Journal
JOURNAL OF ANATOMY
Volume 215, Issue 1, Pages 52-59Publisher
WILEY
DOI: 10.1111/j.1469-7580.2008.01033.x
Keywords
blastocyst; in vitro culture; kidney; maternal diet; preimplantation embryo; renin-angiotensin system; vascular responsiveness
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Funding
- BBSRC [BB/F007450/1] Funding Source: UKRI
- MRC [G0100558] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/F007450/1, G18784] Funding Source: researchfish
- Medical Research Council [G0100558] Funding Source: researchfish
- Biotechnology and Biological Sciences Research Council [BB/F007450, G18784, BB/F007450/1] Funding Source: Medline
- Medical Research Council [G0100558] Funding Source: Medline
- NICHD NIH HHS [U01 HD044635-03, U01 HD044635] Funding Source: Medline
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The development of adult-onset diseases such as type II diabetes, obesity and cardiovascular disease is traditionally attributed to adult lifestyle characteristics such as a lack of physical exercise, poor diet and smoking. However, evidence from both human and animal model studies has demonstrated that environmental factors such as an imbalance or reduction in maternal nutrition during gestation can have adverse effects on offspring metabolism and cardiovascular health. The severity and nature of the phenotypic changes induced in offspring is influenced by the period of gestation manipulated. In particular, the mammalian preimplantation embryo in different animal models displays particular sensitivity to environmental factors, either in vivo (maternal diet) or in vitro (embryo culture) that is associated with the onset of cardiovascular dysfunction in adult life. The detailed mechanisms by which environmental conditions can alter postnatal cardiovascular physiology are poorly understood. However, various factors including endothelial function, vascular responsiveness, the renin-angiotensin system, kidney structure and early postnatal growth dynamics have all been recognize as potential contributors. Here, we review the relationship between preimplantation embryo environment and postnatal cardiovascular disease risk, and consider biochemical, molecular, genetic and physiological pathways implicated in this association.
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