Evidence map›Paper›PMID 34245263›Full record

ArticleThe Journal of clinical endocrinology and metabolism2021

Fetal Cardiac Lipid Sensing Triggers an Early and Sex-related Metabolic Energy Switch in Intrauterine Growth Restriction.

Loïze Maréchal, Benoit Sicotte, Véronique Caron, Michèle Brochu, André Tremblay

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 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

13 citing papers in PubMed, 16 citations in OpenAlex.

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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

5 authors at 2 institutions in 1 country.

Loïze MaréchalDepartment of Pharmacology & Physiology, Faculty of Medicine, Université de Montréal, Montreal, Quebec H3T 1J4, Canada.
Benoit SicotteDepartment of Pharmacology & Physiology, Faculty of Medicine, Université de Montréal, Montreal, Quebec H3T 1J4, Canada.
Véronique CaronResearch Center, CHU Ste-Justine, Montréal, Quebec H3T 1C5, Canada.
Michèle BrochuDepartment of Pharmacology & Physiology, Faculty of Medicine, Université de Montréal, Montreal, Quebec H3T 1J4, Canada.ORCID 0000-0001-5308-8702
André TremblayResearch Center, CHU Ste-Justine, Montréal, Quebec H3T 1C5, Canada.ORCID 0000-0003-1547-9846
Centre Hospitalier Universitaire Sainte-Justine · CAUniversité de Montréal · CA

Funding

CIHR MOP136790CIHR MOP152870
6 · The paper itself

Abstract

contextIntrauterine growth restriction (IUGR) is an immediate outcome of an adverse womb environment, exposing newborns to developing cardiometabolic disorders later in life.

objectiveThis study investigates the cardiac metabolic consequences and underlying mechanism of energy expenditure in developing fetuses under conditions of IUGR.

methodsUsing an animal model of IUGR characterized by uteroplacental vascular insufficiency, mitochondrial function, gene profiling, lipidomic analysis, and transcriptional assay were determined in fetal cardiac tissue and cardiomyocytes.

resultsIUGR fetuses exhibited an upregulation of key genes associated with fatty acid breakdown and β-oxidation (Acadvl, Acadl, Acaa2), and mitochondrial carnitine shuttle (Cpt1a, Cpt2), instigating a metabolic gene reprogramming in the heart. Induction of Ech1, Acox1, Acox3, Acsl1, and Pex11a indicated a coordinated interplay with peroxisomal β-oxidation and biogenesis mainly observed in females, suggesting sexual dimorphism in peroxisomal activation. Concurring with the sex-related changes, mitochondrial respiration rates were stronger in IUGR female fetal cardiomyocytes, accounting for enhanced adenosine 5'-triphosphate production. Mitochondrial biogenesis was induced in fetal hearts with elevated expression of Ppargc1a transcript specifically in IUGR females. Lipidomic analysis identified the accumulation of arachidonic, eicosapentaenoic, and docosapentaenoic polyunsaturated long-chain fatty acids (LCFAs) in IUGR fetal hearts, which leads to nuclear receptor peroxisome proliferator-activated receptor α (PPARα) transcriptional activation in cardiomyocytes. Also, the enrichment of H3K27ac chromatin marks to PPARα-responsive metabolic genes in IUGR fetal hearts outlines an epigenetic control in the early metabolic energy switch.

conclusionThis study describes a premature and sex-related remodeling of cardiac metabolism in response to an unfavorable intrauterine environment, with specific LCFAs that may serve as predictive effectors leading to IUGR.

Indexed as

Energy MetabolismAnimalsAnimals, NewbornFatty AcidsFemaleFetal Growth RetardationFetal HeartMaleMitochondriaMyocytes, CardiacOxidation-ReductionRatsRats, Sprague-DawleySex FactorsFatty Acidscardiomyocyteenergy metabolismfetal growth retardationLCFAsperoxisomeseahorse analysis

Identifiers

PMID34245263
PMCPMC8530737
OpenAlexW3180344901

What Socratic holds

Textmetadata
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 Socratic graph.