Evidence map›Paper›PMID 28698546›Full record

ArticleScientific reports2017

Obesity-induces Organ and Tissue Specific Tight Junction Restructuring and Barrier Deregulation by Claudin Switching.

Rizwan Ahmad, Bilal Rah, Dhundy Bastola, Punita Dhawan, Amar B Singh

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 5% of its field
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

86 citing papers in PubMed, 1 synthesis or guideline pooled it, 148 citations in OpenAlex.

  1. Pooled it
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  10. RNF168 promotes chronic colitis through ANXA7-mediated autophagy and NLRP3-driven pyroptosis.Apoptosis : an international journal on programmed cell death · 2026
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26 more citing papers are in PubMed but not listed here.

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

5 authors at 3 institutions in 1 country.

Rizwan AhmadDepartment of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE, 68198, USA.
Bilal RahDepartment of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE, 68198, USA.
Dhundy BastolaDepartment of Bioinformatics, University of Nebraska Omaha, Omaha, USA.
Punita DhawanDepartment of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE, 68198, USA.
Amar B SinghDepartment of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, NE, 68198, USA. amar.singh@unmc.edu.
University of Nebraska Medical Center · USVA Nebraska Western Iowa Health Care System · USUniversity of Nebraska at Omaha · US

Funding

Role of Claudin-2 in Inflammatory Diseases and Colon CancerR01DK088902 · NIDDK · VANDERBILT UNIVERSITY · PI SINGH, AMAR B · 2011 to 2015
$1.7M
Role of Claudin-2 in Colon TumorigenesisI01BX002761 · VA · OMAHA VA MEDICAL CENTER · PI SINGH, AMAR B · 2016 to 2023
–
BLRD VA I01 BX002761NIDDK NIH HHS R01 DK088902
6 · The paper itself

Abstract

Obesity increases susceptibility to multiple organ disorders, however, underlying mechanisms remain unclear. The subclinical inflammation assisted by obesity-induced gut permeability may underlie obesity-associated co-morbidities. Despite eminent clinical significance of the obesity led gut barrier abnormalities, its precise molecular regulation remains unclear. It is also unknown whether barrier deregulations, similar to the gut, characterize other vital organs in obese individuals. The claudin family of proteins is integral to the tight junction (TJ), the apical cell-cell adhesion and a key regulator of the epithelial barrier. Using comprehensive physiological and biochemical analysis of intestinal and renal tissues from high-fat diet fed mice, critical for maintaining metabolic homeostasis, this study demonstrates that profound TJ-restructuring by organ and tissue-specific claudin switching characterize obese organs. Protein expression and cellular distribution were examined. In-silico analysis further highlighted potential association of select claudins, modulated by the obesity, with signaling and metabolic pathways of pathological significance. In vitro studies using Leptin or DCA-treatment suggested causal significance of obesity-induced changes in tissue microenvironment in regulating barrier deregulations in tissue-specific manner. Overall, current findings advances our understanding of the molecular undertakings of obesity associated changes that help predispose to specific diseases and also identifies novel windows of preventive and/or therapeutic interventions.

Indexed as

AnimalsCell AdhesionClaudinsComputer SimulationDiet, High-FatDisease Models, AnimalFemaleGene Expression RegulationHomeostasisIntestinal MucosaKidneyMaleMetabolic Networks and PathwaysMiceObesityOrgan SpecificityClaudins

Identifiers

PMID28698546
PMCPMC5505957
OpenAlexW2727371443

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.