Evidence map›Paper›PMID 24692847›Full record

Trial reportMediators of inflammation2014

The acute effects of low-dose TNF-α on glucose metabolism and β-cell function in humans.

Tobias Ibfelt, Christian P Fischer, Peter Plomgaard, Gerrit van Hall, Bente Klarlund Pedersen

Open access · goldAbstract readRandomized Controlled Trial
In one paragraph

Trial report in Mediators of inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
1.3field-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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 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

5 authors at 1 institution in 1 country.

Tobias IbfeltDepartment of Infectious Diseases and CMRC, The Centre of Inflammation and Metabolism (CIM), Rigshospitalet, Faculty of Health Sciences, University of Copenhagen, 7641 Blegdamsvej 9, 2100 Copenhagen, Denmark ; Copenhagen Muscle Research Centre, Rigshospitalet, 2100 Copenhagen, Denmark.ORCID 0000-0003-4437-8892
Christian P FischerDepartment of Infectious Diseases and CMRC, The Centre of Inflammation and Metabolism (CIM), Rigshospitalet, Faculty of Health Sciences, University of Copenhagen, 7641 Blegdamsvej 9, 2100 Copenhagen, Denmark ; Copenhagen Muscle Research Centre, Rigshospitalet, 2100 Copenhagen, Denmark.
Peter PlomgaardDepartment of Infectious Diseases and CMRC, The Centre of Inflammation and Metabolism (CIM), Rigshospitalet, Faculty of Health Sciences, University of Copenhagen, 7641 Blegdamsvej 9, 2100 Copenhagen, Denmark ; Copenhagen Muscle Research Centre, Rigshospitalet, 2100 Copenhagen, Denmark.
Gerrit van HallDepartment of Infectious Diseases and CMRC, The Centre of Inflammation and Metabolism (CIM), Rigshospitalet, Faculty of Health Sciences, University of Copenhagen, 7641 Blegdamsvej 9, 2100 Copenhagen, Denmark ; Copenhagen Muscle Research Centre, Rigshospitalet, 2100 Copenhagen, Denmark ; Department of Biomedical Sciences, University of Copenhagen, 2100 Copenhagen, Denmark.
Bente Klarlund PedersenDepartment of Infectious Diseases and CMRC, The Centre of Inflammation and Metabolism (CIM), Rigshospitalet, Faculty of Health Sciences, University of Copenhagen, 7641 Blegdamsvej 9, 2100 Copenhagen, Denmark ; Copenhagen Muscle Research Centre, Rigshospitalet, 2100 Copenhagen, Denmark.
University of Copenhagen · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 2 diabetes is characterized by increased insulin resistance and impaired insulin secretion. Type 2 diabetes is also associated with low-grade inflammation and increased levels of proinflammatory cytokines such as TNF-α. TNF-α has been shown to impair peripheral insulin signaling in vitro and in vivo. However, it is unclear whether TNF-α may also affect endogenous glucose production (EGP) during fasting and glucose-stimulated insulin secretion (GSIS) in vivo. We hypothesized that low-dose TNF- α would increase EGP and attenuate GSIS. Recombinant human TNF-α or placebo was infused in healthy, nondiabetic young men (n = 10) during a 4-hour basal period followed by an intravenous glucose tolerance test (IVGTT). TNF-α lowered insulin levels by 12% during the basal period (P < 0.05). In response to the IVGTT, insulin levels increased markedly in both trials, but there was no difference between trials. Compared to placebo, TNF-α did not affect EGP during the basal period. Our results indicate that TNF-α acutely lowers basal plasma insulin levels but does not impair GSIS. The mechanisms behind this are unknown but we suggest that it may be due to TNF-α increasing clearance of insulin from plasma without impairing beta-cell function or hepatic insulin sensitivity.

Indexed as

AdultBlood GlucoseDiabetes Mellitus, Type 2Double-Blind MethodGlucoseGlucose Tolerance TestHumansInsulinInsulin-Secreting CellsInsulin SecretionMaleRecombinant ProteinsSignal TransductionTumor Necrosis Factor-alphaYoung AdultBlood GlucoseGlucoseInsulinRecombinant ProteinsTumor Necrosis Factor-alpha

Identifiers

PMID24692847
PMCPMC3945645
OpenAlexW1974554179

What OpenQuestion 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 OpenQuestion graph.