Evidence map›Paper›PMID 38816388›Full record

ArticleNature communications2024

Inflammation causes insulin resistance in mice via interferon regulatory factor 3 (IRF3)-mediated reduction in FAHFA levels.

Shuai Yan, Anna Santoro, Micah J Niphakis, Antonio M Pinto, Christopher L Jacobs, Rasheed Ahmad, Radu M Suciu, Bryan R Fonslow, Rachel A Herbst-Graham, Nhi Ngo and 5 more

Abstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing 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

25 citing papers in PubMed.

  1. Review
  2. Article
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  5. Article
  6. Article
  7. Innate immune signalling in the adipocyte.Journal of biochemistry · 2026
    Review
  8. Article
  9. Article
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  12. Article
  13. Review
  14. Article
  15. Review
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  18. 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

15 authors.

Shuai YanDivision of Endocrinology, Diabetes, and Metabolism, Beth Israel Deaconess Medical Center, 330 Brookline Ave, Boston, MA, 02215, USA.
Anna SantoroDivision of Endocrinology, Diabetes, and Metabolism, Beth Israel Deaconess Medical Center, 330 Brookline Ave, Boston, MA, 02215, USA.
Micah J NiphakisLundbeck La Jolla Research Center Inc., 10835 Road To The Cure Dr. #250, San Diego, CA, 92121, USA.
Antonio M PintoThe Salk Institute for Biological Studies, 10010 N. Torey Pines Rd, La Jolla, CA, 92037-1002, USA.ORCID http://orcid.org/0000-0002-1573-8011
Christopher L JacobsDivision of Endocrinology, Diabetes, and Metabolism, Beth Israel Deaconess Medical Center, 330 Brookline Ave, Boston, MA, 02215, USA.ORCID http://orcid.org/0000-0002-6034-1873
Rasheed AhmadImmunology and Microbiology Department, Dasman Diabetes Institute, Jasim Mohamad Al Bahar St., Kuwait City, Kuwait.ORCID http://orcid.org/0000-0001-5746-0743
Radu M SuciuLundbeck La Jolla Research Center Inc., 10835 Road To The Cure Dr. #250, San Diego, CA, 92121, USA.
Bryan R FonslowLundbeck La Jolla Research Center Inc., 10835 Road To The Cure Dr. #250, San Diego, CA, 92121, USA.
Rachel A Herbst-GrahamLundbeck La Jolla Research Center Inc., 10835 Road To The Cure Dr. #250, San Diego, CA, 92121, USA.
Nhi NgoLundbeck La Jolla Research Center Inc., 10835 Road To The Cure Dr. #250, San Diego, CA, 92121, USA.
Cassandra L HenryLundbeck La Jolla Research Center Inc., 10835 Road To The Cure Dr. #250, San Diego, CA, 92121, USA.
Dylan M HerbstLundbeck La Jolla Research Center Inc., 10835 Road To The Cure Dr. #250, San Diego, CA, 92121, USA.
Alan SaghatelianThe Salk Institute for Biological Studies, 10010 N. Torey Pines Rd, La Jolla, CA, 92037-1002, USA.ORCID http://orcid.org/0000-0002-0427-563X
Barbara B KahnDivision of Endocrinology, Diabetes, and Metabolism, Beth Israel Deaconess Medical Center, 330 Brookline Ave, Boston, MA, 02215, USA.ORCID http://orcid.org/0000-0002-4027-0000
Evan D RosenDivision of Endocrinology, Diabetes, and Metabolism, Beth Israel Deaconess Medical Center, 330 Brookline Ave, Boston, MA, 02215, USA. erosen@bidmc.harvard.edu.ORCID http://orcid.org/0000-0003-4603-708X

Funding

Viral Vector Core (VVC)P30CA014195 · NCI · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI Alan Saghatelian · 1985 to 2026
$82.8M
Regulation of the biosynthesis of a novel class of anti-diabetic lipidsR01DK106210 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KAHN, BARBARA B., SAGHATELIAN, ALAN · 2016 to 2024
$6.6M
P&F programP30DK135043 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI Aaron S Leong · 2023 to 2026
$5.4M
Role of IRF3 in Energy and Glucose HomeostasisR01DK102170 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ROSEN, EVAN D · 2015 to 2024
$5.1M
Glucose Transporter Regulation in Obesity and DiabetesR37DK043051 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KAHN, BARBARA B. · 2006 to 2015
$5.0M
GLUCOSE TRANSPORTER REGULATION IN OBESITY AND DIABETESR01DK043051 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KAHN, BARBARA B. · 1992 to 2020
$4.4M
Mechanisms for the regulation of novel lipids in vivoK01DK128075 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI SANTORO, ANNA · 2021 to 2025
$755k
A Hybrid Quadrupole-Orbitrap LC/MSS10OD021815 · OD · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI SAGHATELIAN, ALAN · 2016 to 2016
$580k
Glucose Transporter Regulation in Obesity and DiabetesR56DK043051 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI KAHN, BARBARA B. · 2022 to 2022
$173k
NCI NIH HHS P30 CA014195NIDDK NIH HHS K01 DK128075NIDDK NIH HHS P30 DK135043NIDDK NIH HHS R01 DK043051NIDDK NIH HHS R01 DK102170NIDDK NIH HHS R01 DK106210NIDDK NIH HHS R37 DK043051NIDDK NIH HHS R56 DK043051NIH HHS S10 OD021815U.S. Department of Health & Human Services | NIH | Center for Scientific Review (NIH Center for Scientific Review) DK102170U.S. Department of Health & Human Services | NIH | Center for Scientific Review (NIH Center for Scientific Review) DK106210U.S. Department of Health & Human Services | NIH | Center for Scientific Review (NIH Center for Scientific Review) DK43051U.S. Department of Health & Human Services | NIH | Center for Scientific Review (NIH Center for Scientific Review) K01 128075
6 · The paper itself

Abstract

Obesity-induced inflammation causes metabolic dysfunction, but the mechanisms remain elusive. Here we show that the innate immune transcription factor interferon regulatory factor (IRF3) adversely affects glucose homeostasis through induction of the endogenous FAHFA hydrolase androgen induced gene 1 (AIG1) in adipocytes. Adipocyte-specific knockout of IRF3 protects male mice against high-fat diet-induced insulin resistance, whereas overexpression of IRF3 or AIG1 in adipocytes promotes insulin resistance on a high-fat diet. Furthermore, pharmacological inhibition of AIG1 reversed obesity-induced insulin resistance and restored glucose homeostasis in the setting of adipocyte IRF3 overexpression. We, therefore, identify the adipocyte IRF3/AIG1 axis as a crucial link between obesity-induced inflammation and insulin resistance and suggest an approach for limiting the metabolic dysfunction accompanying obesity.

Indexed as

AdipocytesDiet, High-FatInflammationInsulin ResistanceInterferon Regulatory Factor-3Mice, KnockoutObesity3T3-L1 CellsAnimalsFatty AcidsGlucoseMaleMiceMice, Inbred C57BLFatty AcidsGlucoseInterferon Regulatory Factor-3Irf3 protein, mouse

Identifiers

PMID38816388
PMCPMC11139994

What OpenQuestion holds

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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.