Evidence map›Paper›PMID 33465774›Full record

ReviewAnnals of nutrition & metabolism2020

Gestational Diabetes Mellitus and Developmental Programming.

Anne H Y Chu, Keith M Godfrey

Open access · bronzeAbstract readReview
In one paragraph

Review in Annals of nutrition & metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 3 pooled it
3.1field-weighted citation impact, top 6% 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

47 citing papers in PubMed, 3 syntheses or guidelines pooled it, 74 citations in OpenAlex.

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  19. Pathophysiology of Maternal Obesity and Hypertension in Pregnancy.Journal of cardiovascular development and disease · 2025
    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 2 institutions in 2 countries.

Anne H Y ChuSingapore Institute for Clinical Sciences (SICS), Agency for Science, Technology and Research (A*STAR), Singapore, Singapore.
Keith M GodfreyMRC Lifecourse Epidemiology Unit and NIHR Southampton Biomedical Research Centre, University of Southampton and University Hospital Southampton NHS Foundation Trust, Southampton, United Kingdom, kmg@mrc.soton.ac.uk.
Singapore Institute for Clinical Sciences · SGUniversity of Southampton · GB

Funding

Interdisciplinary Research Network on Early Adversity & Later Life ReversibilityU24AG047867 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI GODFREY, KEITH, MCEWEN, BRUCE S. · 2014 to 2018
$954k
British Heart Foundation RG/15/17/31749Medical Research Council MC_UU_12011/4NIA NIH HHS U24 AG047867
6 · The paper itself

Abstract

During normal pregnancy, increased insulin resistance acts as an adaptation to enhance materno-foetal nutrient transfer and meet the nutritional needs of the developing foetus, particularly in relation to glucose requirements. However, about 1 in 6 pregnancies worldwide is affected by the inability of the mother's metabolism to maintain normoglycaemia, with the combination of insulin resistance and insufficient insulin secretion resulting in gestational diabetes mellitus (GDM). A growing body of epidemiologic work demonstrates long-term implications for adverse offspring health resulting from exposure to GDM in utero. The effect of GDM on offspring obesity and cardiometabolic health may be partly influenced by maternal obesity; this suggests that improving glucose and weight control during early pregnancy, or better still before conception, has the potential to lessen the risk to the offspring. The consequences of GDM for microbiome modification in the offspring and the impact upon offspring immune dysregulation are actively developing research areas. Some studies have suggested that GDM impacts offspring neurodevelopmental and cognitive outcomes; confirmatory studies will need to separate the effect of GDM exposure from the complex interplay of social and environmental factors. Animal and human studies have demonstrated the role of epigenetic modifications in underpinning the predisposition to adverse health in offspring exposed to suboptimal hyperglycaemic in utero environment. To date, several epigenome-wide association studies in human have extended our knowledge on linking maternal diabetes-related DNA methylation marks with childhood adiposity-related outcomes. Identification of such epigenetic marks can help guide future research to develop candidate diagnostic biomarkers and preventive or therapeutic strategies. Longer-term interventions and longitudinal studies will be needed to better understand the causality, underlying mechanisms, or impact of GDM treatments to optimize the health of future generations.

Indexed as

Diabetes, GestationalMaternal Nutritional Physiological PhenomenaPrenatal Exposure Delayed EffectsAnimalsBody CompositionDNA MethylationEpigenesis, GeneticFemaleHumansInsulin ResistanceObesityPregnancyDevelopmental origins of health and diseaseEpigeneticsGestational diabetesLife course epidemiologyNon-communicable disease

Identifiers

PMID33465774
PMCPMC7116810
OpenAlexW3121627202

What OpenQuestion holds

Textmetadata
LicenceTDM
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.