title: Fetal programming and metabolic syndrome.
abstract: Metabolic syndrome is reaching epidemic proportions, particularly in developing countries. In this review, we explore the concept-based on the developmental-origin-of-health-and-disease hypothesis-that reprogramming during critical times of fetal life can lead to metabolic syndrome in adulthood. Specifically, we summarize the epidemiological evidence linking prenatal stress, manifested by low birth weight, to metabolic syndrome and its individual components. We also review animal studies that suggest potential mechanisms for the long-term effects of fetal reprogramming, including the cellular response to stress and both organ- and hormone-specific alterations induced by stress. Although metabolic syndrome in adulthood is undoubtedly caused by multiple factors, including modifiable behavior, fetal life may provide a critical window in which individuals are predisposed to metabolic syndrome later in life.
authors.affiliation: Division of Reproductive Endocrinology and Infertility, Department of Obstetrics, Gynecology and Reproductive Sciences, University of California, San Francisco, California 94115, USA. rinaudop@obgyn.ucsf.edu
authors.forename: Paolo
authors.initials: P
authors.lastname: Rinaudo
authors.forename: Erica
authors.initials: E
authors.lastname: Wang
mesh_terms: D000328:Adult; D000818:Animals; D003585:Cell Biology; D005260:Female; D047109:Fetal Development / Q000502:physiology*; D006801:Humans; D007030:Hypothalamo-Hypophyseal System / Q000502:physiology; D007231:Infant, Newborn; D024821:Metabolic Syndrome / Q000503:physiopathology*; D008954:Models, Biological; D009747:Nutritional Physiological Phenomena; D009928:Organ Specificity; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D013045:Species Specificity; D013312:Stress, Physiological