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生命早期营养与成人疾病结局的关联机制。

Mechanisms behind early life nutrition and adult disease outcome.

机构信息

Elena Velkoska, Department of Medicine, The University of Melbourne, Heidelberg Repatriation Hospital, Heidelberg Heights, 3081, Victoria, Australia.

出版信息

World J Diabetes. 2011 Aug 15;2(8):127-32. doi: 10.4239/wjd.v2.i8.127.

DOI:10.4239/wjd.v2.i8.127
PMID:21954416
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3180529/
Abstract

Obesity is increasing around the globe. While adult lifestyle factors undoubtedly contribute to the incidence of obesity and its attendant disorders, mounting evidence suggests that programming of obesity may occur following under- and over-nutrition during development. As hypothalamic control of appetite and energy expenditure is set early in life and can be perturbed by certain exposures such as undernutrition and altered metabolic and hormonal signals, in utero exposure to altered maternal nutrition and inadequate nutrition during early postnatal life may contribute to programming of obesity in offspring. Data from animal studies indicate both intrauterine and postnatal environments are critical determinants of the development of pathways regulating energy homeostasis. This review summarizes recent evidence of the impact of maternal nutrition as well as postnatal nutrition of the offspring on subsequent obesity and disease risk of the offspring. While much of the experimental work reviewed here was conducted in the rodent, these observations provide useful insights into avenues for future research into developing preventive measures to curb the obesity epidemic.

摘要

肥胖症在全球范围内不断增加。虽然成年人的生活方式因素无疑促成了肥胖症及其相关疾病的发生,但越来越多的证据表明,肥胖症的发生可能是由于在发育过程中营养不足和营养过剩。由于食欲和能量消耗的下丘脑控制在生命早期就已确定,并且可能会受到某些暴露的干扰,如营养不良和代谢及激素信号改变,因此,胎儿期暴露于改变了的母体营养和新生儿期营养不足可能会导致后代肥胖的发生。来自动物研究的数据表明,宫内和产后环境都是调节能量平衡通路发育的关键决定因素。本综述总结了近期关于母体营养以及后代产后营养对后代肥胖和疾病风险的影响的证据。虽然这里回顾的大部分实验工作都是在啮齿动物中进行的,但这些观察结果为未来研究提供了有用的思路,以制定预防措施来遏制肥胖症的流行。

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本文引用的文献

1
Early life influences on obesity risk: maternal overnutrition and programming of obesity.早年生活对肥胖风险的影响:母亲营养过剩与肥胖的程序化
Expert Rev Endocrinol Metab. 2009 Nov;4(6):625-637. doi: 10.1586/eem.09.45.
2
Chronic high-fat diet in fathers programs β-cell dysfunction in female rat offspring.父亲慢性高脂肪饮食使雌性子代大鼠胰岛β细胞功能障碍。
Nature. 2010 Oct 21;467(7318):963-6. doi: 10.1038/nature09491.
3
Hypothalamic neuroendocrine circuitry is programmed by maternal obesity: interaction with postnatal nutritional environment.下丘脑神经内分泌回路由母体肥胖编程:与产后营养环境的相互作用。
PLoS One. 2009 Jul 16;4(7):e6259. doi: 10.1371/journal.pone.0006259.
4
Maternal obesity induced by diet in rats permanently influences central processes regulating food intake in offspring.饮食诱导的大鼠母体肥胖会永久性地影响调节后代食物摄入的中枢过程。
PLoS One. 2009 Jun 11;4(6):e5870. doi: 10.1371/journal.pone.0005870.
5
Identification and importance of brown adipose tissue in adult humans.成人棕色脂肪组织的识别及其重要性。
N Engl J Med. 2009 Apr 9;360(15):1509-17. doi: 10.1056/NEJMoa0810780.
6
Maternal obesity is necessary for programming effect of high-fat diet on offspring.母体肥胖是高脂饮食对后代产生编程效应所必需的。
Am J Physiol Regul Integr Comp Physiol. 2009 May;296(5):R1464-72. doi: 10.1152/ajpregu.91015.2008. Epub 2009 Feb 25.
7
Maternal nutritional history predicts obesity in adult offspring independent of postnatal diet.母亲的营养史可独立于产后饮食预测成年后代的肥胖情况。
J Physiol. 2009 Feb 15;587(Pt 4):905-15. doi: 10.1113/jphysiol.2008.163477. Epub 2008 Dec 22.
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Established maternal obesity in the rat reprograms hypothalamic appetite regulators and leptin signaling at birth.大鼠孕期已存在的母体肥胖会在出生时对下丘脑食欲调节因子和瘦素信号进行重编程。
Int J Obes (Lond). 2009 Jan;33(1):115-22. doi: 10.1038/ijo.2008.213. Epub 2008 Nov 4.
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Obesity (Silver Spring). 2008 Oct;16(10):2323-30. doi: 10.1038/oby.2008.351. Epub 2008 Jul 24.
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