Abstract

Simple SummaryMaternal obesity is associated with increased farrowing difficulties and influences the fetus, but the effect on placental inflammation, oxidative stress, and vascular development in swine remains unclear. In this study, we tested the hypothesis that maternal obesity blocks placental vascular development associated with maternal obesity-increased placental inflammation and oxidative stress in swine. The objective of this study was to evaluate the influence of body condition of sows to placental pro-inflammatory and oxidative stress status and placental angiogenesis. we found that higher backfat thickness in sows is associated with enhanced oxidative stress, increased expression of pro-inflammation cytokines, and inhibited angiogenesis in the placenta. Therefore, reasonable control of body conditions during reproductive cycles may improve placenta development and maintain a healthy placenta environment.In sows, excess backfat during late gestation is associated with increased farrowing difficulties and influences the fetus, but the impact of backfat thickness on placental inflammation, oxidative stress, and vascular development has not been defined. In this study, 120 sows were divided into six groups based on backfat thickness (≤16, 17–18, 19–20, 21–22, 23–24, and ≥25 mm) in late gestation. The placental lipids, reactive oxygen species (ROS), malondialdehyde (MDA), and total antioxidant capacity (TAC) levels, inflammatory-related cytokine and angiogenesis were determined. The concentrations of triglycerides, total cholesterol, low density lipoprotein cholesterol (LDL–C), and free fatty acid (FFA) linearly increased (p < 0.05) associated with increased late gestation backfat. ROS and MDA increased and TAC decreased (p < 0.05) as the backfat thickness increased. The mRNA expression of toll-like receptors (TLR) 2, TLR4, tumor necrosis factor (TNF) α, interleukin (IL)–1β, IL–6, and monocyte chemoattractant protein (MCP)–1 increased with increased backfat in late gestation. There were no differences in IL–8 and IL–10 mRNA expression among sows with different backfat thickness. Placental vessel density initially increased and then decreased with increasing backfat thickness of sows. Similarly, the mRNA levels of vascular endothelial growth factor (VEGF) were also increased and then decreased. Excessive backfat in late gestation was associated with greater oxidative stress, greater expression of proinflammatory cytokines, and decreased expression of placental angiogenic regulators.

Highlights

  • During gestation, the placenta plays a central role in fetal growth and development, and in the communication between dam and fetus [1]

  • Recent studies have shown that maternal obesity is associated with a lipotoxic placental environment [4] and increased inflammation [4,5] and oxidative stress [4,6] in obese women

  • Cotyledonary arteriole diameters are markedly greater in obese than control ewes at midgestation, and the expression of angiogenic factors is lower in obese than control ewes [3]

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Summary

Introduction

The placenta plays a central role in fetal growth and development, and in the communication between dam and fetus [1]. Maternal obesity influences the placenta, and the fetus placenta is associated with reproductive disorders in human beings [2] and some animal species, like sheep [3]. Recent studies have shown that maternal obesity is associated with a lipotoxic placental environment [4] and increased inflammation [4,5] and oxidative stress [4,6] in obese women. Maternal obesity enhances the placental inflammatory signaling pathways in obese ewes at mid-gestation [7]. Placental vascular development and blood flow are critical to fetal growth and development [8]. Placental vascular development is important to ensure optimum health of offspring

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