Evidence map›Paper›PMID 32888406›Full record

ArticleCell metabolism2020

A Cell-Autonomous Signature of Dysregulated Protein Phosphorylation Underlies Muscle Insulin Resistance in Type 2 Diabetes.

Thiago M Batista, Ashok Kumar Jayavelu, Nicolai J Wewer Albrechtsen, Salvatore Iovino, Jasmin Lebastchi, Hui Pan, Jonathan M Dreyfuss, Anna Krook, Juleen R Zierath, Matthias Mann and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Cell metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
7.9field-weighted citation impact, top 2% 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

66 citing papers in PubMed, 104 citations in OpenAlex.

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  6. Expanding the understanding of insulin resistance in brain and periphery.Trends in endocrinology and metabolism: TEM · 2026
    Review
  7. Review
  8. The insulin signalling network.Nature metabolism · 2025
    Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Insulin resistance in type 2 diabetes mellitus.Nature reviews. Endocrinology · 2025
    Review
  14. Article
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  20. Article

6 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

11 authors at 6 institutions in 4 countries.

Thiago M BatistaSection of Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215, USA.
Ashok Kumar JayaveluDepartment of Proteomics and Signal Transduction, Max Planck Institute of Biochemistry, 82152 Martinsried, Germany.
Nicolai J Wewer AlbrechtsenDepartment of Proteomics and Signal Transduction, Max Planck Institute of Biochemistry, 82152 Martinsried, Germany; Novo Nordisk Foundation Center for Protein Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen 2200, Denmark; Department of Clinical Biochemistry, Rigshospitalet, University of Copenhagen, Copenhagen 2100, Denmark.
Salvatore IovinoSection of Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215, USA.
Jasmin LebastchiSection of Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215, USA.
Hui PanBioinformatics and Biostatistics Core, Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215, USA.
Jonathan M DreyfussBioinformatics and Biostatistics Core, Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215, USA.
Anna KrookDepartment of Physiology and Pharmacology, Karolinska Institutet, Stockholm 171 77, Sweden.
Juleen R ZierathNovo Nordisk Foundation Center for Basic Metabolic Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen 2200, Denmark; Section of Integrative Physiology, Department of Molecular Medicine and Surgery, Karolinska Institutet, Stockholm 171 76, Sweden.
Matthias MannDepartment of Proteomics and Signal Transduction, Max Planck Institute of Biochemistry, 82152 Martinsried, Germany; Novo Nordisk Foundation Center for Protein Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen 2200, Denmark.
C Ronald KahnSection of Integrative Physiology and Metabolism, Joslin Diabetes Center, Harvard Medical School, Boston, MA 02215, USA. Electronic address: c.ronald.kahn@joslin.harvard.edu.
Harvard University · USJoslin Diabetes Center · USNovo Nordisk Foundation · DKKarolinska Institutet · SEMax Planck Institute of Biochemistry · DEUniversity of Copenhagen · DK

Funding

SPECIAL ASSAY COREP30DK036836 · NIDDK · JOSLIN DIABETES CENTER · PI ROHIT N. KULKARNI · 1986 to 2026
$50.5M
INSULIN RECEPTOR STRUCTURE AND TURNOVERR37DK031036 · NIDDK · JOSLIN DIABETES CENTER · PI KAHN, C RONALD · 2000 to 2019
$12.9M
Insulin Receptor Substrates and Insulin ActionR01DK033201 · NIDDK · JOSLIN DIABETES CENTER · PI KAHN, C RONALD · 1986 to 2016
$10.6M
Role of PI 3-Kinase Isoforms in Insulin ActionR01DK055545 · NIDDK · JOSLIN DIABETES CENTER · PI KAHN, C RONALD · 1999 to 2020
$8.3M
The Insulin Receptor and Its Signaling MechanismsR01DK031036 · NIDDK · JOSLIN DIABETES CENTER · PI C RONALD KAHN · 1986 to 2026
$4.2M
NIDDK NIH HHS P30 DK036836NIDDK NIH HHS R01 DK031036NIDDK NIH HHS R01 DK033201NIDDK NIH HHS R01 DK055545NIDDK NIH HHS R37 DK031036
6 · The paper itself

Abstract

Skeletal muscle insulin resistance is the earliest defect in type 2 diabetes (T2D), preceding and predicting disease development. To what extent this reflects a primary defect or is secondary to tissue cross talk due to changes in hormones or circulating metabolites is unknown. To address this question, we have developed an in vitro disease-in-a-dish model using iPS cells from T2D patients differentiated into myoblasts (iMyos). We find that T2D iMyos in culture exhibit multiple defects mirroring human disease, including an altered insulin signaling, decreased insulin-stimulated glucose uptake, and reduced mitochondrial oxidation. More strikingly, global phosphoproteomic analysis reveals a multidimensional network of signaling defects in T2D iMyos going beyond the canonical insulin-signaling cascade, including proteins involved in regulation of Rho GTPases, mRNA splicing and/or processing, vesicular trafficking, gene transcription, and chromatin remodeling. These cell-autonomous defects and the dysregulated network of protein phosphorylation reveal a new dimension in the cellular mechanisms underlying the fundamental defects in T2D.

Indexed as

Cell LineDiabetes Mellitus, Type 2HumansInduced Pluripotent Stem CellsInsulin ResistanceModels, BiologicalMuscle, SkeletalPhosphorylationrho GTP-Binding ProteinsSignal Transductionrho GTP-Binding Proteinschromatin remodelingglucose transportinsulin resistanceiPSCmitochondrial oxidationmRNA splicingphosphoproteomicsskeletal muscletype 2 diabetesvesicle trafficking

Identifiers

PMID32888406
PMCPMC7875546
OpenAlexW3082099734

What OpenQuestion holds

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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.