Blackmore H L, Ozanne S E
Level 4 Metabolic Research Laboratories, Institute of Metabolic Sciences, University of Cambridge, Addenbrookes Hospital, Cambridge, UK.
J Dev Orig Health Dis. 2013 Oct;4(5):338-47. doi: 10.1017/S2040174412000761.
It is widely recognized that environmental insults during adulthood including smoking, lack of exercise and a poor diet increases an individual's risk of cardiovascular disease (CVD). However, research initiated over the last two decades has highlighted that our risk of CVD can be programmed following adverse exposures during early development. Such adverse exposures may include, undernutrition, placental insufficiency, hypoxia, overnutrition and obesity. This review aims to address the current Western obesity crisis by addressing the long-term impact of maternal overnutrition and obesity on the offspring's future risk of CVD. Although current human studies have observed the presence of adverse CVD markers in children born to obese mothers, animal models have proved vital in understanding the underlying mechanisms involved. Mechanisms suggested to be involved in the programming of CVD in the offspring include increased oxidative stress, inflammation, lipotoxicity and epigenetics. CVD remains the greatest cause of death worldwide, therefore further understanding of the mechanisms mediating these effects is important in the development of intervention strategies.
人们普遍认识到，成年期的环境损害，包括吸烟、缺乏运动和不良饮食，会增加个体患心血管疾病（CVD）的风险。然而，过去二十年来开展的研究强调，我们患心血管疾病的风险可能在早期发育过程中遭受不良暴露后就被编程了。此类不良暴露可能包括营养不足、胎盘功能不全、缺氧、营养过剩和肥胖。本综述旨在通过探讨母亲营养过剩和肥胖对后代未来患心血管疾病风险的长期影响，来应对当前西方的肥胖危机。尽管目前的人体研究已经观察到肥胖母亲所生孩子中存在不良心血管疾病标志物，但动物模型已被证明在理解其中涉及的潜在机制方面至关重要。提示与后代心血管疾病编程有关的机制包括氧化应激增加、炎症、脂毒性和表观遗传学。心血管疾病仍然是全球最大的死因，因此进一步了解介导这些影响的机制对于制定干预策略很重要。
