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母体围产期营养不良改变乳汁中的乳糖和转铁蛋白:与代谢性疾病的发生有关?

Maternal perinatal undernutrition modifies lactose and serotranferrin in milk: relevance to the programming of metabolic diseases?

机构信息

Environnement Périnatal et Croissance (EA4489), Université Lille-Nord de France, Equipe Dénutritions Maternelles Périnatales, Université de Lille, Villeneuve d'Ascq, France;

Unité de Glycobiologie Structurale et Fonctionnelle (UMR8576), Université de Lille, Villeneuve d'Ascq, France;

出版信息

Am J Physiol Endocrinol Metab. 2015 Mar 1;308(5):E393-401. doi: 10.1152/ajpendo.00452.2014. Epub 2014 Dec 30.

DOI:10.1152/ajpendo.00452.2014
PMID:25550282
Abstract

A close link between intrauterine growth restriction and development of chronic adult diseases such as obesity, diabetes, and hypertension has been established both in humans and animals. Modification of growth velocity during the early postnatal period (i.e., lactation) may also sensitize to the development of metabolic syndrome in adulthood. This suggests that milk composition may have long-lasting programming/deprogramming metabolic effects in the offspring. We therefore assess the effects of maternal perinatal denutrition on breast milk composition in a food-restricted 50% (FR50) rat model. Monosaccharides and fatty acids were characterized by gas chromatography, and proteins were profiled by surface-enhanced laser desorption/ionization-time-of-flight analysis in milk samples from FR50 and control rat dams. Milk analysis of FR50 rats demonstrated that maternal undernutrition decreases lactose concentration and modulates lipid profile at postnatal day 10 by increasing the unsaturated fatty acids/saturated fatty acids and diminishes serotransferrin levels at postnatal day 21. Our data indicate that maternal perinatal undernutrition modifies milk composition both quantitatively and qualitatively. These modifications by maternal nutrition open new perspectives to identify molecules that could be used in artificial milk to protect from the subsequent development of metabolic diseases.

摘要

宫内生长受限与肥胖、糖尿病和高血压等慢性成人疾病的发展之间存在密切联系,这在人类和动物中都得到了证实。在生命早期(即哺乳期)改变生长速度也可能使成年后更容易发生代谢综合征。这表明,牛奶成分可能对后代的代谢具有持久的编程/去编程作用。因此,我们在限制食物摄入的 50%(FR50)大鼠模型中评估了母体围产期营养不良对母乳成分的影响。通过气相色谱法对单糖和脂肪酸进行了特征分析,并通过表面增强激光解吸/电离-飞行时间分析对 FR50 和对照大鼠母鼠乳汁样本中的蛋白质进行了分析。对 FR50 大鼠的乳汁分析表明,母体营养不良会降低乳糖浓度,并通过增加不饱和脂肪酸/饱和脂肪酸在产后第 10 天改变脂质谱,并在产后第 21 天降低转铁蛋白水平。我们的数据表明,母体围产期营养不良会同时在数量和质量上改变乳汁成分。这些由母体营养引起的变化为鉴定可用于人工乳汁的分子以预防随后发生代谢疾病提供了新的视角。

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