Evidence map›Paper›PMID 29107964›Full record

ArticlePloS one2017

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

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 and 2 more

Abstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

52 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  10. Effects of Amazake Produced with DifferentFoods (Basel, Switzerland) · 2023
    Article
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  19. Ameliorating Effects ofInternational journal of molecular sciences · 2022
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

June-Chul LeeDepartment of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea.
Hae-Youn LeeDepartment of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea.
Tae Kang KimDepartment of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea.
Min-Soo KimDepartment of Life and Nanopharmaceutical Sciences and Department of Biology, Kyung Hee University, Seoul, Republic of Korea.
Young Mi ParkDepartment of Health Sciences and Technology, SAIHST, Sungkyunkwan University, Seoul, Republic of Korea.
Jinyoung KimDepartment of Medicine, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea.
Kihyoun ParkDepartment of Health Sciences and Technology, SAIHST, Sungkyunkwan University, Seoul, Republic of Korea.
Mi-Na KweonDepartment of Convergence Medicine, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea.
Seok-Hyung KimDepartment of Health Sciences and Technology, SAIHST, Sungkyunkwan University, Seoul, Republic of Korea.
Jin-Woo BaeDepartment of Life and Nanopharmaceutical Sciences and Department of Biology, Kyung Hee University, Seoul, Republic of Korea.
Kyu Yeon HurDepartment of Health Sciences and Technology, SAIHST, Sungkyunkwan University, Seoul, Republic of Korea.
Myung-Shik LeeSeverance Biomedical Science Institute and Department of Internal Medicine, Yonsei University College of Medicine, Seoul, Republic of Korea.ORCID http://orcid.org/0000-0003-3292-1720

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

AnimalsColitisDiet, High-FatIntestinal MucosaMiceMice, Inbred C57BLMicrobiotaRNA, Ribosomal, 16SRNA, Ribosomal, 16S

Identifiers

PMID29107964
PMCPMC5673181

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.