Evidence map›Paper›PMID 30131390›Full record

ArticleDiabetes2018

Increased β-Cell Workload Modulates Proinsulin-to-Insulin Ratio in Humans.

Teresa Mezza, Pietro M Ferraro, Vinsin A Sun, Simona Moffa, Chiara M A Cefalo, Giuseppe Quero, Francesca Cinti, Gian Pio Sorice, Alfredo Pontecorvi, Franco Folli and 3 more

Open access · greenAbstract read
PubMed Publisher
In one paragraph

Article in Diabetes, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
4.5field-weighted citation impact, top 5% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

  1. Pooled it
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  3. What Does the Proinsulin/C-Peptide Ratio Reflect?Diabetes, obesity & metabolism · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 3 institutions in 1 country.

Teresa MezzaEndocrinologia e Diabetologia, Fondazione Policlinico Universitario Agostino Gemelli IRCSS, Rome, Italy.ORCID 0000-0001-5407-9576
Pietro M FerraroUniversità Cattolica del Sacro Cuore, Rome, Italy.
Vinsin A SunEndocrinologia e Diabetologia, Fondazione Policlinico Universitario Agostino Gemelli IRCSS, Rome, Italy.
Simona MoffaEndocrinologia e Diabetologia, Fondazione Policlinico Universitario Agostino Gemelli IRCSS, Rome, Italy.
Chiara M A CefaloEndocrinologia e Diabetologia, Fondazione Policlinico Universitario Agostino Gemelli IRCSS, Rome, Italy.
Giuseppe QueroUniversità Cattolica del Sacro Cuore, Rome, Italy.
Francesca CintiEndocrinologia e Diabetologia, Fondazione Policlinico Universitario Agostino Gemelli IRCSS, Rome, Italy.
Gian Pio SoriceEndocrinologia e Diabetologia, Fondazione Policlinico Universitario Agostino Gemelli IRCSS, Rome, Italy.
Alfredo PontecorviEndocrinologia e Diabetologia, Fondazione Policlinico Universitario Agostino Gemelli IRCSS, Rome, Italy.
Franco FolliEndocrinology and Metabolism, Department of Health Science, University of Milano, Azienda Socio Sanitaria Territoriale Santi Paolo e Carlo, Ospedale San Paolo e Ospedale San Carlo, Milan, Italy.
Andrea MariInstitute of Neuroscience, National Research Council, Padua, Italy.ORCID 0000-0002-1436-5591
Sergio AlfieriUniversità Cattolica del Sacro Cuore, Rome, Italy.
Andrea GiaccariEndocrinologia e Diabetologia, Fondazione Policlinico Universitario Agostino Gemelli IRCSS, Rome, Italy andrea.giaccari@unicatt.it.ORCID 0000-0002-7462-7792
Università Cattolica del Sacro Cuore · ITNational Research Council · ITOspedale San Paolo · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increased proinsulin secretion, which characterizes type 2 diabetes and insulin resistance, may be due to an intrinsic, primitive defect in proinsulin processing or be secondary to increased demand on β-cells (hyperinsulinemia secondary to insulin resistance). An alternative way to investigate the relation between relative hyperproinsulinemia and increased secretory demand is to study the dynamic changes in the proinsulin-to-insulin ratio after partial pancreatectomy, a model of acute increased β-cell workload on the remaining pancreas. To pursue this aim, patients without diabetes, scheduled for partial pancreatectomy, underwent 4-h mixed-meal tests and hyperinsulinemic-euglycemic clamps before and after surgery. After acute β-cell mass reduction, no changes were observed in the fasting proinsulin-to-insulin ratio, whereas the fold change in the proinsulin-to-insulin ratio significantly increased over time after the meal. Further, our data demonstrate that whole-body insulin resistance is associated with underlying defects in proinsulin secretion, which become detectable only in the presence of increased insulin secretion demand.

Indexed as

Blood GlucoseFemaleGlucose Clamp TechniqueHumansInsulinInsulin-Secreting CellsLipidsMaleMiddle AgedPancreatectomyProinsulinBlood GlucoseInsulinLipidsProinsulin

Identifiers

PMID30131390
OpenAlexW2888559318

What OpenQuestion holds

Textmetadata
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.