Evidence map›Paper›PMID 28864016›Full record

ArticlePlacenta2017

Effects of maternal diabetes and fetal sex on human placenta mitochondrial biogenesis.

Shaoning Jiang, April M Teague, Jeanie B Tryggestad, Christopher E Aston, Timothy Lyons, Steven D Chernausek

Open access · greenAbstract read
In one paragraph

Article in Placenta, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
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, 48 citations in OpenAlex.

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  9. The role of microRNAs in pregnancies complicated by maternal diabetes.Clinical science (London, England : 1979) · 2024
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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

6 authors at 2 institutions in 2 countries.

Shaoning JiangDepartment of Pediatrics, Section of Diabetes and Endocrinology, Harold Hamm Diabetes Center, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
April M TeagueDepartment of Pediatrics, Section of Diabetes and Endocrinology, Harold Hamm Diabetes Center, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
Jeanie B TryggestadDepartment of Pediatrics, Section of Diabetes and Endocrinology, Harold Hamm Diabetes Center, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
Christopher E AstonDepartment of Pediatrics, Biomedical and Behavioral Methodology Core, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
Timothy LyonsCentre for Experimental Medicine, Queen's University of Belfast, Belfast, UK.
Steven D ChernausekDepartment of Pediatrics, Section of Diabetes and Endocrinology, Harold Hamm Diabetes Center, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA. Electronic address: steven-chernausek@ouhsc.edu.
University of Oklahoma Health Sciences Center · USQueen's University Belfast · GB

Funding

Tracking and Evaluation CoreU54GM104938 · NIGMS · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI TIMOTHY M VANWAGONER · 2013 to 2026
$68.2M
TRAINING COREP20MD000528 · NIMHD · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI STEPHENS, LANCER · 2003 to 2016
$17.8M
Prenatal Conditions and the Pathway to Obesity and Diabetes in ChildrenR01DK089034 · NIDDK · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI CHERNAUSEK, STEVEN D · 2010 to 2014
$1.4M
NIDDK NIH HHS R01 DK089034NIGMS NIH HHS U54 GM104938NIMHD NIH HHS P20 MD000528
6 · The paper itself

Abstract

Abnormal placental function in maternal diabetes affects fetal health and can predispose offspring to metabolic diseases in later life. There are fetal sex-specific differences in placenta structure and gene expression, which may affect placental responses to maternal diabetes. The present study examined the effects of maternal diabetes on indices of mitochondrial biogenesis in placentae from male and female offspring. Mitochondrial DNA (mtDNA) copy number and expression of key regulators of mitochondrial biogenesis were assessed in placentae from 19 diabetic and 23 non-diabetic women. The abundance of peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) and mitochondria transcription factor A (TFAM) were lower in female placentae compared to males, but not mtDNA content. In male offspring, maternal diabetes was associated with decreased placental PGC-1α and TFAM, and mitochondrial DNA (mtDNA) content. Male placental TFAM levels were highly correlated with PGC-1α and mtDNA content. However, despite decreased PGC-1α, concomitant changes in TFAM and mtDNA content by diabetes were not observed in females. In addition, TFAM abundance in female placentae was not correlated with PGC-1α or mtDNA content. In summary, placental PGC-1α/TFAM/mitochondrial biogenesis pathway is affected by maternal diabetes and offspring sex. Decreased PGC-1α in response to maternal diabetes plausibly contributes to impaired mitochondrial biogenesis in placentae of male offspring, which may affect long-term health and explain some of enhanced risk of future metabolic diseases in males.

Indexed as

Organelle BiogenesisAdultBlood GlucoseDiabetes, GestationalDNA-Binding ProteinsDNA, MitochondrialFemaleHumansLongitudinal StudiesMaleMitochondrial ProteinsPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPlacentaPregnancySex FactorsTranscription FactorsBlood GlucoseDNA-Binding ProteinsDNA, MitochondrialMitochondrial ProteinsPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPPARGC1A protein, humanTFAM protein, humanTranscription FactorsFetal sexMaternal diabetesMitochondrial DNAPGC-1αPlacentaTFAM

Identifiers

PMID28864016
PMCPMC5659203
OpenAlexW2622627400

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.