Evidence map›Paper›PMID 35745174›Full record

ArticleNutrients2022

Role of Beta Cell Function and Insulin Resistance in the Development of Gestational Diabetes Mellitus.

Jonas Ellerbrock, Benthe Spaanderman, Joris van Drongelen, Eva Mulder, Veronica Lopes van Balen, Veronique Schiffer, Laura Jorissen, Robert-Jan Alers, Jeanine Leenen, Chahinda Ghossein-Doha and 1 more

Open access · goldAbstract read
In one paragraph

Article in Nutrients, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
8.7field-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.

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

28 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
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  5. Association betweenFrontiers in endocrinology · 2026
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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

11 authors at 3 institutions in 1 country.

Jonas EllerbrockSchool for Oncology and Developmental Biology (GROW), Maastricht University, 6229 ER Maastricht, The Netherlands.ORCID 0000-0001-6142-3777
Benthe SpaandermanDepartment of Obstetrics and Gynecology, Radboud University Medical Center, 6500 HB Nijmegen, The Netherlands.
Joris van DrongelenDepartment of Obstetrics and Gynecology, Radboud University Medical Center, 6500 HB Nijmegen, The Netherlands.
Eva MulderSchool for Oncology and Developmental Biology (GROW), Maastricht University, 6229 ER Maastricht, The Netherlands.
Veronica Lopes van BalenDepartment of Obstetrics and Gynecology, Maastricht University Medical Center, 6229 ER Maastricht, The Netherlands.
Veronique SchifferSchool for Oncology and Developmental Biology (GROW), Maastricht University, 6229 ER Maastricht, The Netherlands.
Laura JorissenSchool for Oncology and Developmental Biology (GROW), Maastricht University, 6229 ER Maastricht, The Netherlands.ORCID 0000-0003-4513-163X
Robert-Jan AlersSchool for Oncology and Developmental Biology (GROW), Maastricht University, 6229 ER Maastricht, The Netherlands.ORCID 0000-0003-4478-7207
Jeanine LeenenDepartment of Finance, Zuyderland Medical Center, 6419 PC Heerlen, The Netherlands.
Chahinda Ghossein-DohaSchool for Oncology and Developmental Biology (GROW), Maastricht University, 6229 ER Maastricht, The Netherlands.
Marc SpaandermanSchool for Oncology and Developmental Biology (GROW), Maastricht University, 6229 ER Maastricht, The Netherlands.
Maastricht University · NLRadboud University Nijmegen · NLZuyderland Medisch Centrum · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGestational diabetes mellitus (GDM) is a pregnancy complication characterized by second trimester hyperglycemia. Untreated, GDM is related to an increased risk for adverse pregnancy outcomes. Both beta cell dysfunction and insulin resistance underlie impaired glucose tolerance. Understanding the dominant mechanism predisposing to GDM may be important to provide effective treatment in order to improve perinatal outcomes. We hypothesize that insulin resistance rather that beta cell dysfunction predisposes to GDM.

methodsA 75g oral glucose tolerance test (OGTT) was performed on 2112 second-trimester pregnant women to determine the relationship between insulin resistance (HOMA-IR), beta cell function (HOMA-β), and the prevalence of abnormal glucose handling.

resultsHigh insulin resistance raised the risk of GDM (relative risk (RR) 6.1, 95% confidence interval (CI) (4.4-8.5)), as did beta cell dysfunction (RR 3.8, 95% CI (2.7-5.4)). High insulin resistance, but not beta cell function, enhances the necessity for additional glucose lowering medication on top of a low carbohydrate diet in women diagnosed with GDM.

conclusionsBoth high insulin resistance and beta cell dysfunction increase the risk of GDM. As increased insulin resistance, rather than beta cell function, is related to an insufficient response to a low carbohydrate diet, we speculate that insulin sensitizers rather than insulin therapy may be the most targeted therapeutic modality in diet-insensitive GDM.

Indexed as

Diabetes, GestationalInsulin ResistanceInsulin-Secreting CellsBlood GlucoseFemaleHumansInsulinPregnancyBlood GlucoseInsulinbeta cell functionGDMgestational diabetes mellitusHOMA-IRHOMA-βinsulin resistanceOGTT

Identifiers

PMID35745174
PMCPMC9231208
OpenAlexW4282841538

What OpenQuestion holds

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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.