Evidence map›Paper›PMID 11375421›Full record

ArticleThe Journal of clinical investigation2001

Syntaxin 4 heterozygous knockout mice develop muscle insulin resistance.

C Yang, K J Coker, J K Kim, S Mora, D C Thurmond, A C Davis, B Yang, R A Williamson, G I Shulman, J E Pessin

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

56 citing papers in PubMed, 118 citations in OpenAlex.

  1. Article
  2. Article
  3. Vamp3/syntaxin 4 mediates the basolateral membrane fusion of TfR transcytosis across the BBB and is exploited by pathogenicProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Cardiac SNARE Expression in Health and Disease.Frontiers in endocrinology · 2019
    Article
  15. Article
  16. Molecular Regulatory Mechanism of Exocytosis in the Salivary Glands.International journal of molecular sciences · 2018
    Review
  17. Exocytosis proteins as novel targets for diabetes prevention and/or remediation?American journal of physiology. Regulatory, integrative and comparative physiology · 2017
    Review
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 1 country.

C YangDepartment of Physiology and Biophysics, The University of Iowa, Iowa City, Iowa 52242, USA.
K J Coker
J K Kim
S Mora
D C Thurmond
A C Davis
B Yang
R A Williamson
G I Shulman
J E Pessin
University of Iowa · USBayer (United States) · USHoward Hughes Medical Institute · USYale University · US

Funding

Mechanisms of Lipid-Induced Hepatic Insulin ResistanceR01DK040936 · NIDDK · YALE UNIVERSITY · PI SHULMAN, GERALD I · 1989 to 2015
$5.1M
INTRACELLULAR TRAFFICKING OF GLUT4 CONTAINING VESICLESR01DK055811 · NIDDK · UNIVERSITY OF IOWA · PI PESSIN, JEFFREY E. · 2000 to 2009
$3.3M
SITE SPECIFIC ANTIINSULIN RECEPTOR ANTIBODIESP30DK025295 · NIDDK · UNIVERSITY OF IOWA · PI BAR, ROBERT S · 1986 to 2002
$2.6M
Interleukin-10 and Regulation of Skeletal Muscle Insulin ActionR01DK080756 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI KIM, JASON K · 2008 to 2012
$1.6M
REGULATION OF INSULIN STIMULATED GLUT4 TRANSLOCATIONF32DK009813 · NIDDK · UNIVERSITY OF IOWA · PI THURMOND, DEBBIE C · 1998 to 1999
–
NIDDK NIH HHS DK-25295NIDDK NIH HHS DK-55811NIDDK NIH HHS F32 DK009813NIDDK NIH HHS R01 DK040936NIDDK NIH HHS R01 DK055811NIDDK NIH HHS R01 DK080756
6 · The paper itself

Abstract

To investigate the physiological function of syntaxin 4 in the regulation of GLUT4 vesicle trafficking, we used homologous recombination to generate syntaxin 4-knockout mice. Homozygotic disruption of the syntaxin 4 gene results in early embryonic lethality, whereas heterozygous knockout mice, Syn4(+/-), had normal viability with no significant impairment in growth, development, or reproduction. However, the Syn4(+/-) mice manifested impaired glucose tolerance with a 50% reduction in whole-body glucose uptake. This defect was attributed to a 50% reduction in skeletal muscle glucose transport determined by 2-deoxyglucose uptake during hyperinsulinemic-euglycemic clamp procedures. In parallel, insulin-stimulated GLUT4 translocation in skeletal muscle was also significantly reduced in these mice. In contrast, Syn4(+/-) mice displayed normal insulin-stimulated glucose uptake and metabolism in adipose tissue and liver. Together, these data demonstrate that syntaxin 4 plays a critical physiological role in insulin-stimulated glucose uptake in skeletal muscle. Furthermore, reduction in syntaxin 4 protein levels in this tissue can account for the impairment in whole-body insulin-stimulated glucose metabolism in this animal model.

Indexed as

Muscle ProteinsAdipocytesAdipose Tissue, BrownAnimalsBiological TransportGlucoseGlucose Clamp TechniqueGlucose Tolerance TestGlucose Transporter Type 4GlycogenGlycolysisHeterozygoteInsulin ResistanceLiverMembrane ProteinsMiceGlucoseGlucose Transporter Type 4GlycogenMembrane ProteinsMonosaccharide Transport ProteinsMuscle ProteinsQa-SNARE ProteinsSlc2a4 protein, mouse

Identifiers

PMID11375421
PMCPMC209300
OpenAlexW2139648742

What OpenQuestion holds

Textmetadata
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.