Evidence mapPaperPMID 38169108Full record

ArticlePhysiological reports2024

Extracellular vesicles from obese and diabetic mouse plasma alter C2C12 myotube glucose uptake and gene expression.

Christopher R Pitzer, Hector G Paez, Peter J Ferrandi, Junaith S Mohamed, Stephen E Alway

Open access · goldAbstract read
In one paragraph

Article in Physiological reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.7field-weighted citation impact, top 33% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. 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

5 authors at 1 institution in 1 country.

Christopher R PitzerCenter for Muscle, Metabolism and Neuropathology, Division of Regenerative and Rehabilitation Sciences, College of Health Professions, The University of Tennessee Health Science Center, Memphis, Tennessee, USA.ORCID 0009-0001-2529-4880
Hector G PaezCenter for Muscle, Metabolism and Neuropathology, Division of Regenerative and Rehabilitation Sciences, College of Health Professions, The University of Tennessee Health Science Center, Memphis, Tennessee, USA.ORCID 0000-0002-7381-6006
Peter J FerrandiCenter for Muscle, Metabolism and Neuropathology, Division of Regenerative and Rehabilitation Sciences, College of Health Professions, The University of Tennessee Health Science Center, Memphis, Tennessee, USA.ORCID 0009-0002-8785-1280
Junaith S MohamedCenter for Muscle, Metabolism and Neuropathology, Division of Regenerative and Rehabilitation Sciences, College of Health Professions, The University of Tennessee Health Science Center, Memphis, Tennessee, USA.ORCID 0000-0002-1518-4856
Stephen E AlwayCenter for Muscle, Metabolism and Neuropathology, Division of Regenerative and Rehabilitation Sciences, College of Health Professions, The University of Tennessee Health Science Center, Memphis, Tennessee, USA.ORCID 0000-0002-0378-4707
University of Tennessee Health Science Center · US

Funding

Department of Defense W81XWH2110187
6 · The paper itself

Abstract

Recent studies have indicated a role for circulating extracellular vesicles (EVs) in the pathogenesis of multiple diseases. However, most in vitro studies have used variable and arbitrary doses of EVs rather than interpreting EVs as an existing component of standard skeletal muscle cell culture media. The current study provides an initial investigation into the effects of circulating EVs on the metabolic phenotype of C2C12 myotubes by replacing EVs from fetal bovine serum with circulating EVs from control mice or mice with obesity and type 2 diabetes (OT2D). We report that EVs associated with OT2D decrease 2-NBDG uptake (a proxy measure of glucose uptake) in the insulin-stimulated state compared to controls. OT2D associated EV treatment also significantly decreased myosin heavy chain type 1 (MHCI) mRNA abundance in myotubes but had no effect on mRNA expression of any other myosin heavy chain isoforms. OT2D-associated circulating EVs also significantly increased lipid accumulation within myotubes without altering the expression of a selection of genes important for lipid entry, synthesis, or catabolism. The data indicate that, in a severely diabetic state, circulating EVs may contribute to insulin resistance and alter gene expression in myotubes in a manner consistent with the skeletal muscle phenotype observed in OT2D.

Indexed as

Diabetes Mellitus, Type 2Extracellular VesiclesAnimalsGene ExpressionGlucoseLipidsMiceMuscle Fibers, SkeletalMyosin Heavy ChainsObesityRNA, MessengerGlucoseLipidsMyosin Heavy ChainsRNA, Messengerextracellular vesiclesmetabolismmuscleobesitytype 2 diabetes

Identifiers

PMID38169108
PMCPMC10761623
OpenAlexW4390542422

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.