Evidence map›Paper›PMID 33188009›Full record

ArticleBMJ open diabetes research & care2020

Placental proteome abnormalities in women with gestational diabetes and large-for-gestational-age newborns.

Emma Assi, Francesca D'Addio, Chiara Mandò, Anna Maestroni, Cristian Loretelli, Moufida Ben Nasr, Vera Usuelli, Ahmed Abdelsalam, Andy Joe Seelam, Ida Pastore and 8 more

Abstract read
In one paragraph

Article in BMJ open diabetes research & care, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

18 citing papers in PubMed, 1 synthesis or guideline pooled it.

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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

18 authors.

Emma AssiInternational Center for T1D Pediatric Clinical Research Center Romeo ed Enrica Invernizzi, Department of Biomedical and Clinical Sciences, Università di Milano, Milano, Italy.
Francesca D'AddioInternational Center for T1D Pediatric Clinical Research Center Romeo ed Enrica Invernizzi, Department of Biomedical and Clinical Sciences, Università di Milano, Milano, Italy.
Chiara Mandò"G. Pardi" Laboratory of Maternal-Fetal Translational Research, Department of Biomedical and Clinical Sciences "L. Sacco", Università di Milano, Milano, Lombardia, Italy.
Anna MaestroniInternational Center for T1D Pediatric Clinical Research Center Romeo ed Enrica Invernizzi, Department of Biomedical and Clinical Sciences, Università di Milano, Milano, Italy.
Cristian LoretelliInternational Center for T1D Pediatric Clinical Research Center Romeo ed Enrica Invernizzi, Department of Biomedical and Clinical Sciences, Università di Milano, Milano, Italy.
Moufida Ben NasrInternational Center for T1D Pediatric Clinical Research Center Romeo ed Enrica Invernizzi, Department of Biomedical and Clinical Sciences, Università di Milano, Milano, Italy.
Vera UsuelliInternational Center for T1D Pediatric Clinical Research Center Romeo ed Enrica Invernizzi, Department of Biomedical and Clinical Sciences, Università di Milano, Milano, Italy.
Ahmed AbdelsalamInternational Center for T1D Pediatric Clinical Research Center Romeo ed Enrica Invernizzi, Department of Biomedical and Clinical Sciences, Università di Milano, Milano, Italy.
Andy Joe SeelamInternational Center for T1D Pediatric Clinical Research Center Romeo ed Enrica Invernizzi, Department of Biomedical and Clinical Sciences, Università di Milano, Milano, Italy.
Ida PastoreDepartment of Endocrinology, ASST Fatebenefratelli-Sacco, Milano, Lombardia, Italy.
Cinzia MagagnottiProMiFa, Protein Microsequencing Facility, Ospedale San Raffaele, Milano, Lombardia, Italy.
Reza AbdiTransplantation Research Center, Renal Division, Brigham & Women's, Harvard University, Boston, Massachusetts, USA.
Basset El EssawyTransplantation Research Center, Renal Division, Brigham & Women's, Harvard University, Boston, Massachusetts, USA.
Franco FolliEndocrinologia e Metabolismo, Dipartimento di Scienze della Salute, Universita di Milano, Milano, Italy.ORCID 0000-0001-9824-5222
Domenico CorradiDepartment of Biomedical, Biotechnological and Translational Sciences, Unit of Pathology, University of Parma, Parma, Emilia-Romagna, Italy.
Gianvincenzo ZuccottiInternational Center for T1D Pediatric Clinical Research Center Romeo ed Enrica Invernizzi, Department of Biomedical and Clinical Sciences, Università di Milano, Milano, Italy.
Irene Cetin"G. Pardi" Laboratory of Maternal-Fetal Translational Research, Department of Biomedical and Clinical Sciences "L. Sacco", Università di Milano, Milano, Lombardia, Italy.
Paolo FiorinaInternational Center for T1D Pediatric Clinical Research Center Romeo ed Enrica Invernizzi, Department of Biomedical and Clinical Sciences, Università di Milano, Milano, Italy paolo.fiorina@childrens.harvard.edu.ORCID 0000-0002-1093-7724

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionGestational diabetes mellitus (GDM) is the most frequent metabolic complication during pregnancy and is associated with development of short-term and long-term complications for newborns, with large-for-gestational-age (LGA) being particularly common. Interestingly, the mechanism behind altered fetal growth in GDM is only partially understood. RESEARCH DESIGN AND

methodsA proteomic approach was used to analyze placental samples obtained from healthy pregnant women (n=5), patients with GDM (n=12) and with GDM and LGA (n=5). Effects of altered proteins on fetal development were tested in vitro in human embryonic stem cells (hESCs).

resultsHere, we demonstrate that the placental proteome is altered in pregnant women affected by GDM with LGA, with at least 37 proteins differentially expressed to a higher degree (p<0.05) as compared with those with GDM but without LGA. Among these proteins, 10 are involved in regulating tissue differentiation and/or fetal growth and development, with bone marrow proteoglycan (PRG2) and dipeptidyl peptidase-4 (DPP-4) being highly expressed. Both PRG2 and DPP-4 altered the transcriptome profile of stem cells differentiation markers when tested in vitro in hESCs, suggesting a potential role in the onset of fetal abnormalities.

conclusionsOur findings suggest that placental dysfunction may be directly responsible for abnormal fetal growth/development during GDM. Once established on a larger population, inhibitors of the pathways involving those altered factors may be tested in conditions such as GDM and LGA, in which therapeutic approaches are still lacking.

Indexed as

Diabetes, GestationalFetal MacrosomiaProteomeCesarean SectionFemaleHumansInfant, NewbornPregnancyProteomicsProteomediabetesgestationalplacentaproteomics

Identifiers

PMID33188009
PMCPMC7668299

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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.