The placental vasculature is affected by changes in gene expression and glycogen-rich cells in a diet-induced obesity mouse model.

Maternal obesity is a risk factor for pregnancy complications. Obesity caused by a high-fat diet (HFD) may alter maternal glucose/glycogen metabolism. Here, our objective was to investigate whether the placental vasculature is altered via changes in gene expression and glycogen-rich cells using a pr...

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Main Authors: Hui Zhao, Ronald J Wong, David K Stevenson
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2023-01-01
Series:PLoS ONE
Online Access:https://doi.org/10.1371/journal.pone.0294185
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author Hui Zhao
Ronald J Wong
David K Stevenson
author_facet Hui Zhao
Ronald J Wong
David K Stevenson
author_sort Hui Zhao
collection DOAJ
description Maternal obesity is a risk factor for pregnancy complications. Obesity caused by a high-fat diet (HFD) may alter maternal glucose/glycogen metabolism. Here, our objective was to investigate whether the placental vasculature is altered via changes in gene expression and glycogen-rich cells using a preclinical mouse model of diet-induced obesity. We subjected female FVB/N mice to one of three feeding regimens: regular chow (RC) given at preconception and during pregnancy (Control); RC given at preconception and then a HFD during pregnancy (HFD-P); or HFD initiated 4 weeks preconception and during pregnancy (HFD-PreCP). Daily food consumption and weekly maternal weights were recorded. Maternal blood glucose levels were measured at preconception and 4 gestational epochs (E6.5-E9.5, E10.5-E12.5, E13.5-E15.5, E16.5-E19.5). At E8.5-E16.5, total RNA in placentas were isolated for gene expression analyses. Placentas were also collected for HE and periodic acid Schiff's (PAS) staining and glycogen content assays. Dams in the HFD-P and HFD-PreCP groups gained significantly more weight than controls. Pre- and antenatal glucose levels were also significantly higher (15%-30%) in HFD-PreCP dams. Expression of several placental genes were also altered in HFD dams compared with controls. Consumption of the HFD also led to phenotypic and morphologic changes in glycogen trophoblasts (GlyTs) and uterine natural killer (uNK) cells. Alterations in vascularity were also observed in the labyrinth of HFD-PreCP placentas, which correlated with decreased placental efficiency. Overall, we observed that a HFD induces gestational obesity in mice, alters expression of placental genes, affects glucose homeostasis, and alters glycogen-positive GlyTs and uNK cells. All these changes may lead to impaired placental vascular development, and thus heighten the risk for pregnancy complications.
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spelling doaj-art-386ffc7a506a4133957d2b01d4d4defe2025-08-20T01:59:21ZengPublic Library of Science (PLoS)PLoS ONE1932-62032023-01-011811e029418510.1371/journal.pone.0294185The placental vasculature is affected by changes in gene expression and glycogen-rich cells in a diet-induced obesity mouse model.Hui ZhaoRonald J WongDavid K StevensonMaternal obesity is a risk factor for pregnancy complications. Obesity caused by a high-fat diet (HFD) may alter maternal glucose/glycogen metabolism. Here, our objective was to investigate whether the placental vasculature is altered via changes in gene expression and glycogen-rich cells using a preclinical mouse model of diet-induced obesity. We subjected female FVB/N mice to one of three feeding regimens: regular chow (RC) given at preconception and during pregnancy (Control); RC given at preconception and then a HFD during pregnancy (HFD-P); or HFD initiated 4 weeks preconception and during pregnancy (HFD-PreCP). Daily food consumption and weekly maternal weights were recorded. Maternal blood glucose levels were measured at preconception and 4 gestational epochs (E6.5-E9.5, E10.5-E12.5, E13.5-E15.5, E16.5-E19.5). At E8.5-E16.5, total RNA in placentas were isolated for gene expression analyses. Placentas were also collected for HE and periodic acid Schiff's (PAS) staining and glycogen content assays. Dams in the HFD-P and HFD-PreCP groups gained significantly more weight than controls. Pre- and antenatal glucose levels were also significantly higher (15%-30%) in HFD-PreCP dams. Expression of several placental genes were also altered in HFD dams compared with controls. Consumption of the HFD also led to phenotypic and morphologic changes in glycogen trophoblasts (GlyTs) and uterine natural killer (uNK) cells. Alterations in vascularity were also observed in the labyrinth of HFD-PreCP placentas, which correlated with decreased placental efficiency. Overall, we observed that a HFD induces gestational obesity in mice, alters expression of placental genes, affects glucose homeostasis, and alters glycogen-positive GlyTs and uNK cells. All these changes may lead to impaired placental vascular development, and thus heighten the risk for pregnancy complications.https://doi.org/10.1371/journal.pone.0294185
spellingShingle Hui Zhao
Ronald J Wong
David K Stevenson
The placental vasculature is affected by changes in gene expression and glycogen-rich cells in a diet-induced obesity mouse model.
PLoS ONE
title The placental vasculature is affected by changes in gene expression and glycogen-rich cells in a diet-induced obesity mouse model.
title_full The placental vasculature is affected by changes in gene expression and glycogen-rich cells in a diet-induced obesity mouse model.
title_fullStr The placental vasculature is affected by changes in gene expression and glycogen-rich cells in a diet-induced obesity mouse model.
title_full_unstemmed The placental vasculature is affected by changes in gene expression and glycogen-rich cells in a diet-induced obesity mouse model.
title_short The placental vasculature is affected by changes in gene expression and glycogen-rich cells in a diet-induced obesity mouse model.
title_sort placental vasculature is affected by changes in gene expression and glycogen rich cells in a diet induced obesity mouse model
url https://doi.org/10.1371/journal.pone.0294185
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