Evidence map›Paper›PMID 19741162›Full record

ArticleDiabetes2009

Insulin resistance and altered systemic glucose metabolism in mice lacking Nur77.

Lily C Chao, Kevin Wroblewski, Zidong Zhang, Liming Pei, Laurent Vergnes, Olga R Ilkayeva, Shi Ying Ding, Karen Reue, Matthew J Watt, Christopher B Newgard and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed
3.4field-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

89 citing papers in PubMed, 155 citations in OpenAlex.

  1. Trial
  2. Article
  3. Nr4a1 β-cell specific deletion impairs glucose tolerance in female mice.American journal of physiology. Endocrinology and metabolism · 2026
    Article
  4. Review
  5. Review
  6. Functional and Genetic Insights into the Role of theAnimals : an open access journal from MDPI · 2025
    Article
  7. Controversy and multiple roles of the solitary nucleus receptor Nur77 in disease and physiology.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
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  19. Dihydroartemisinin alleviates AngII-induced vascular smooth muscle cell proliferation and inflammatory response by blocking the FTO/NR4A3 axis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022
    Article
  20. Article

29 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

13 authors at 6 institutions in 2 countries.

Lily C ChaoHoward Hughes Medical Institute, Department of Pathology and Laboratory Medicine, University of California-Los Angeles, Los Angeles, California, USA.
Kevin Wroblewski
Zidong Zhang
Liming Pei
Laurent Vergnes
Olga R Ilkayeva
Shi Ying Ding
Karen Reue
Matthew J Watt
Christopher B Newgard
Paul F Pilch
Andrea L Hevener
Peter Tontonoz
University of California, Los Angeles · USBoston Medical Center · USDuke Medical Center · USDuke University · USHoward Hughes Medical Institute · USMonash University · AU

Funding

ULTRASTRUCTURE OF THE INTIMA IN EARLY LESION FORMATIONP01HL030568 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI FOGELMAN, ALAN M · 1985 to 2019
$55.2M
Pediatric Scientist Development Program (PSDP) [K12]K12HD000850 · NICHD · YALE UNIVERSITY · PI Sallie R. Permar · 1987 to 2026
$44.1M
ACTIVATION OF HEXOSE TRANSPORT BY INSULINR01DK030425 · NIDDK · BOSTON UNIVERSITY MEDICAL CAMPUS · PI PILCH, PAUL F · 1986 to 2012
$3.5M
Regulation of Glucose Metabolism by Skeletal Muscle Nuclear Receptor 4AK08DK081683 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CHAO, LILY CHIH-CHEN · 2008 to 2010
$423k
Howard Hughes Medical InstituteNHLBI NIH HHS HL030568NHLBI NIH HHS P01 HL030568NICHD NIH HHS HD-00850NICHD NIH HHS K12 HD000850NIDDK NIH HHS DK-081683-01NIDDK NIH HHS DK-30425NIDDK NIH HHS K08 DK081683NIDDK NIH HHS R01 DK030425
6 · The paper itself

Abstract

objectiveNur77 is an orphan nuclear receptor with pleotropic functions. Previous studies have identified Nur77 as a transcriptional regulator of glucose utilization genes in skeletal muscle and gluconeogenesis in liver. However, the net functional impact of these pathways is unknown. To examine the consequence of Nur77 signaling for glucose metabolism in vivo, we challenged Nur77 null mice with high-fat feeding. RESEARCH DESIGN AND

methodsWild-type and Nur77 null mice were fed a high-fat diet (60% calories from fat) for 3 months. We determined glucose tolerance, tissue-specific insulin sensitivity, oxygen consumption, muscle and liver lipid content, muscle insulin signaling, and expression of glucose and lipid metabolism genes.

resultsMice with genetic deletion of Nur77 exhibited increased susceptibility to diet-induced obesity and insulin resistance. Hyperinsulinemic-euglycemic clamp studies revealed greater high-fat diet-induced insulin resistance in both skeletal muscle and liver of Nur77 null mice compared with controls. Loss of Nur77 expression in skeletal muscle impaired insulin signaling and markedly reduced GLUT4 protein expression. Muscles lacking Nur77 also exhibited increased triglyceride content and accumulation of multiple even-chained acylcarnitine species. In the liver, Nur77 deletion led to hepatic steatosis and enhanced expression of lipogenic genes, likely reflecting the lipogenic effect of hyperinsulinemia.

conclusionsCollectively, these data demonstrate that loss of Nur77 influences systemic glucose metabolism and highlight the physiological contribution of muscle Nur77 to this regulatory pathway.

Indexed as

Insulin ResistanceAnimalsBlood GlucoseCalorimetry, IndirectDietary FatsFatty LiverGlucoseGlucose Clamp TechniqueGlucose Transporter Type 4GlycolysisInsulinLipid MetabolismMiceMice, KnockoutMuscle, SkeletalNuclear Receptor Subfamily 4, Group A, Member 1Blood GlucoseDietary FatsGlucoseGlucose Transporter Type 4InsulinNr4a1 protein, mouseNuclear Receptor Subfamily 4, Group A, Member 1Receptor, InsulinSlc2a4 protein, mouse

Identifiers

PMID19741162
PMCPMC2780886
OpenAlexW2113139156

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.