Evidence map›Paper›PMID 24689038›Full record

ArticleBioMed research international2014

Decreased thioredoxin-1 and increased HSP90 expression in skeletal muscle in subjects with type 2 diabetes or impaired glucose tolerance.

M Venojärvi, A Korkmaz, S Aunola, K Hällsten, K Virtanen, J Marniemi, J-P Halonen, O Hänninen, P Nuutila, M Atalay

Open access · hybridAbstract read
In one paragraph

Article in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

9 citing papers in PubMed, 17 citations in OpenAlex.

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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 4 institutions in 1 country.

M VenojärviInstitute of Biomedicine, Exercise Medicine, University of Eastern Finland, P.O. Box 1627, 70211 Kuopio, Finland.
A KorkmazInstitute of Biomedicine, Physiology, University of Eastern Finland, P.O. Box 1627, 70211 Kuopio, Finland.
S AunolaDepartment of Health, Functional Capacity and Welfare, Functional Capacity Unit, National Institute for Health and Welfare, 20720 Turku, Finland.
K HällstenPET Centre, University of Turku, 20520 Turku, Finland.
K VirtanenPET Centre, University of Turku, 20520 Turku, Finland.
J MarniemiDepartment of Chronic Disease Prevention, Population Studies Unit, National Institute for Health and Welfare, 20520 Turku, Finland.
J-P HalonenSocial Insurance Institution, Research Department, 20720 Turku, Finland.
O HänninenInstitute of Biomedicine, Physiology, University of Eastern Finland, P.O. Box 1627, 70211 Kuopio, Finland.
P NuutilaPET Centre, University of Turku, 20520 Turku, Finland.
M AtalayInstitute of Biomedicine, Physiology, University of Eastern Finland, P.O. Box 1627, 70211 Kuopio, Finland.
University of Eastern Finland · FITurku PET Centre · FIFinnish Institute for Health and Welfare · FISocial Insurance Institution · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In diabetes, the endogenous defence systems are overwhelmed, causing various types of stress in tissues. In this study, newly diagnosed or diet-treated type 2 diabetics (T2D) (n = 10) were compared with subjects with impaired glucose tolerance (IGT) (n = 8). In both groups, at resting conditions, blood samples were drawn for assessing metabolic indices and skeletal muscle samples (m. vastus lateralis) were taken for the measurements of cellular defence markers: thioredoxin-1 (TRX-1) and stress proteins HSP72, HSP90. The protein level of TRX-1 was 36.1% lower (P = 0.031) and HSP90 was 380% higher (P < 0.001) in the T2D than in the IGT subjects, with no significant changes in HSP72. However, after the adjustment of both analyses with HOMA-IR only HSP90 difference remained significant. In conclusion, level of TRX-1 in skeletal muscle tissue was lower while that of HSP90 was higher in T2D than in IGT subjects. This may impair antioxidant defence and lead to disruptions of protein homoeostasis and redox regulation of cellular defences. Because HSP90 may be involved in sustaining functional insulin signalling pathway in type 2 diabetic muscles and higher HSP90 levels can be a consequence of type 2 diabetes, our results are potentially important for the diabetes research.

Indexed as

Blood GlucoseDiabetes Mellitus, Type 2FemaleGlucose IntoleranceHSP72 Heat-Shock ProteinsHSP90 Heat-Shock ProteinsHumansMaleMiddle AgedMuscle, SkeletalThioredoxinsBlood GlucoseHSP72 Heat-Shock ProteinsHSP90 Heat-Shock ProteinsThioredoxins

Identifiers

PMID24689038
PMCPMC3932292
OpenAlexW2092036484

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Registered trials

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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.