title: Experimental models of developmental programming: consequences of exposure to an energy rich diet during development.
abstract: Studies in both humans and experimental animals addressing the 'Fetal Origins of Adult Disease' hypothesis have established a relationship between an adverse intrauterine environment and offspring disease in adult life. This phenomenon, termed 'fetal programming' describes a process whereby a stimulus in utero establishes a permanent response in the fetus leading to enhanced susceptibility to later disease. However, the environment, during periods of developmental plasticity in postnatal life, can also 'programme' function. Thus, the terms 'developmental programming' and the 'Developmental Origins of Adult Health and Disease' are preferentially utilized. The 'Thrifty Phenotype' hypothesis explained the association between insufficient in utero nutrition and the later development of Type 2 diabetes. Most recently the 'Predictive Adaptive Response' hypothesis proposes that the degree of mismatch between the pre- and postnatal environments is an important determinant of subsequent disease. Epidemiological studies have indicated that fetal growth restriction correlates with later disease, implying that fetal nutritional deprivation is a strong programming stimulus. This prompted the development of experimental animal models using controlled maternal calorie, protein or macronutrient deficiency during key periods of gestation. However, in many societies, maternal and postnatal nutrition are either sufficient or excessive. Here, we examine findings from a range of nutritional studies examining maternal and/or postnatal nutritional excess. There is supportive evidence from a limited number of studies to test the 'Predictive Adaptive Response' hypothesis. These suggest that maternal over-nutrition is deleterious to the health of offspring and can result in a phenotype of the offspring that is characteristic of metabolic syndrome.
authors.affiliation: Maternal and Fetal Research Unit, Division of Reproductive Health, Endocrinology and Development, GKT School of Medicine, St Thomas' Hospital, Lambeth Palace Road, London SE1 7EH, UK. james.armitage@kcl.ac.uk
authors.forename: James A
authors.initials: JA
authors.lastname: Armitage
authors.forename: Paul D
authors.initials: PD
authors.lastname: Taylor
authors.forename: Lucilla
authors.initials: L
authors.lastname: Poston
mesh_terms: D000222:Adaptation, Physiological; D000818:Animals; D002319:Cardiovascular System / Q000196:embryology / Q000503:physiopathology; D004032:Diet; D004195:Disease Models, Animal; D004734:Energy Metabolism; D005260:Female; D006801:Humans; D018811:Maternal Exposure / Q000009:adverse effects; D024821:Metabolic Syndrome / Q000196:embryology / Q000209:etiology / Q000503:physiopathology; D023421:Models, Animal; D008954:Models, Biological; D009765:Obesity / Q000196:embryology* / Q000209:etiology / Q000503:physiopathology*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D039401:Prenatal Nutritional Physiological Phenomena