title: Leptin in pregnancy and development: a contributor to adulthood disease?
abstract: Emerging research has highlighted the importance of leptin in fetal growth and development independent of its essential role in the maintenance of hunger and satiety through the modulation of neuropeptide Y and proopiomelanocortin neurons. Alterations in maternal-placental-fetal leptin exchange may modify the development of the fetus and contribute to the increased risk of developing disease in adulthood. In addition, leptin also plays an important role in reproductive functions, with plasma leptin concentrations rising in pregnant women, peaking during the third trimester. Elevated plasma leptin concentrations occur at the completion of organogenesis, and research in animal models has demonstrated that leptin is involved in the development and maturation of a number of organs, including the heart, brain, kidneys, and pancreas. Elevated maternal plasma leptin is associated with maternal obesity, and reduced fetal plasma leptin is correlated with intrauterine growth restriction. Alterations in plasma leptin during development may be associated with an increased risk of developing a number of adulthood diseases, including cardiovascular, metabolic, and renal diseases via altered fetal development and organogenesis. Importantly, research has shown that leptin antagonism after birth significantly reduces maturation of numerous organs. Conversely, restoration of the leptin deficiency after birth in growth-restricted animals restores the offspring's body weight and improves organogenesis. Therefore, leptin appears to play a major role in organogenesis, which may adversely affect the risk of developing a number of diseases in adulthood. Therefore, greater understanding of the role of leptin during development may assist in the prevention and treatment of a number of disease states that occur in adulthood.
authors.affiliation: Department of Physiology, University of Melbourne, Parkville, Australia;
authors.forename: Jessica F
authors.initials: JF
authors.lastname: Briffa
authors.affiliation: Centre for Chronic Disease Prevention and Management, College of Health and Biomedicine, Victoria University, St. Albans, Australia; and.
authors.forename: Andrew J
authors.initials: AJ
authors.lastname: McAinch
authors.affiliation: Department of Human Biosciences, Latrobe University, Bundoora, Australia.
authors.forename: Tania
authors.initials: T
authors.lastname: Romano
authors.affiliation: Department of Physiology, University of Melbourne, Parkville, Australia;
authors.forename: Mary E
authors.initials: ME
authors.lastname: Wlodek
authors.affiliation: Department of Physiology, University of Melbourne, Parkville, Australia; Deanne.Skelly@unimelb.edu.au.
authors.forename: Deanne H
authors.initials: DH
authors.lastname: Hryciw
mesh_terms: D000328:Adult; D000818:Animals; D004194:Disease / Q000209:etiology*; D005260:Female; D047109:Fetal Development; D006801:Humans; D020738:Leptin / Q000097:blood*; D008431:Maternal-Fetal Exchange / Q000502:physiology; D011247:Pregnancy / Q000097:blood*; D011297:Prenatal Exposure Delayed Effects / Q000097:blood*; D012307:Risk Factors
chemical_list: D020738:Leptin
keywords: adulthood diseases; intrauterine growth restriction; leptin; maternal obesity; organogenesis