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[母亲肥胖与子代骨骼肌发育——代谢紊乱的胎儿起源]

[Maternal obesity and the development of skeletal muscle in offspring--fetal origin of metabolic disorders].

作者信息

Grabiec Kamil, Milewska Marta, Grzelkowska-Kowalczyk Katarzyna

机构信息

Katedra Nauk Fizjologicznych, Wydział Medycyny Weterynaryjnej, Szkoła Główna Gospodarstwa Wiejskiego w Warszawie, ul. Nowoursynowska 159, Warsaw.

出版信息

Postepy Hig Med Dosw (Online). 2012 Jan 4;66:1-10. doi: 10.5604/973505.

DOI:10.5604/973505
PMID:22371399
Abstract

Suboptimal fetal environments due to inadequate maternal nutrition, obesity, inflammation or gestational diabetes expose the fetus to humoral cues that alter metabolism and growth parameters leading to metabolic disturbances later in life. The fetal stage is crucial for the development of skeletal muscle, a tissue playing an important role in metabolism. Maternal obesity induces inflammation in the fetus causing modifications in the development of fetal skeletal muscle. Changes in the normal course of myogenesis may arise through several mechanisms: changes in WNT/β-catenin signaling pathway, decreased AMPK activity evoked by TNF-α, increased activity of NF-κB in response to inflammation, which leads to a decrease in myogenic factor MyoD, and increased expression of TGF β1. Modification in fetal development associated with maternal obesity is attributed to epigenetic changes. Polyunsaturated fatty acids supplied in the diet did affect the development of insulin-sensitive tissues during both the fetal and postnatal period. The specific phenotype of skeletal muscle fibers may play a role in the development of obesity, i.e. fiber phenotype I (slow, oxidative) may protect against obesity and insulin resistance. Exploring the mechanisms of direct impact of maternal obesity on the development of tissues in the offspring may help to reduce the occurrence of metabolic diseases in later life.

摘要

由于母体营养不足、肥胖、炎症或妊娠期糖尿病导致的胎儿环境欠佳,会使胎儿暴露于体液信号中,这些信号会改变新陈代谢和生长参数,从而导致日后生活中的代谢紊乱。胎儿期对于骨骼肌的发育至关重要,骨骼肌是一种在新陈代谢中起重要作用的组织。母体肥胖会在胎儿体内引发炎症,导致胎儿骨骼肌发育发生改变。正常的肌生成过程中的变化可能通过多种机制产生:WNT/β-连环蛋白信号通路的变化、TNF-α诱发的AMPK活性降低、炎症反应导致的NF-κB活性增加(这会导致肌源性因子MyoD减少)以及TGF β1表达增加。与母体肥胖相关的胎儿发育改变归因于表观遗传变化。饮食中提供的多不饱和脂肪酸在胎儿期和出生后时期均会影响胰岛素敏感组织的发育。骨骼肌纤维的特定表型可能在肥胖的发生中起作用,即I型纤维(慢肌、氧化型)可能对肥胖和胰岛素抵抗具有保护作用。探究母体肥胖对后代组织发育的直接影响机制,可能有助于减少日后生活中代谢疾病的发生。

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