Evidence mapPaperPMID 22286551Full record

Trial reportDiabetologia2012

Steroid-induced insulin resistance and impaired glucose tolerance are both associated with a progressive decline of incretin effect in first-degree relatives of patients with type 2 diabetes.

D H Jensen, K Aaboe, J E Henriksen, A Vølund, J J Holst, S Madsbad, T Krarup

2 registry-linked trialsOpen access · bronzeAbstract readClinical Trial
PubMed Publisher
In one paragraph

Trial report in Diabetologia, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
5.5field-weighted citation impact, top 3% 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.

NCT07224334 phase1recruitingstarted 2025, after this paper: background citation

Alpha to Beta Cell Communication in Health and Disease

Ran2025Enrolled30Registered outcomes3Posted comparisons0ConditionsDiabetes (DM)Armsdexamethasone, Exendin-9 is a 30 amino acid peptide that is an established competitive antagonist of the GLP-1 receptor. Subjects will receive exendin-9 by intravenous infusion at a rate of 600 pmol/kg/min
Open the trial in the graph
NCT00784745 nacompletednot on this map

Is Insulin Resistance and/or Glucose Intolerance Pathogenetic in the Development of a Reduced Incretin Effect

TypeinterventionalSponsorUniversity Hospital, Gentofte, CopenhagenRan2008 to 2009Enrolled21ConditionsInsulin Resistance, Glucose IntoleranceArmsDexamethasone
3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 66 citations in OpenAlex.

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  9. Effects of Anterior Pituitary Adenomas' Hormones on Glucose Metabolism and Its Clinical Implications.Diabetes, metabolic syndrome and obesity : targets and therapy · 2023
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  18. The incretin effect in obese adolescents with and without type 2 diabetes: impaired or intact?American journal of physiology. Endocrinology and metabolism · 2016
    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

7 authors at 5 institutions in 1 country.

D H JensenDepartment of Endocrinology, Bispebjerg University Hospital, Bispebjerg Bakke 23, DK-2400 Copenhagen, Denmark. David_hebbelstrup_Jensen@hotmail.com
K Aaboe
J E Henriksen
A Vølund
J J Holst
S Madsbad
T Krarup
Bispebjerg Hospital · DKHerlev Hospital · DKHvidovre Hospital · DKOdense University Hospital · DKUniversity of Copenhagen · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims/hypothesisThe aim of this study was to evaluate the separate impact of insulin resistance and impaired glucose tolerance (IGT) on the incretin effect.

methodsTwenty-one healthy glucose-tolerant first-degree relatives of patients with type 2 diabetes underwent a 75 g OGTT, an isoglycaemic i.v. glucose test and a mixed meal to evaluate the incretin effect before and after treatment with dexamethasone to increase insulin resistance. Beta cell glucose sensitivity, beta cell index and fasting proinsulin were measured as indices of beta cell function.

resultsAfter dexamethasone, ten individuals had increased insulin resistance but normal glucose tolerance (NGT), while 11 individuals with an equal increase in insulin resistance developed IGT. In the NGT and IGT groups, the incretin effects were 71 ± 3.2% and 67 ± 4.6% (p = 0.4) before treatment, but decreased significantly in both groups to 58 ± 5.2% and 32 ± 8.8% (p < 0.05 between groups) after treatment. Dexamethasone increased total glucagon-like peptide-1 and glucose-dependent insulinotropic peptide responses to the OGTT. The impaired incretin effect in NGT was observed in the absence of reductions in beta cell glucose sensitivity and beta cell index during i.v. glucose, corrected for insulin resistance, but in parallel with increased proinsulin/C-peptide ratio. CONCLUSION/

interpretationInsulin resistance and IGT, representing two stages in the path towards diabetes, are associated with differential reductions in the incretin effect seen before the development of IGT and overt type 2 diabetes. The reduction is unrelated to secretion of incretin hormones, but is related to insulin resistance and subtle beta cell defects, and is further aggravated on development of IGT.

trial registrationClinicalTrials.gov NCT00784745.

fundingThis study was supported by a grant from the Novo Nordisk Foundation.

Indexed as

AdultBlood GlucoseDexamethasoneFemaleGlucocorticoidsGlucose IntoleranceGlucose Tolerance TestHumansIncretinsInsulin ResistanceMaleYoung AdultBlood GlucoseDexamethasoneGlucocorticoidsIncretins

Identifiers

PMID22286551
OpenAlexW2019567818

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

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.