graduate Institute of Veterinary Pathobiology, National Chung Hsing University, Taichung 402, Taiwan
4
National Laboratory Animal Center, National Applied Research Laboratories, Taipei 115, Taiwan
5
Liver Center, Cathay General Hospital Medical Center, Taipei 106, Taiwan
6
School of Medicine, Taipei Medical University College of Medicine, Taipei 110, Taiwan
7
Department of Exercise and Health Science, National Taipei University of Nursing and Health Sciences, Taipei 112, Taiwan
These authors contribute equally to this work.
Present Address: P.O. Box 1-86, Nangang, Taipei City 11599, Taiwan.
*
Authors to whom correspondence should be addressed.
Received: 25 August 2017 / Revised: 24 October 2017 / Accepted: 2 November 2017 / Published: 6 November 2017
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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. View Full-Text
Keywords: gut microbiota; humanized gnotobiotic mice; nonalcoholic fatty liver disease; high-fat diet gut microbiota; humanized gnotobiotic mice; nonalcoholic fatty liver disease; high-fat diet
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MDPI and ACS Style

Chiu, C.-C.; Ching, Y.-H.; Li, Y.-P.; Liu, J.-Y.; Huang, Y.-T.; Huang, Y.-W.; Yang, S.-S.; Huang, W.-C.; Chuang, H.-L. Nonalcoholic Fatty Liver Disease Is Exacerbated in High-Fat Diet-Fed Gnotobiotic Mice by Colonization with the Gut Microbiota from Patients with Nonalcoholic Steatohepatitis. Nutrients 2017, 9, 1220.

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