Evidence map›Paper›PMID 25070616›Full record

ReviewMetabolism: clinical and experimental2014

β-Cell function in type 2 diabetes.

Ele Ferrannini, Andrea Mari

Registry-linked trialAbstract readReview
PubMed Publisher
In one paragraph

Review in Metabolism: clinical and experimental, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02502344 (The Research About the Influence of Medical Interventions in the Period of Insulin Resistance on Prevalence of Abnormal Glucose Tolerance), which is not on this map. Cited by 57 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 2 pooled it
12.3field-weighted citation impact, top 1% 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.

NCT02502344 phase4unknown statusstarted 2015, after this paper: background citation

The Research About the Influence of Medical Interventions in the Period of Insulin Resistance on Prevalence of Abnormal Glucose Tolerance

Ran2015Enrolled60Registered outcomes1Posted comparisons0ConditionsInsulin ResistanceArmshealthy lifestyle, Metformin
PMID 15561905PMID 18502303PMID 22385956other papers from this trial
Open the trial in the graph
3 · Its place in the literature

Who cites it

57 citing papers in PubMed, 2 syntheses or guidelines pooled it, 131 citations in OpenAlex.

  1. Pooled it
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  19. Mechanism and recent updates on insulin-related disorders.World journal of clinical cases · 2023
    Review
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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

2 authors at 1 institution in 1 country.

Ele FerranniniDepartment of Clinical & Experimental Medicine, University of Pisa, Italy. Electronic address: ferranni@ifc.cnr.it.
Andrea MariC N R Institute of Biomedical Engineering, Padova, Italy.
University of Pisa · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Different in vivo tests explore different aspects of β-cell function. Because intercorrelation of insulin secretion indices is modest, no single in vivo test allows β-cell function to be assessed with accuracy and specificity comparable to insulin sensitivity. Physiologically-based mathematical modeling is necessary to interpret insulin secretory responses in terms of relevant parameters of β-cell function. Models can be used to analyze intravenous glucose tests, but secretory responses to intravenous glucose may be paradoxical in subjects with diabetes. Use of oral glucose (or mixed meal) data may be preferable not only for simplicity but also for physiological interpretation. While the disposition index focuses on the relationship between insulin secretion and insulin resistance, secretion parameters reflecting the dynamic response to changing glucose levels over a time frame of minutes or hours--such as β-cell glucose sensitivity--are key to explain changes in glucose tolerance and are largely independent of insulin sensitivity. Pathognomonic of the β-cell defect of type 2 diabetes is a reduced glucose sensitivity, which is accompanied by normal or raised absolute insulin secretion rates--compensatory to the attendant insulin resistance--and impaired incretin-induced potentiation. As β-cell mass is frequently within the range of nondiabetic individuals, these defects are predominantly functional and potentially reversible. Any intervention, on lifestyle or with drugs, that improves glucose tolerance does so primarily through increased β-cell glucose sensitivity. So far, however, no intervention has proven unequivocally capable of modifying the natural course of β-cell dysfunction.

Indexed as

Blood GlucoseDiabetes Mellitus, Type 2GlucoseHumansInsulinInsulin ResistanceInsulin-Secreting CellsBlood GlucoseGlucoseInsulinClinical testingInsulin secretionType 2 diabetesβ-cell function

Identifiers

PMID25070616
OpenAlexW2016963008

What OpenQuestion 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 OpenQuestion graph.