Evidence map›Paper›PMID 39071288›Full record

ArticlebioRxiv : the preprint server for biology2025

Targeting IRE1α improves insulin sensitivity and thermogenesis and suppresses metabolically active adipose tissue macrophages in male obese mice.

Dan Wu, Venkateswararao Eeda, Zahra Maria, Komal Rawal, Audrey Wang, Oana Herlea-Pana, Ram Babu Undi, Hui-Ying Lim, Weidong Wang

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors.

Dan WuDepartment of Genetics, Heersink School of Medicine, UAB Comprehensive Diabetes Center, University of Alabama at Birmingham, 1918 University Blvd, Birmingham, Alabama, 35233, United States.
Venkateswararao EedaDepartment of Medicine, Division of Endocrinology, The University of Oklahoma Health Science Center, 941 Stanton L. Young Boulevard, Oklahoma City, Oklahoma 73104, United States.
Zahra MariaDepartment of Medicine, Division of Endocrinology, The University of Oklahoma Health Science Center, 941 Stanton L. Young Boulevard, Oklahoma City, Oklahoma 73104, United States.
Komal RawalDepartment of Medicine, Division of Endocrinology, The University of Oklahoma Health Science Center, 941 Stanton L. Young Boulevard, Oklahoma City, Oklahoma 73104, United States.
Audrey WangIndian Springs School, 190 Woodward Dr, Pelham, Alabama 35124.
Oana Herlea-PanaDepartment of Medicine, Division of Endocrinology, The University of Oklahoma Health Science Center, 941 Stanton L. Young Boulevard, Oklahoma City, Oklahoma 73104, United States.
Ram Babu UndiDepartment of Physiology, Harold Hamm Diabetes Center, The University of Oklahoma Health Science Center, 941 Stanton L. Young Boulevard, Oklahoma City, Oklahoma 73104, United States.
Hui-Ying LimDepartment of Genetics, Heersink School of Medicine, UAB Comprehensive Diabetes Center, University of Alabama at Birmingham, 1918 University Blvd, Birmingham, Alabama, 35233, United States.
Weidong WangDepartment of Genetics, Heersink School of Medicine, UAB Comprehensive Diabetes Center, University of Alabama at Birmingham, 1918 University Blvd, Birmingham, Alabama, 35233, United States.ORCID 0000-0003-3619-0953

Funding

Tissue Pathology Shared ResourceP30CA225520 · NCI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI Wade Williams · 2018 to 2026
$27.1M
Pilot Project ProgramP30GM122744 · NIGMS · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI LE, YUN ZHENG · 2017 to 2021
$5.5M
Preclinical Validation of PPARg Acetylation Inhibitors for Diabetes Prevention and TreatmentR01DK128848 · NIDDK · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI WANG, WEIDONG · 2021 to 2025
$2.4M
Developing proinsulin misfolding inhibitors for beta cell protection and diabetes treatmentR01DK130174 · NIDDK · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI Weidong Wang · 2022 to 2026
$1.9M
Cytoprotection and the mechanism of action of a natural product Khellin against ER stressR01DK116017 · NIDDK · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI WANG, WEIDONG · 2018 to 2021
$1.6M
NCI NIH HHS P30 CA225520NIDDK NIH HHS R01 DK116017NIDDK NIH HHS R01 DK128848NIDDK NIH HHS R01 DK130174NIGMS NIH HHS P30 GM122744
6 · The paper itself

Abstract

Overnutrition engenders the expansion of adipose tissue and the accumulation of immune cells, in particular, macrophages, in the adipose tissue, leading to chronic low-grade inflammation and insulin resistance. In obesity, several proinflammatory subpopulations of adipose tissue macrophages (ATMs) identified hitherto include the conventional "M1-like" CD11C-expressing ATM and the newly discovered metabolically activated CD9-expressing ATM; however, the relationship among ATM subpopulations is unclear. The ER stress sensor inositol-requiring enzyme 1α (IRE1α) is activated in the adipocytes and immune cells under obesity. It is unknown whether targeting IRE1α is capable of reversing insulin resistance and obesity and modulating the metabolically activated ATMs. We report that pharmacological inhibition of IRE1α RNase significantly ameliorates insulin resistance and glucose intolerance in male mice with diet-induced obesity. IRE1α inhibition also increases thermogenesis and energy expenditure, and hence protects against high fat diet-induced obesity. Our study shows that the "M1-like" CD11c

Identifiers

PMID39071288
PMCPMC11275733

What OpenQuestion holds

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LicenceCC BY
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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.