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产前高脂饮食会改变大鼠胎盘的形态、营养转运蛋白表达及mTORC1信号通路。

Prenatal high-fat diet alters placental morphology, nutrient transporter expression, and mtorc1 signaling in rat.

作者信息

Song Lin, Sun Bo, Boersma Gretha J, Cordner Zachary A, Yan Jianqun, Moran Timothy H, Tamashiro Kellie L K

机构信息

Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, People's Republic of China.

Department of Psychiatry & Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.

出版信息

Obesity (Silver Spring). 2017 May;25(5):909-919. doi: 10.1002/oby.21821. Epub 2017 Mar 23.

DOI:10.1002/oby.21821
PMID:28332771
Abstract

OBJECTIVE

This study aimed to determine how the rat placenta and fetus respond to maternal high-fat (HF) diet during gestation and to identify the possible mechanisms.

METHODS

Pregnant Sprague-Dawley rats were fed with standard chow (13.5% fat) or HF (60% fat) diet during gestation. Placentas were collected on gestation day 21.

RESULTS

HF dams had greater fat mass, higher plasma leptin, lower plasma adiponectin, and impaired glucose tolerance during pregnancy. The placental labyrinth thickness was reduced in both male and female fetuses of HF dams. In HF male placentas, glucose transporter 3 gene expression, system A amino acid transporter (SNAT) 2 gene expression, and SNAT2 protein expression were increased through the activation of the mTORC1 4EBP1 branch. In HF female placentas, gene expression of insulin-like growth factor 2 (IGF2) and IGF2 receptor was elevated compared to placentas of females fed standard chow. Although male and female placentas responded differently to prenatal HF diet exposure, both male and female fetal weight was not altered by maternal HF diet.

CONCLUSIONS

Placenta responds and adapts to maternal metabolic changes by altering placental layer thickness, mTORC1 signaling, expression of nutrient transporters, and growth factors in a sex-specific manner.

摘要

目的

本研究旨在确定妊娠期间大鼠胎盘和胎儿对母体高脂(HF)饮食的反应,并确定可能的机制。

方法

妊娠期间,给怀孕的斯普拉格-道利大鼠喂食标准饲料(脂肪含量13.5%)或高脂(脂肪含量60%)饲料。在妊娠第21天收集胎盘。

结果

高脂饮食组母鼠孕期脂肪量增加、血浆瘦素水平升高、血浆脂联素水平降低,且糖耐量受损。高脂饮食组母鼠的雄性和雌性胎儿的胎盘迷路厚度均减小。在高脂饮食组雄性胎盘中,葡萄糖转运蛋白3基因表达、A系统氨基酸转运体(SNAT)2基因表达以及SNAT2蛋白表达通过mTORC1 4EBP1分支的激活而增加。与喂食标准饲料的雌性大鼠的胎盘相比,高脂饮食组雌性胎盘中胰岛素样生长因子2(IGF2)及其受体的基因表达升高。尽管雄性和雌性胎盘对产前高脂饮食暴露的反应不同,但母体高脂饮食并未改变雄性和雌性胎儿的体重。

结论

胎盘通过以性别特异性方式改变胎盘层厚度、mTORC1信号传导、营养转运体表达和生长因子,对母体代谢变化做出反应并进行适应。

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