Placenta-Mediated Maternal-Fetal Nutrient Transport in Pregnancy Disorders: A Comprehensive Review A Community-Based Cross-Sectional Study
Abstract
Background: The course of fetal growth relies on how much nutrition is accessible.This supply hinges on how well the placenta can move vital molecules such as fatty acids, glucose, and amino acids delivered via placental transfer.Objective: The aim of this study is to show how placental programming influences newborn weight in pregnancies that are normal as well as those affected by obesity.It also considers how obesity in pregnancy is linked to a greater chance of atypical fetal size, including unusually small or unusually large infants.Methods: A PRISMA-guided systematic review was carried out, using an extensive search of several databases like PubMed, ScienceDirect, and ResearchGate.Sources from 2020 through 2026 were used for this work.Results: Fetal tissues contain docosahexaenoic acid and arachidonic acid during pregnancy.Some proteins, like FATPs, FAT/CD36, and FABPs, move fatty acids by crossing placental membranes.Liver X receptors, peroxisome proliferator-activated receptors, and sterol regulatory element-binding proteins are transcription factors involved in placental gene regulation.Maternal obesity causes lipotoxicity and inflammation in the placenta, which can affect angiogenic signaling and endothelial metabolism.Gestationalore GLUT1 in babies that were large for their gestational age (LGA) than in babies that were small for their gestational age (SGA).SGA was linked to lower SNAT2, and LGA-obese mothers had lower SNAT4.FATP1 was lower in SGA yet higher in LGA.Conclusion: This review assembles evidence that maternal obesity impairs placental vascular performance, emphasizing the interplay between angiogenic mediators and endothelial metabolic activity to produce dysfunction.
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BibTeX
@article{leke2026placentamediated,
title = {{Placenta-Mediated Maternal-Fetal Nutrient Transport in Pregnancy Disorders: A Comprehensive Review A Community-Based Cross-Sectional Study}},
author = {André Léké and Maurice Biendo},
journal = {Archives of Clinical and Biomedical Research},
year = {2026},
month = oct,
doi = {10.26502/acbr.50170535},
url = {https://u-picardie.hal.science/hal-05795110v1},
note = {CC BY},
}
RIS
TY - JOUR
TI - Placenta-Mediated Maternal-Fetal Nutrient Transport in Pregnancy Disorders: A Comprehensive Review A Community-Based Cross-Sectional Study
AU - André Léké
AU - Maurice Biendo
PY - 2026
DA - 2026/10/12
JO - Archives of Clinical and Biomedical Research
DO - 10.26502/acbr.50170535
UR - https://u-picardie.hal.science/hal-05795110v1
AB - Background: The course of fetal growth relies on how much nutrition is accessible.This supply hinges on how well the placenta can move vital molecules such as fatty acids, glucose, and amino acids delivered via placental transfer.Objective: The aim of this study is to show how placental programming influences newborn weight in pregnancies that are normal as well as those affected by obesity.It also considers how obesity in pregnancy is linked to a greater chance of atypical fetal size, including unusually small or unusually large infants.Methods: A PRISMA-guided systematic review was carried out, using an extensive search of several databases like PubMed, ScienceDirect, and ResearchGate.Sources from 2020 through 2026 were used for this work.Results: Fetal tissues contain docosahexaenoic acid and arachidonic acid during pregnancy.Some proteins, like FATPs, FAT/CD36, and FABPs, move fatty acids by crossing placental membranes.Liver X receptors, peroxisome proliferator-activated receptors, and sterol regulatory element-binding proteins are transcription factors involved in placental gene regulation.Maternal obesity causes lipotoxicity and inflammation in the placenta, which can affect angiogenic signaling and endothelial metabolism.Gestationalore GLUT1 in babies that were large for their gestational age (LGA) than in babies that were small for their gestational age (SGA).SGA was linked to lower SNAT2, and LGA-obese mothers had lower SNAT4.FATP1 was lower in SGA yet higher in LGA.Conclusion: This review assembles evidence that maternal obesity impairs placental vascular performance, emphasizing the interplay between angiogenic mediators and endothelial metabolic activity to produce dysfunction.
SN - 2572-5017
ER -