Evidence map›Paper›PMID 22028180›Full record

Trial reportDiabetes2011

Influence of hyperinsulinemia and insulin resistance on in vivo β-cell function: their role in human β-cell dysfunction.

Andrea Mari, Andrea Tura, Andrea Natali, Christian Anderwald, Beverley Balkau, Nebojsa Lalic, Mark Walker, Ele Ferrannini, RISC Investigators

Open access · hybridAbstract readClinical Trial
In one paragraph

Trial report in Diabetes, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
5.3field-weighted citation impact, top 4% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Linking neuronal brain activity to the glucose metabolism.Theoretical biology & medical modelling · 2013
    Trial
  4. Review
  5. Article
  6. Article
  7. Insulin regulates arginine-stimulated insulin secretion in humans.Metabolism: clinical and experimental · 2022
    Article
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  9. Review
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  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
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  17. Review
  18. 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

9 authors at 5 institutions in 4 countries.

Andrea MariNational Research Council Institute of Biomedical Engineering, Padova, Italy. andrea.mari@isib.cnr.it
Andrea Tura
Andrea Natali
Christian Anderwald
Beverley Balkau
Nebojsa Lalic
Mark Walker
Ele Ferrannini
RISC Investigators
National Research Council · ITUniversity of Pisa · ITCenter for Health, Exercise and Sport Sciences · RSInserm · FRMedical University of Vienna · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveRecent work has shown that insulin stimulates its own secretion in insulin-sensitive humans, suggesting that insulin resistance in the β-cell could cause β-cell dysfunction. We have tested whether insulin exposure and insulin sensitivity modulate β-cell function in subjects with normal glucose tolerance (NGT) and whether they contribute to dysglycemia in impaired glucose regulation (IGR). RESEARCH DESIGN AND

methodsInsulin sensitivity (by euglycemic clamp), insulin-induced secretory response at isoglycemia (IISR) (as C-peptide percent change from basal during the clamp), glucose-induced secretory response (GISR) to an intravenous glucose bolus, and β-cell glucose sensitivity (β-GS) (by oral glucose tolerance test [OGTT] modeling) were measured in 1,151 NGT and 163 IGR subjects from the RISC (Relationship between Insulin Sensitivity and Cardiovascular Disease) study.

resultsIn NGT, IISR was related to both insulin sensitivity and antecedent insulin exposure; GISR was related to insulin exposure. IISR was positively, if weakly, related to β-GS (r= 0.16, P < 0.0001). Both IISR (-23 [39] vs. -9 [2]%, median [interquartile range], P < 0.03) and β-GS (69 [47] vs. 118 [83] pmol ⋅ min(-1) ⋅ m(-2) ⋅ mmol(-1) ⋅ L, P < 0.0001) were decreased in IGR compared with NGT. Insulin sensitivity and β-GS were the major determinants of mean OGTT glucose in both NGT and IGR, with a minor role for IISR. In a multivariate logistic model, IGR was predicted by β-GS (odds ratio 4.84 [95% CI 2.89-8.09]) and insulin sensitivity (3.06 [2.19-4.27]) but not by IISR (1.11 [0.77-1.61]).

conclusionsPre-exposure to physiological hyperinsulinemia stimulates insulin secretion to a degree that depends on insulin sensitivity. However, this phenomenon has limited impact on β-cell dysfunction and dysglycemia.

Indexed as

AdultBlood GlucoseFemaleGlucoseGlucose Clamp TechniqueGlucose Tolerance TestHumansHyperinsulinismInsulinInsulin ResistanceInsulin-Secreting CellsInsulin SecretionMaleMiddle AgedBlood GlucoseGlucoseInsulin

Identifiers

PMID22028180
PMCPMC3219936
OpenAlexW2170965963

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.