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代谢综合征:母体营养不足与胎儿编程的作用。

Metabolic syndrome: role of maternal undernutrition and fetal programming.

机构信息

Department of Cardiac Biochemistry, All India Institute of Medical Sciences, New Delhi, 110049, India,

出版信息

Rev Endocr Metab Disord. 2013 Sep;14(3):229-40. doi: 10.1007/s11154-013-9266-4.

Abstract

Development of metabolic syndrome is attributed to genes, dietary intake, physical activity and environmental factors. Fetal programming due to maternal nutrition is also an important factor especially in developing countries where intrauterine growth retardation followed by excess nutrition postnatally is causing mismatch predisposing individuals to development of metabolic syndrome and its components. Several epidemiological and animal studies have provided evidence for the link between intrauterine growth retardation and adult metabolic diseases. Deficiency of macronutrients, protein and carbohydrates, during pregnancy and gestation results in lower infant birth weight, a surrogate marker of fetal growth and subsequently insulin resistance, glucose intolerance, hypertension and adiposity in adulthood. The role of micronutrients is less extensively studied but however gaining attention with several recent studies focusing on this aspect. Several mechanisms have been proposed to explain the developmental origin of adult diseases important among them being alteration of hypothalamic pituitary axis, epigenetic regulation of gene expression and oxidative stress. All of these mechanisms may be acting at different time during gestation and contributing to development of metabolic syndrome in adulthood.

摘要

代谢综合征的发展归因于基因、饮食摄入、身体活动和环境因素。由于母体营养而导致的胎儿编程也是一个重要因素,特别是在发展中国家,宫内生长迟缓随后是出生后过度营养导致个体易发生代谢综合征及其组分。一些流行病学和动物研究为宫内生长迟缓与成人代谢性疾病之间的联系提供了证据。在怀孕期间和妊娠期缺乏宏量营养素、蛋白质和碳水化合物会导致婴儿出生体重降低,这是胎儿生长的替代标志物,随后在成年时会导致胰岛素抵抗、葡萄糖耐量降低、高血压和肥胖。微量营养素的作用研究得较少,但随着最近的一些研究集中在这方面,它越来越受到关注。已经提出了几种机制来解释成人疾病的发育起源,其中重要的是下丘脑-垂体轴的改变、基因表达的表观遗传调控和氧化应激。所有这些机制可能在妊娠的不同时间起作用,并导致成年期代谢综合征的发生。

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