Evidence map›Paper›PMID 27207548›Full record

ArticleDiabetes2016

Integrin-Linked Kinase in Muscle Is Necessary for the Development of Insulin Resistance in Diet-Induced Obese Mice.

Li Kang, Shilpa Mokshagundam, Bradley Reuter, Daniel S Lark, Claire C Sneddon, Chandani Hennayake, Ashley S Williams, Deanna P Bracy, Freyja D James, Ambra Pozzi and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.5field-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

28 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
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  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Integrin-linked kinase (ILK): the known vs. the unknown and perspectives.Cellular and molecular life sciences : CMLS · 2022
    Review
  13. Article
  14. Article
  15. Autoregulation of insulin receptor signaling through MFGE8 and the αvβ5 integrin.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  16. Article
  17. Review
  18. Review
  19. 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

12 authors at 2 institutions in 1 country.

Li KangDepartment of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN Mouse Metabolic Phenotyping Center, Vanderbilt University, Nashville, TN Division of Molecular and Clinical Medicine, School of Medicine, University of Dundee, Dundee, U.K. l.kang@dundee.ac.uk.
Shilpa MokshagundamDepartment of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN.
Bradley ReuterDepartment of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN.
Daniel S LarkDepartment of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN.
Claire C SneddonDivision of Molecular and Clinical Medicine, School of Medicine, University of Dundee, Dundee, U.K.
Chandani HennayakeDivision of Molecular and Clinical Medicine, School of Medicine, University of Dundee, Dundee, U.K.
Ashley S WilliamsDepartment of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN.
Deanna P BracyDepartment of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN Mouse Metabolic Phenotyping Center, Vanderbilt University, Nashville, TN.
Freyja D JamesDepartment of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN Mouse Metabolic Phenotyping Center, Vanderbilt University, Nashville, TN.
Ambra PozziDepartment of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN Division of Nephrology, Department of Medicine, Vanderbilt University, Nashville, TN Department of Medicine, Veterans Affairs Hospital, Nashville, TN.
Roy ZentDivision of Nephrology, Department of Medicine, Vanderbilt University, Nashville, TN Department of Medicine, Veterans Affairs Hospital, Nashville, TN.
David H WassermanDepartment of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN Mouse Metabolic Phenotyping Center, Vanderbilt University, Nashville, TN.
Vanderbilt University · USVeterans Health Administration · US

Funding

Vanderbilt Mouse Metabolic Physiology CenterU24DK059637 · NIDDK · VANDERBILT UNIVERSITY · PI WASSERMAN, DAVID H · 2001 to 2015
$14.9M
INTEGRATED CONTROL OF MUSCLE GLUCOSE UPTAKE IN VIVOR01DK054902 · NIDDK · VANDERBILT UNIVERSITY · PI WASSERMAN, DAVID H · 1999 to 2020
$5.9M
Vanderbilt Student Research Training ProgramT35DK007383 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI William Heerman · 1986 to 2026
$4.1M
Betal Integrin and Renal TubulogenesisR01DK075594 · NIDDK · VANDERBILT UNIVERSITY · PI ZENT, ROY · 2008 to 2015
$2.6M
The P450 Epoxygenases as Pro-Oncogenic EnzymesR01CA162433 · NCI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI POZZI, AMBRA · 2012 to 2016
$1.9M
Integrin/TGF-beta Axis in Tubulointerstitial FibrosisR01DK095761 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI POZZI, AMBRA · 2013 to 2016
$1.4M
Structure Function Analysis of Integrins alpha1beta1 and alpha2beta2R01DK083187 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI SANDERS, CHARLES R, ZENT, ROY · 2010 to 2013
$1.3M
Integrated Control of Muscle Glucose Uptake in VivoR56DK054902 · NIDDK · VANDERBILT UNIVERSITY · PI WASSERMAN, DAVID H · 2009 to 2009
$388k
Role of Collagen Binding Receptors in GlomerulosclerosisI01BX002025 · VA · VETERANS HEALTH ADMINISTRATION · PI AMBRA POZZI · 2013 to 2026
–
The ILK/PINCH/Parvin complex in renal tubulogenesisI01BX002196 · VA · VETERANS HEALTH ADMINISTRATION · PI ZENT, ROY · 2013 to 2025
–
BLRD VA I01 BX002025BLRD VA I01 BX002196NCI NIH HHS R01 CA162433NIDDK NIH HHS R01 DK054902NIDDK NIH HHS R01 DK075594NIDDK NIH HHS R01 DK083187NIDDK NIH HHS R01 DK095761NIDDK NIH HHS R56 DK054902NIDDK NIH HHS T35 DK007383NIDDK NIH HHS U24 DK059637
6 · The paper itself

Abstract

Diet-induced muscle insulin resistance is associated with expansion of extracellular matrix (ECM) components, such as collagens, and the expression of collagen-binding integrin, α2β1. Integrins transduce signals from ECM via their cytoplasmic domains, which bind to intracellular integrin-binding proteins. The integrin-linked kinase (ILK)-PINCH-parvin (IPP) complex interacts with the cytoplasmic domain of β-integrin subunits and is critical for integrin signaling. In this study we defined the role of ILK, a key component of the IPP complex, in diet-induced muscle insulin resistance. Wild-type (ILK(lox/lox)) and muscle-specific ILK-deficient (ILK(lox/lox)HSAcre) mice were fed chow or a high-fat (HF) diet for 16 weeks. Body weight was not different between ILK(lox/lox) and ILK(lox/lox)HSAcre mice. However, HF-fed ILK(lox/lox)HSAcre mice had improved muscle insulin sensitivity relative to HF-fed ILK(lox/lox) mice, as shown by increased rates of glucose infusion, glucose disappearance, and muscle glucose uptake during a hyperinsulinemic-euglycemic clamp. Improved muscle insulin action in the HF-fed ILK(lox/lox)HSAcre mice was associated with increased insulin-stimulated phosphorylation of Akt and increased muscle capillarization. These results suggest that ILK expression in muscle is a critical component of diet-induced insulin resistance, which possibly acts by impairing insulin signaling and insulin perfusion through capillaries.

Indexed as

Insulin ResistanceAnimalsDiet, High-FatExtracellular MatrixGlucoseGlucose Clamp TechniqueInsulinMiceMice, Inbred C57BLMice, ObeseMuscle, SkeletalObesityProtein Serine-Threonine KinasesScaffold Protein ILKSignal TransductionGlucoseInsulinProtein Serine-Threonine KinasesScaffold Protein ILK

Identifiers

PMID27207548
PMCPMC4878430
OpenAlexW2316751472

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.