Evidence map›Paper›PMID 31665641›Full record

ArticleCell reports2019

Maternal Lipid Metabolism Directs Fetal Liver Programming following Nutrient Stress.

Caitlyn E Bowman, Ebru S Selen Alpergin, Kyle Cavagnini, Danielle M Smith, Susanna Scafidi, Michael J Wolfgang

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

18 citing papers in PubMed, 28 citations in OpenAlex.

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  15. Regulation of maternal-fetal metabolic communication.Cellular and molecular life sciences : CMLS · 2021
    Review
  16. Article
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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 1 institution in 1 country.

Caitlyn E BowmanDepartment of Biological Chemistry, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Ebru S Selen AlperginDepartment of Biological Chemistry, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Kyle CavagniniDepartment of Biological Chemistry, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Danielle M SmithDepartment of Biological Chemistry, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Susanna ScafidiAnesthesiology and Critical Care Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Michael J WolfgangDepartment of Biological Chemistry, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA; Pharmacology and Molecular Sciences, The Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. Electronic address: mwolfga1@jhmi.edu.
Johns Hopkins Medicine · US

Funding

BIOCHEMISTRY, CELLULAR AND MOLECULAR BIOLOGY PROGRAMT32GM007445 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI GREEN, RACHEL · 1985 to 2021
$24.1M
Regulation of Neuronal Lipid Homeostasis By ThioesterasesR01NS072241 · NINDS · JOHNS HOPKINS UNIVERSITY · PI WOLFGANG, MICHAEL J. · 2011 to 2020
$4.0M
Role of Hepatic Fatty Acid Oxidation in Metabolic HomeostasisR01DK116746 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI WOLFGANG, MICHAEL J. · 2018 to 2021
$1.8M
Role of fatty acid oxidation after pediatric head injuryR01NS110808 · NINDS · JOHNS HOPKINS UNIVERSITY · PI SCAFIDI, SUSANNA · 2019 to 2023
$1.8M
Mechanisms of metabolic adaptation after traumatic brain injuryR01NS111230 · NINDS · JOHNS HOPKINS UNIVERSITY · PI SCAFIDI, SUSANNA · 2019 to 2023
$1.8M
NIDDK NIH HHS R01 DK116746NIGMS NIH HHS T32 GM007445NINDS NIH HHS R01 NS072241NINDS NIH HHS R01 NS110808NINDS NIH HHS R01 NS111230
6 · The paper itself

Abstract

The extreme metabolic demands of pregnancy require coordinated metabolic adaptations between mother and fetus to balance fetal growth and maternal health with nutrient availability. To determine maternal and fetal contributions to metabolic flexibility during gestation, pregnant mice with genetic impairments in mitochondrial carbohydrate and/or lipid metabolism were subjected to nutrient deprivation. The maternal fasting response initiates a fetal liver transcriptional program marked by upregulation of lipid- and peroxisome proliferator-activated receptor alpha (Pparα)-regulated genes. Impaired maternal lipid metabolism alters circulating lipid metabolite concentrations and enhances the fetal response to fasting, which is largely dependent on fetal Pparα. Maternal fasting also improves metabolic deficits in fetal carbohydrate metabolism by increasing the availability of alternative substrates. Impairment of both carbohydrate and lipid metabolism in pregnant dams further exacerbates the fetal liver transcriptional response to nutrient deprivation. Together, these data demonstrate a regulatory role for mitochondrial macronutrient metabolism in mediating maternal-fetal metabolic communication, particularly when nutrients are limited.

Indexed as

Fetal DevelopmentLipid MetabolismNutrientsStress, PhysiologicalAnimalsBiological TransportCarbohydrate MetabolismFastingFatty AcidsFemaleFetusFood DeprivationLiverMetabolomeMetabolomicsMiceFatty AcidsMonocarboxylic Acid TransportersNutrientsPPAR alphaPyruvatescarnitine palmitoyltransferase 2Cpt2fatty acid oxidationmetabolismmitochondriamitochondrial pyruvate carrier. MPCperoxisome proliferator-activated receptor alphaPPARαpregnancypyruvate

Identifiers

PMID31665641
PMCPMC6896898
OpenAlexW2982584633

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.