Evidence map›Paper›PMID 30936140›Full record

ArticleDiabetes2019

Skeletal Muscle-Specific Activation of G

Derek B J Bone, Jaroslawna Meister, Jonas R Knudsen, Diptadip Dattaroy, Amanda Cohen, Regina Lee, Huiyan Lu, Daniel Metzger, Thomas E Jensen, Jürgen Wess

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

10 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Adipocyte GNature communications · 2022
    Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Lack of adipocyte purinergic P2YProceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  10. Review
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

10 authors at 3 institutions in 3 countries.

Derek B J BoneMolecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD.
Jaroslawna MeisterMolecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD.
Jonas R KnudsenSection of Molecular Physiology, Department of Nutrition, Exercise and Sports, University of Copenhagen, Copenhagen, Denmark.
Diptadip DattaroyMolecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD.
Amanda CohenMolecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD.
Regina LeeMolecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD.
Huiyan LuMouse Transgenic Core Facility, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD.
Daniel MetzgerInstitut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS UMR 7104, INSERM U1258, Université de Strasbourg, Illkirch, France.
Thomas E JensenSection of Molecular Physiology, Department of Nutrition, Exercise and Sports, University of Copenhagen, Copenhagen, Denmark.ORCID 0000-0001-6139-8268
Jürgen WessMolecular Signaling Section, Laboratory of Bioorganic Chemistry, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD jurgenw@niddk.nih.gov.ORCID 0000-0003-0818-1232
National Institute of Diabetes and Digestive and Kidney Diseases · USUniversity of Copenhagen · DKCentre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Skeletal muscle (SKM) insulin resistance plays a central role in the pathogenesis of type 2 diabetes. Because G-protein-coupled receptors (GPCRs) represent excellent drug targets, we hypothesized that activation of specific functional classes of SKM GPCRs might lead to improved glucose homeostasis in type 2 diabetes. At present, little is known about the in vivo metabolic roles of the various distinct GPCR signaling pathways operative in SKM. In this study, we tested the hypothesis that selective activation of SKM G

Indexed as

Insulin ResistanceAdenylate KinaseAnimalsDiabetes Mellitus, Type 2GlucoseGlucose IntoleranceGTP-Binding Protein alpha Subunits, Gq-G11HumansMiceMice, ObeseMice, TransgenicMuscle, SkeletalMyoblasts, SkeletalObesityReceptors, G-Protein-CoupledSignal TransductionAdenylate KinaseGlucoseGTP-Binding Protein alpha Subunits, Gq-G11Receptors, G-Protein-Coupled

Identifiers

PMID30936140
PMCPMC6610017
OpenAlexW2927420404

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.