Evidence map›Paper›PMID 33674694›Full record

ArticleScientific reports2021

DSS-induced colitis is associated with adipose tissue dysfunction and disrupted hepatic lipid metabolism leading to hepatosteatosis and dyslipidemia in mice.

Jeonghyeon Kwon, Chungho Lee, Sungbaek Heo, Bobae Kim, Chang-Kee Hyun

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
10.8field-weighted citation impact, top 1% 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

77 citing papers in PubMed, 107 citations in OpenAlex.

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  13. Colon-targeted pH-responsive tofacitinib beads improve ulcerative colitis outcomes with lower systemic exposure.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2026
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  15. A Feline Milk-DrivedMicroorganisms · 2026
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17 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 1 institution in 1 country.

Jeonghyeon KwonSchool of Life Science, Handong Global University, Pohang, Gyungbuk, 37554, South Korea.
Chungho LeeSchool of Life Science, Handong Global University, Pohang, Gyungbuk, 37554, South Korea.
Sungbaek HeoSchool of Life Science, Handong Global University, Pohang, Gyungbuk, 37554, South Korea.
Bobae KimSchool of Life Science, Handong Global University, Pohang, Gyungbuk, 37554, South Korea.
Chang-Kee HyunSchool of Life Science, Handong Global University, Pohang, Gyungbuk, 37554, South Korea. ckhyun@handong.edu.
Handong Global University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Considering high prevalence of non-alcoholic fatty liver diseases (NAFLD) in patients with inflammatory bowel disease (IBD), this study aimed to elucidate molecular mechanisms for how intestinal inflammatory conditions are causally linked to hepatic steatosis and dyslipidemia. Both younger and older mice treated with acute or chronic dextran sodium sulfate (DSS) developed colitis, which was evidenced by weight loss, colon length shortening, and elevated disease activity index and inflammation score. They also showed decreased expression of intestinal barrier function-related proteins and elevated plasma lipopolysaccharide level, indicating DSS-induced barrier dysfunction and thereby increased permeability. Interestingly, they displayed phenotypes of hepatic fat accumulation and abnormal blood lipid profiles. This DSS-induced colitis-associated lipid metabolic dysfunction was due to overall disruption of metabolic processes including fatty acid oxidation, lipogenesis, lipolysis, reverse cholesterol transport, bile acid synthesis, and white adipose tissue browning and brown adipose tissue thermogenesis, most of which are mediated by key regulators of energy homeostasis such as FGF21, adiponectin, and irisin, via SIRT1/PGC-1α- and LXRα-dependent pathways. Our study suggests a potential molecular mechanism underlying the comorbidity of NAFLD and IBD, which could provide a key to understanding how the two diseases are pathogenically linked and discovering critical therapeutic targets for their treatment.

Indexed as

Adipose TissueAnimalsColitisComorbidityDextran SulfateDisease Models, AnimalDyslipidemiasInflammationInflammatory Bowel DiseasesLipogenesisLipolysisLiverMaleMiceMice, Inbred C57BLNon-alcoholic Fatty Liver DiseaseDextran Sulfate

Identifiers

PMID33674694
PMCPMC7935975
OpenAlexW3134260427

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.