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早期生活营养环境对哺乳动物繁殖力的影响。

Effect of the early-life nutritional environment on fecundity and fertility of mammals.

机构信息

School of Veterinary Medicine and Science, University of Nottingham, Loughborough LE12 5RA, UK.

出版信息

Philos Trans R Soc Lond B Biol Sci. 2009 Nov 27;364(1534):3419-27. doi: 10.1098/rstb.2009.0121.

DOI:10.1098/rstb.2009.0121
PMID:19833652
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2781843/
Abstract

The early-life developmental environment is instrumental in shaping our overall adult health and well-being. Early-life diet and endocrine exposure may independently, or in concert with our genetic constitution, induce a pathophysiological process that amplifies with age and leads to premature morbidity and mortality. Recently, this has become known as 'programming' but is akin to 'maternal effects' described for many years in the biological sciences and is defined as any influence that acts during critical developmental windows to induce long-term changes in the organisms' phenotype. To date, such delayed maternal effects have largely been characterized in terms of susceptibility to cardiovascular or metabolic disease. Here, we review evidence from experimental animal species, non-human primates and man for an effect of the early-life nutritional environment on adult fecundity and fertility. In addition, using a database of pedigree sheep, we also specifically test the hypothesis that being born small for gestational age with or without post-natal growth acceleration directly programmes fertility. We conclude that there is a lack of compelling evidence to suggest pre-natal undernutrition may directly reduce adult fecundity and fertility, but may exert some effects secondarily via an increased incidence of 'metabolic syndrome'. Possible effects of being born relatively large on subsequent fecundity and fertility warrant further investigation.

摘要

生命早期的发育环境对我们成年后的整体健康和幸福感起着重要作用。生命早期的饮食和内分泌暴露可能会独立地或与我们的遗传构成一起,诱导一个随着年龄增长而加剧的病理生理过程,导致过早发病和死亡。最近,这种现象被称为“编程”,但类似于生物科学中多年来描述的“母体效应”,被定义为在关键发育窗口期间对生物体表型产生长期影响的任何影响。迄今为止,这种延迟的母体效应在很大程度上是根据对心血管或代谢疾病的易感性来描述的。在这里,我们回顾了实验动物物种、非人类灵长类动物和人类的证据,证明生命早期的营养环境对成年生育力和生育能力有影响。此外,我们还使用绵羊谱系数据库,专门测试了这样一个假设,即出生时的胎儿大小小于胎龄或出生后生长加速是否直接编程生育能力。我们得出的结论是,没有令人信服的证据表明产前营养不良可能直接降低成年生育力和生育能力,但可能通过增加“代谢综合征”的发生率而产生一些间接影响。出生时相对较大对随后的生育力和生育能力的可能影响值得进一步研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41f2/2781843/11d287847671/rstb20090121f05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41f2/2781843/65c3a2ecffdf/rstb20090121f01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41f2/2781843/6a62f8795779/rstb20090121f02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41f2/2781843/58e094dcb572/rstb20090121f03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41f2/2781843/ce771e109d93/rstb20090121f04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41f2/2781843/11d287847671/rstb20090121f05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41f2/2781843/65c3a2ecffdf/rstb20090121f01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41f2/2781843/6a62f8795779/rstb20090121f02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41f2/2781843/58e094dcb572/rstb20090121f03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41f2/2781843/ce771e109d93/rstb20090121f04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/41f2/2781843/11d287847671/rstb20090121f05.jpg

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