Evidence map›Paper›PMID 31133649›Full record

ArticleExperimental & molecular medicine2019

Insulin resistance mediates high-fat diet-induced pulmonary fibrosis and airway hyperresponsiveness through the TGF-β1 pathway.

Yoon Hee Park, Eun Yi Oh, Heejae Han, Misuk Yang, Hye Jung Park, Kyung Hee Park, Jae-Hyun Lee, Jung-Won Park

Open access · goldAbstract read
In one paragraph

Article in Experimental & molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

49 citing papers in PubMed, 68 citations in OpenAlex.

  1. Article
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  4. Insulin Resistance and Inflammation.International journal of molecular sciences · 2026
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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

8 authors at 1 institution in 1 country.

Yoon Hee ParkInstitute for Allergy, Yonsei University College of Medicine, Seoul, Korea.
Eun Yi OhInstitute for Allergy, Yonsei University College of Medicine, Seoul, Korea.
Heejae HanInstitute for Allergy, Yonsei University College of Medicine, Seoul, Korea.
Misuk YangInstitute for Allergy, Yonsei University College of Medicine, Seoul, Korea.
Hye Jung ParkDepartment of Internal Medicine and Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, Korea.
Kyung Hee ParkInstitute for Allergy, Yonsei University College of Medicine, Seoul, Korea.
Jae-Hyun LeeInstitute for Allergy, Yonsei University College of Medicine, Seoul, Korea.
Jung-Won ParkInstitute for Allergy, Yonsei University College of Medicine, Seoul, Korea. parkjw@yuhs.ac.ORCID http://orcid.org/0000-0003-0249-8749
Yonsei University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prior studies have reported the presence of lung fibrosis and enhanced airway hyperresponsiveness (AHR) in mice with high-fat-diet (HFD)-induced obesity. This study evaluated the role of TGF-β1 in HFD-induced AHR and lung fibrosis in a murine model. We generated HFD-induced obesity mice and performed glucose and insulin tolerance tests. HFD mice with or without ovalbumin sensitization and challenge were also treated with an anti-TGF-β1 neutralizing antibody. AHR to methacholine, inflammatory cells in the bronchoalveolar lavage fluid (BALF), and histological features were evaluated. Insulin was intranasally administered to normal diet (ND) mice, and in vitro insulin stimulation of BEAS-2b cells was performed. HFD-induced obesity mice had increased insulin resistance, enhanced AHR, peribronchial and perivascular fibrosis, and increased numbers of macrophages in the BALF. However, they did not have meaningful eosinophilic or neutrophilic inflammation in the lungs compared with ND mice. The HFD enhanced TGF-β1 expression in the bronchial epithelium, but we found no differences in the expression of interleukin (IL)-4 or IL-5 in lung homogenates. Administration of the anti-TGF-β1 antibody attenuated HFD-induced AHR and lung fibrosis. It also attenuated goblet cell hyperplasia, but did not affect the AHR and inflammatory cell infiltration induced by OVA challenge. The intranasal administration of insulin enhanced TGF-β1 expression in the bronchial epithelium and lung fibrosis. Stimulating BEAS-2b cells with insulin also increased TGF-β1 production by 24 h. We concluded that HFD-induced obesity-associated insulin resistance enhances TGF-β1 expression in the bronchial epithelium, which may play an important role in the development of lung fibrosis and AHR in obesity.

Indexed as

Insulin ResistanceAnimalsDiet, High-FatLungMaleMice, Inbred C57BLPulmonary FibrosisSignal TransductionTransforming Growth Factor beta1Transforming Growth Factor beta1

Identifiers

PMID31133649
PMCPMC6536500
OpenAlexW2946233024

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.