Evidence map›Paper›PMID 19219422›Full record

ArticleDiabetologia2009

Involvement of TNF-alpha in abnormal adipocyte and muscle sortilin expression in obese mice and humans.

V Kaddai, J Jager, T Gonzalez, R Najem-Lendom, S Bonnafous, A Tran, Y Le Marchand-Brustel, P Gual, J-F Tanti, M Cormont

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Diabetologia, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 11% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.

  1. Pooled it
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  15. Sortilin as a Biomarker for Cardiovascular Disease Revisited.Frontiers in cardiovascular medicine · 2021
    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

10 authors at 5 institutions in 1 country.

V KaddaiINSERM U895, Mediterranean Center of Molecular Medicine (C3M), Bâtiment Archimed, Nice Cedex 3, France.
J Jager
T Gonzalez
R Najem-Lendom
S Bonnafous
A Tran
Y Le Marchand-Brustel
P Gual
J-F Tanti
M Cormont
Centre Méditerranéen de Médecine Moléculaire · FRHôpital l'Archet · FRInserm · FRUniversité Côte d'Azur · FRCentre Hospitalier Universitaire de Nice · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims/hypothesisInsulin resistance is caused by numerous factors including inflammation. It is characterised by defective insulin stimulation of adipocyte and muscle glucose transport, which requires the glucose transporter GLUT4 translocation towards the plasma membrane. Defects in insulin signalling can cause insulin resistance, but alterations in GLUT4 trafficking could also play a role. Our goal was to determine whether proteins controlling GLUT4 trafficking are altered in insulin resistance linked to obesity.

methodsUsing real-time RT-PCR, we searched for selected transcripts that were differentially expressed in adipose tissue and muscle in obese mice and humans. Using various adipocyte culture models and in vivo mice treatment, we searched for the involvement of TNF-alpha in these alterations in obesity.

resultsSortilin mRNA and protein were downregulated in adipose tissue from obese db/db and ob/ob mice, and also in muscle. Importantly, sortilin mRNA was also decreased in morbidly obese human diabetic patients. Sortilin and TNF-alpha (also known as TNF) mRNA levels were inversely correlated in mice and human adipose tissues. TNF-alpha decreased sortilin mRNA and protein levels in cultured mouse and human adipocytes, an effect partly prevented by the peroxisome proliferator-activated receptor gamma activator rosiglitazone. TNF-alpha also inhibited adipocyte and muscle sortilin mRNA when injected to mice. CONCLUSIONS/

interpretationSortilin, an essential player in adipocyte and muscle glucose metabolism through the control of GLUT4 localisation, is downregulated in obesity and TNF-alpha is likely to be involved in this defect. Chronic low-grade inflammation in obesity could thus contribute to insulin resistance by modulating proteins that control GLUT4 trafficking.

Indexed as

Adaptor Proteins, Vesicular TransportAdipocytesAdultAnimalsBariatric SurgeryDNA PrimersDown-RegulationEpididymisFemaleHumansMaleMiceMice, ObeseMiddle AgedMuscle, SkeletalObesityAdaptor Proteins, Vesicular TransportDNA PrimersRNA, MessengerSortilinTumor Necrosis Factor-alpha

Identifiers

PMID19219422
OpenAlexW1980849907

What Socratic 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 Socratic graph.