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Obesogenic diet-induced gut barrier dysfunction and pathobiont expansion aggravate experimental colitis.

Authors
 June-Chul Lee  ;  Hae-Youn Lee  ;  Tae Kang Kim  ;  Min-Soo Kim  ;  Young Mi Park  ;  Jinyoung Kim  ;  Kihyoun Park  ;  Mi-Na Kweon  ;  Seok-Hyung Kim  ;  Jin-Woo Bae  ;  Kyu Yeon Hur  ;  Myung-Shik Lee 
Citation
 PLOS ONE, Vol.12(11) : e0187515, 2017 
Journal Title
 PLOS ONE 
Issue Date
2017
MeSH
Animals ; Colitis/pathology* ; Diet, High-Fat/adverse effects* ; Intestinal Mucosa/microbiology ; Intestinal Mucosa/physiopathology* ; Mice ; Mice, Inbred C57BL ; Microbiota/genetics ; RNA, Ribosomal, 16S/genetics
Abstract
Consumption of a typical Western diet is a risk factor for several disorders. Metabolic syndrome is the most common disease associated with intake of excess fat. However, the incidence of inflammatory bowel disease is also greater in subjects consuming a Western diet, although the mechanism of this phenomenon is not clearly understood. We examined the morphological and functional changes of the intestine, the first site contacting dietary fat, in mice fed a high-fat diet (HFD) inducing obesity. Paneth cell area and production of antimicrobial peptides by Paneth cells were decreased in HFD-fed mice. Goblet cell number and secretion of mucin by goblet cells were also decreased, while intestinal permeability was increased in HFD-fed mice. HFD-fed mice were more susceptible to experimental colitis, and exhibited severe colonic inflammation, accompanied by the expansion of selected pathobionts such as Atopobium sp. and Proteobacteria. Fecal microbiota transplantation transferred the susceptibility to DSS-colitis, and antibiotic treatment abrogated colitis progression. These data suggest that an experimental HFD-induced Paneth cell dysfunction and subsequent intestinal dysbiosis characterized by pathobiont expansion can be predisposing factors to the development of inflammatory bowel disease.
Files in This Item:
T201704497.pdf Download
DOI
10.1371/journal.pone.0187515
Appears in Collections:
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers
Yonsei Authors
Lee, Myung Shik(이명식) ORCID logo https://orcid.org/0000-0003-3292-1720
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/161324
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