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高脂饮食诱导的肥胖表型会导致小鼠出现母胎受限、胎盘功能不全和胎儿生长受限。

Obesity phenotype induced by high-fat diet leads to maternal-fetal constraint, placental inefficiency, and fetal growth restriction in mice.

作者信息

Sanches Ana Paula Varela, de Oliveira Josilene Lopes, Ferreira Maíra Schuchter, Lima Bruna de Souza, Miyamoto Josiane Érica, Simino Laís Angélica de Paula, Torsoni Márcio Alberto, Torsoni Adriana Souza, Milanski Marciane, Ignácio-Souza Letícia

机构信息

Laboratory of Metabolic Disorders, School of Applied Sciences, University of Campinas, UNICAMP, Limeira, São Paulo, Brazil.

Laboratory of Metabolic Disorders, School of Applied Sciences, University of Campinas, UNICAMP, Limeira, São Paulo, Brazil; Obesity and Comorbidities Research Center, University of Campinas, Campinas, Brazil.

出版信息

J Nutr Biochem. 2022 Jun;104:108977. doi: 10.1016/j.jnutbio.2022.108977. Epub 2022 Mar 3.

DOI:10.1016/j.jnutbio.2022.108977
PMID:35248701
Abstract

The aim of this study was to investigate certain parameters regarding the maternal-fetal outcomes in a diet-induced obesity model. Obese, glucose-intolerant females who were exposed to a high-fat diet prior to pregnancy had lower placental efficiency and lower birth weight pups compared to the controls. Simple linear regression analyses showed that maternal obesity disrupts the proportionality between maternal and fetal outcomes during pregnancy. Maternal obesity is correlated with fetal outcomes, perhaps because of problems with hormonal signaling and exacerbation of inflammation in the maternal metabolic environment. The maternal obese phenotype altered the thickness of the placental layer, the transport of fatty acids, and the expression of growth factors. For example, lower expression of epidermal growth factor receptor (EGFR) mRNA in the obesity-prone group may have contributed to the rupture of the placental layers, leading to adverse fetal outcomes. Furthermore, maintenance of maternal glucose homeostasis and overexpression of placental growth factor (PGF) in the obesity-resistant group likely protected the placenta and fetuses from morphological and functional damage.

摘要

本研究的目的是调查饮食诱导肥胖模型中与母胎结局相关的某些参数。与对照组相比,孕前暴露于高脂饮食的肥胖、糖耐量不耐受女性的胎盘效率较低,幼崽出生体重也较低。简单线性回归分析表明,孕期母体肥胖会破坏母体与胎儿结局之间的比例关系。母体肥胖与胎儿结局相关,这可能是由于激素信号问题以及母体代谢环境中炎症加剧所致。母体肥胖表型改变了胎盘层厚度、脂肪酸转运以及生长因子的表达。例如,易肥胖组中表皮生长因子受体(EGFR)mRNA表达较低可能导致了胎盘层破裂,从而导致不良胎儿结局。此外,抗肥胖组中母体葡萄糖稳态的维持以及胎盘生长因子(PGF)的过表达可能保护了胎盘和胎儿免受形态和功能损伤。

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