ArticlePloS one2015
Is Placental Mitochondrial Function a Regulator that Matches Fetal and Placental Growth to Maternal Nutrient Intake in the Mouse?
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers.
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.
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.
Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- Reduced bioenergetics and mitochondrial fragmentation in human primary cytotrophoblasts induced by an EGFR-targeting chemical mixture.Chemosphere · 2024Article
- Review
- Environmental Exposures around Conception: Developmental Pathways Leading to Lifetime Disease Risk.International journal of environmental research and public health · 2021Review
- Placental mitochondrial DNA mutational load and perinatal outcomes: Findings from a multi-ethnic pregnancy cohort.Mitochondrion · 2021Article
- Nutrients, Mitochondrial Function, and Perinatal Health.Nutrients · 2020Review
- Article
- Perinatal Nutrition and Programmed Risk for Neuropsychiatric Disorders: A Focus on Animal Models.Biological psychiatry · 2019Review
- Sex-Specific Effects of Nanoparticle-Encapsulated MitoQ (nMitoQ) Delivery to the Placenta in a Rat Model of Fetal Hypoxia.Frontiers in physiology · 2019Article
- Impact of Obesity and Hyperglycemia on Placental Mitochondria.Oxidative medicine and cellular longevity · 2018Article
- Acute nutritional stress during pregnancy affects placental efficiency, fetal growth and adult glucose homeostasis.Oncotarget · 2017Article
- Role of microRNA-130b in placental PGC-1α/TFAM mitochondrial biogenesis pathway.Biochemical and biophysical research communications · 2017Article
- Prenatal exposure to tobacco smoke leads to increased mitochondrial DNA content in umbilical cord serum associated to reduced gestational age.International journal of environmental health research · 2017Article
- Increased Cord Blood Betatrophin Levels in the Offspring of Mothers with Gestational Diabetes.PloS one · 2016Article
- Article
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundEffective fetal growth requires adequate maternal nutrition coupled to active transport of nutrients across the placenta, which, in turn requires ATP. Epidemiological and experimental evidence has shown that impaired maternal nutrition in utero results in an adverse postnatal phenotype for the offspring. Placental mitochondrial function might link maternal food intake to fetal growth since impaired placental ATP production, in response to poor maternal nutrition, could be a pathway linking maternal food intake to reduced fetal growth.
methodWe assessed the effects of maternal diet on placental water content, ATP levels and mitochondrial DNA (mtDNA) content in mice at embryonic (E) day 18 (E18). Females maintained on either low- (LPD) or normal- (NPD) protein diets were mated with NPD males.
resultsFetal dry weight and placental efficiency (embryo/placental fresh weight) were positively correlated (r = 0.53, P = 0.0001). Individual placental dry weight was reduced by LPD (P = 0.003), as was the expression of amino acid transporter Slc38a2 and of growth factor Igf2. Placental water content, which is regulated by active transport of solutes, was increased by LPD (P = 0.0001). However, placental ATP content was also increased (P = 0.03). To investigate the possibility of an underlying mitochondrial stress response, we studied cultured human trophoblast cells (BeWos). High throughput imaging showed that amino acid starvation induces changes in mitochondrial morphology that suggest stress-induced mitochondrial hyperfusion. This is a defensive response, believed to increase mitochondrial efficiency, that could underlie the increase in ATP observed in placenta.
conclusionsThese findings reinforce the pathophysiological links between maternal diet and conceptus mitochondria, potentially contributing to metabolic programming. The quiet embryo hypothesis proposes that pre-implantation embryo survival is best served by a relatively low level of metabolism. This may extend to post-implantation trophoblast responses to nutrition.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.