Regulation of placental amino acid transport in health and disease.

fetal development fetal growth restriction fetal overgrowth human maternal–fetal exchange prenatal programming syncytiotrophoblast

Journal

Acta physiologica (Oxford, England)
ISSN: 1748-1716
Titre abrégé: Acta Physiol (Oxf)
Pays: England
ID NLM: 101262545

Informations de publication

Date de publication:
06 May 2024
Historique:
revised: 19 04 2024
received: 29 01 2024
accepted: 23 04 2024
medline: 7 5 2024
pubmed: 7 5 2024
entrez: 7 5 2024
Statut: aheadofprint

Résumé

Abnormal fetal growth, i.e., intrauterine growth restriction (IUGR) or fetal growth restriction (FGR) and fetal overgrowth, is associated with increased perinatal morbidity and mortality and is strongly linked to the development of metabolic and cardiovascular disease in childhood and later in life. Emerging evidence suggests that changes in placental amino acid transport may contribute to abnormal fetal growth. This review is focused on amino acid transport in the human placenta, however, relevant animal models will be discussed to add mechanistic insights. At least 25 distinct amino acid transporters with different characteristics and substrate preferences have been identified in the human placenta. Of these, System A, transporting neutral nonessential amino acids, and System L, mediating the transport of essential amino acids, have been studied in some detail. Importantly, decreased placental Systems A and L transporter activity is strongly associated with IUGR and increased placental activity of these two amino acid transporters has been linked to fetal overgrowth in human pregnancy. An array of factors in the maternal circulation, including insulin, IGF-1, and adiponectin, and placental signaling pathways such as mTOR, have been identified as key regulators of placental Systems A and L. Studies using trophoblast-specific gene targeting in mice have provided compelling evidence that changes in placental Systems A and L are mechanistically linked to altered fetal growth. It is possible that targeting specific placental amino acid transporters or their upstream regulators represents a novel intervention to alleviate the short- and long-term consequences of abnormal fetal growth in the future.

Identifiants

pubmed: 38711335
doi: 10.1111/apha.14157
doi:

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

e14157

Subventions

Organisme : NIH HHS
ID : HD105701
Pays : United States
Organisme : NIH HHS
ID : HD065007
Pays : United States
Organisme : NIH HHS
ID : HD068370
Pays : United States

Informations de copyright

© 2024 Scandinavian Physiological Society. Published by John Wiley & Sons Ltd.

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Auteurs

Hiroshi Shimada (H)

Department of Obstetrics and Gynecology, University of Colorado, Anschutz Medical Campus, Aurora, Colorado, USA.
Department of Obstetrics and Gynecology, Sapporo Medical University, Sapporo, Japan.

Theresa L Powell (TL)

Department of Obstetrics and Gynecology, University of Colorado, Anschutz Medical Campus, Aurora, Colorado, USA.
Department of Pediatrics, University of Colorado, Anschutz Medical Campus, Aurora, Colorado, USA.

Thomas Jansson (T)

Department of Obstetrics and Gynecology, University of Colorado, Anschutz Medical Campus, Aurora, Colorado, USA.

Classifications MeSH