title: Fetal programming of appetite and obesity.
abstract: Obesity and related metabolic disorders are prevalent health issues in modern society and are commonly attributed to lifestyle and dietary factors. However, the mechanisms by which environmental factors modulate the physiological systems that control weight regulation and the aetiology of metabolic disorders, which manifest in adult life, may have their roots before birth. The 'fetal origins' or 'fetal programming' paradigm is based on the observation that environmental changes can reset the developmental path during intrauterine development leading to obesity and cardiovascular and metabolic disorders later in life. The pathogenesis is not based on genetic defects but on altered genetic expression as a consequence of an adaptation to environmental changes during fetal development. While many endocrine systems can be affected by fetal programming recent experimental studies suggest that leptin and insulin resistance are critical endocrine defects in the pathogenesis of programming-induced obesity and metabolic disorders. However, it remains to be determined whether postnatal obesity is a consequence of programming of appetite regulation and whether hyperphagia is the main underlying cause of the increased adiposity and the development of metabolic disorders.
authors.affiliation: Liggins Institute for Medical Research, Faculty of Medical and Health Sciences, University of Auckland, Private Bag 92019, Auckland, New Zealand. bh.breier@aucland.ac.nz
authors.forename: B H
authors.initials: BH
authors.lastname: Breier
authors.forename: M H
authors.initials: MH
authors.lastname: Vickers
authors.forename: B A
authors.initials: BA
authors.lastname: Ikenasio
authors.forename: K Y
authors.initials: KY
authors.lastname: Chan
authors.forename: W P
authors.initials: WP
authors.lastname: Wong
mesh_terms: D000818:Animals; D001066:Appetite / Q000502:physiology*; D004702:Endocrine Glands / Q000196:embryology / Q000503:physiopathology; D005260:Female; D005333:Fetus / Q000503:physiopathology; D006801:Humans; D007333:Insulin Resistance / Q000502:physiology; D020738:Leptin / Q000502:physiology; D009765:Obesity / Q000196:embryology* / Q000209:etiology; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects
chemical_list: D020738:Leptin