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EMBRYONIC AND FETAL PROGRAMMING OF PHYSIOLOGICAL DISORDERS IN ADULTHOOD
Citation:
LAU, C. S. AND J. M. ROGERS. EMBRYONIC AND FETAL PROGRAMMING OF PHYSIOLOGICAL DISORDERS IN ADULTHOOD. Birth Defects Research, Part C: Embryo Today: Reviews. John Wiley & Sons, Ltd., Indianapolis, IN, 72(4):300-312, (2004).
Description:
In the past decade, numerous epidemiological studies have indicated strong inverse associations between birth weight and risk of coronary heart disease, hypertension, type 2-diabetes and other diseases in adulthood. The ¿Barker hypothesis¿ thus postulates that a number of organ structures and functions undergo programming during embryonic and fetal life. This developmental programming determines the set-points of physiological and metabolic responses in adult life. Alterations of nutrient availability during gestation may lead to developmental adaptations, via hormonal maneuvers by the embryo and fetus that re-adjust these set-points. These adaptive measures have short-term benefits to the embryo and fetus, so that the newborn will be better prepared for the adverse environment (e.g. undernutrition). However, adequate nutritional support during postnatal life that enables catch-up growth may create metabolic conflicts that predispose the adult to aberrant physiological functions and ultimately, increased risk of disease. It is plausible that other adverse in utero conditions, including exposure to developmental toxiciants may similarly alter the adult disease susceptibility. This paper provides an overview of the Barker hypothesis, its supporting evidence, the current advances in understanding the biological mechanisms underlying this phenomenon, and its implications for developmental toxicology.