Evidence map›Paper›PMID 35268071›Full record

ArticleNutrients2022

Untargeted Metabolome Analysis Reveals Reductions in Maternal Hepatic Glucose and Amino Acid Content That Correlate with Fetal Organ Weights in a Mouse Model of Fetal Alcohol Spectrum Disorders.

Nipun Saini, Manjot S Virdee, Kaylee K Helfrich, Sze Ting Cecilia Kwan, Sandra M Mooney, Susan M Smith

Open access · goldAbstract read
In one paragraph

Article in Nutrients, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
4.2field-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

9 citing papers in PubMed, 11 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

6 authors at 1 institution in 1 country.

Nipun SainiUNC Nutrition Research Institute, University of North Carolina at Chapel Hill, Kannapolis, NC 28081, USA.ORCID 0000-0001-6775-3486
Manjot S VirdeeUNC Nutrition Research Institute, University of North Carolina at Chapel Hill, Kannapolis, NC 28081, USA.
Kaylee K HelfrichUNC Nutrition Research Institute, University of North Carolina at Chapel Hill, Kannapolis, NC 28081, USA.ORCID 0000-0002-9811-1029
Sze Ting Cecilia KwanUNC Nutrition Research Institute, University of North Carolina at Chapel Hill, Kannapolis, NC 28081, USA.ORCID 0000-0002-5280-9253
Sandra M MooneyUNC Nutrition Research Institute, University of North Carolina at Chapel Hill, Kannapolis, NC 28081, USA.
Susan M SmithUNC Nutrition Research Institute, University of North Carolina at Chapel Hill, Kannapolis, NC 28081, USA.
University of North Carolina at Chapel Hill · US

Funding

UNIV OF NORTH CAROLINA CLINICAL NUTRITION RESEARCH UNITP30DK056350 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Venkata Saroja Voruganti · 1999 to 2026
$31.6M
Craniofacial Morphogenesis in Prenatal Alcohol ExposureR01AA011085 · NIAAA · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SMITH, SUSAN M. · 2001 to 2025
$6.3M
Prenatal alcohol exposure disrupts maternal-fetal iron metabolism in FASDR01AA022999 · NIAAA · UNIV OF NORTH CAROLINA CHAPEL HILL · PI KLING, PAMELA J, SMITH, SUSAN M. · 2014 to 2018
$1.6M
Maternal Fetal Metabolic Disruption in Prenatal Alcohol ExposureR00AA028291 · NIAAA · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Nipun Saini · 2024 to 2026
$710k
Maternal Fetal Metabolic Disruption in Prenatal Alcohol ExposureK99AA028291 · NIAAA · UNIV OF NORTH CAROLINA CHAPEL HILL · PI SAINI, NIPUN · 2021 to 2022
$275k
NIAAA NIH HHS K99 AA028291NIAAA NIH HHS R00 AA028291NIAAA NIH HHS R01 AA011085NIAAA NIH HHS R01 AA022999NIAAA NIH HHS R01 AA11085NIAAA NIH HHS R01 AA22999NIDDK NIH HHS P30 DK056350UNC Nutrition Research Institute Internal Funding
6 · The paper itself

Abstract

Prenatal alcohol exposure (PAE) causes fetal growth restrictions. A major driver of fetal growth deficits is maternal metabolic disruption; this is under-investigated following PAE. Untargeted metabolomics on the dam and fetus exposed to alcohol (ALC) revealed that the hepatic metabolome of ALC and control (CON) dams were distinct, whereas that of ALC and CON fetuses were similar. Alcohol reduced maternal hepatic glucose content and enriched essential amino acid (AA) catabolites, N-acetylated AA products, urea content, and free fatty acids. These alterations suggest an attempt to minimize the glucose gap by increasing gluconeogenesis using AA and glycerol. In contrast, ALC fetuses had unchanged glucose and AA levels, suggesting an adequate draw of maternal nutrients, despite intensified stress on ALC dams. Maternal metabolites including glycolytic intermediates, AA catabolites, urea, and one-carbon-related metabolites correlated with fetal liver and brain weights, whereas lipid metabolites correlated with fetal body weight, indicating they may be drivers of fetal weight outcomes. Together, these data suggest that ALC alters maternal hepatic metabolic activity to limit glucose availability, thereby switching to alternate energy sources to meet the high-energy demands of pregnancy. Their correlation with fetal phenotypic outcomes indicates the influence of maternal metabolism on fetal growth and development.

Indexed as

Fetal Alcohol Spectrum DisordersPrenatal Exposure Delayed EffectsAmino AcidsAnimalsFemaleGlucoseLiverMetabolomeMicePregnancyAmino AcidsGlucoseamino acidsfetal weightgluconeogenesisglucosehepatic metabolismmaternal–fetal metabolismpregnancyprenatal alcohol exposureuntargeted metabolomics

Identifiers

PMID35268071
PMCPMC8912878
OpenAlexW4221131431

What Socratic holds

Textmetadata
LicenceCC BY
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.