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Developmental Origins of Adult DiseaseLangley-Evans S.C. · McMullen S.
School of Biosciences, University of Nottingham, Nottingham, UK Corresponding Author
Prof. Simon Langley-Evans
School of Biosciences, University of Nottingham, Sutton Bonington
Loughborough, LE12 5RD (UK)
Tel. +44 115 951 6139, Fax +44 115 951 6122
Variation in the quality or quantity of nutrients consumed during pregnancy can exert permanent and powerful effects upon the developing fetus. This programming of fetal development is emerging as a new risk factor for non-communicable diseases of adulthood, including coronary heart disease and the metabolic syndrome. Epidemiological studies show that indicators of nutritional deficit in pregnancy are associated with greater risk of diabetes and cardiovascular mortality. The study of programming in relation to disease processes has been advanced by the development of animal models, which have utilized both under- and overfeeding of specific nutrients in pregnancy. Studies of this nature support the nutritional programming hypothesis and provide tools with which to examine the mechanisms through which programming may occur. Studies of animals subject to undernutrition in utero generally exhibit changes in the structure of key organs, such as the kidney and pancreas. These effects are consistent with the concept that programming influences remodel the development of organs. The causal pathways which extend from tissue remodelling to disease processes are relatively well characterised. In contrast, the processes which drive disordered organ development are poorly understood. It is noteworthy that minor perturbation of maternal nutritional status can programme fetal development. It is suggested therefore that programming is a product of altered expression of key genes. This drives the tissue remodelling response and future disease risk.
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