Gardiner Helena M
Institute of Reproductive and Developmental Biology, Faculty of Medicine, Imperial College, Queen Charlotte's and Chelsea Hospital, London, UK.
Early Hum Dev. 2007 Dec;83(12):819-23. doi: 10.1016/j.earlhumdev.2007.09.011. Epub 2007 Sep 25.
The "fetal origins hypothesis" proposes that a fetus' adaptation to its intrauterine environment and postnatal stressors may have life-long consequences and that the fetal response to an environmental challenge may result in programming of different organ systems, depending on the timing of the insult. Growth restriction in the last trimester of pregnancy has been associated with later cardiovascular disease, not only through disturbances of normal cardiovascular and neuro-hormonal control mechanisms, but also because the "catch-up growth" observed in growth restricted infants disturbs the "thrifty phenotype" that permits an individual to live within its predicted environment. Problems in testing the fetal programming hypothesis include the measurement of an individual's failure to achieve their growth potential and the absence of an effective early measurement of later cardiovascular risk. However, individuals studied during fetal life are now reaching adulthood and will provide us with new insights into vascular programming.
“胎儿起源假说”提出,胎儿对其子宫内环境和出生后应激源的适应可能会产生终身影响,并且胎儿对环境挑战的反应可能会导致不同器官系统的编程,这取决于损伤发生的时间。妊娠晚期的生长受限不仅与随后的心血管疾病有关,这是由于正常心血管和神经激素控制机制受到干扰,还因为在生长受限婴儿中观察到的“追赶生长”扰乱了使个体能够在其预测环境中生存的“节俭表型”。检验胎儿编程假说存在的问题包括测量个体未能实现其生长潜力,以及缺乏对后期心血管风险的有效早期测量。然而,在胎儿期接受研究的个体现已成年,这将为我们提供有关血管编程的新见解。