Evidence map›Paper›PMID 33165596›Full record

ArticleThe Journal of clinical endocrinology and metabolism2021

Placental Inositol Reduced in Gestational Diabetes as Glucose Alters Inositol Transporters and IMPA1 Enzyme Expression.

Reshma A Pillai, Mohammed O Islam, Preben Selvam, Neha Sharma, Anne H Y Chu, Oliver C Watkins, Keith M Godfrey, Rohan M Lewis, Shiao Y Chan

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical endocrinology and metabolism, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.7field-weighted citation impact, top 11% 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

19 citing papers in PubMed, 26 citations in OpenAlex.

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  6. Inositol-Exchange Activity in Human Primordial Placenta.International journal of molecular sciences · 2024
    Article
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  8. Article
  9. Nutrition research reviews · 2023
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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 4 institutions in 2 countries.

Reshma A PillaiDepartment of Obstetrics & Gynaecology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
Mohammed O IslamDepartment of Obstetrics & Gynaecology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
Preben SelvamDepartment of Obstetrics & Gynaecology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
Neha SharmaDepartment of Obstetrics & Gynaecology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
Anne H Y ChuSingapore Institute for Clinical Sciences, Agency for Science, Technology and Research (A*STAR), Singapore.
Oliver C WatkinsDepartment of Obstetrics & Gynaecology, Yong Loo Lin School of Medicine, National University of 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.
Rohan M LewisFaculty of Medicine, University of Southampton, Southampton, United Kingdom.
Shiao Y ChanDepartment of Obstetrics & Gynaecology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.
National University of Singapore · SGAgency for Science, Technology and Research · SGUniversity Hospital Southampton NHS Foundation Trust · GBUniversity of Southampton · GB

Funding

British Heart Foundation RG/15/17/31749Department of Health NF-SI-0515-10042Medical Research Council MC_PC_21001Medical Research Council MC_PC_21003Medical Research Council MC_UP_A620_1014Medical Research Council MC_UU_12011/4
6 · The paper itself

Abstract

contextPerturbed inositol physiology in insulin-resistant conditions has led to proposals of inositol supplementation for gestational diabetes (GDM) prevention, but placental inositol biology is poorly understood.

objectiveInvestigate associations of maternal glycemia with placental inositol content, determine glucose effects on placental expression of inositol enzymes and transporters, and examine relations with birthweight. DESIGN AND

participantsCase-control study of placentae from term singleton pregnancies (GDM n = 24, non-GDM n = 26), and culture of another 9 placentae in different concentrations of glucose and myo-inositol for 48 hours.

main outcome measuresPlacental inositol was quantified by the Megazyme assay. Relative expression of enzymes involved in myo-inositol metabolism and plasma membrane inositol transport was determined by quantitative RT-PCR and immunoblotting. Linear regression analyses were adjusted for maternal age, body mass index, ethnicity, gestational age, and sex.

resultsPlacental inositol content was 17% lower in GDM compared with non-GDM. Higher maternal mid-gestation glycemia were associated with lower placental inositol. Increasing fasting glycemia was associated with lower protein levels of the myo-inositol synthesis enzyme, IMPA1, and the inositol transporters, SLC5A11 and SLC2A13, the expression of which also correlated with placental inositol content. In vitro, higher glucose concentrations reduced IMPA1 and SLC5A11 mRNA expression. Increasing fasting glycemia positively associated with customized birthweight percentile as expected in cases with low placental inositol, but this association was attenuated with high placental inositol.

conclusionGlycemia-induced dysregulation of placental inositol synthesis and transport may be implicated in reduced placental inositol content in GDM, and this may in turn be permissive to accelerated fetal growth.

Indexed as

AdultBlood GlucoseCase-Control StudiesCells, CulturedDiabetes, GestationalDown-RegulationFemaleGene Expression RegulationGlucoseGlucose Transport Proteins, FacilitativeHumansInfant, NewbornInositolMalePhosphoric Monoester HydrolasesPlacentaBlood GlucoseGlucoseGlucose Transport Proteins, FacilitativeInositolmyo-inositol-1 (or 4)-monophosphatasePhosphoric Monoester HydrolasesSLC2A13 protein, humanSLC5A11 protein, humanSodium-Glucose Transport Proteinsbirthweightglycemiainositolmyo-inositolplacentapregnancy

Identifiers

PMID33165596
PMCPMC7116629
OpenAlexW3101372680

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.