title: Maternal undernutrition and fetal developmental programming of obesity: the glucocorticoid connection.
abstract: An adequate maternal nutrition during pregnancy is crucial for the health outcome of offspring in adulthood. Maternal undernutrition during critical periods of fetal development can program the fetus for metabolic syndrome (MetS) later in life, especially when postnatally challenged with a hypernutritive diet. Adipogenesis, which begins in utero and accelerates in neonatal life, is a major candidate for developmental programming. During fetal development, the hypothalamic-pituitary-adrenal (HPA) axis is extremely susceptible to programming, and the HPA tone is increased throughout life in undernourished conditions. As a consequence, an alteration in the expression and function of glucocorticoid (GC) receptors and of the major GC regulatory enzymes (11β-hydroxysteroid dehydrogenase 1 and -2) occurs. In this review, we will give insights into the role of maternoplacental adverse interactions under the specific context of maternal undernutrition, for later-in-life MetS development, with a special emphasis on the role of GCs.
authors.affiliation: Department of Biochemistry, Faculty of Medicine, University of Porto, Porto, Portugal.
authors.forename: Ana
authors.initials: A
authors.lastname: Correia-Branco
authors.affiliation: Department of Biochemistry, Faculty of Medicine, University of Porto, Porto, Portugal Center for Biotechnology and Fine Chemistry, School of Biotechnology, Portuguese Catholic University, Porto, Portugal.
authors.forename: Elisa
authors.initials: E
authors.lastname: Keating
authors.affiliation: Department of Biochemistry, Faculty of Medicine, University of Porto, Porto, Portugal fmartel@med.up.pt.
authors.forename: Fátima
authors.initials: F
authors.lastname: Martel
mesh_terms: D043205:11-beta-Hydroxysteroid Dehydrogenase Type 1 / Q000378:metabolism; D043209:11-beta-Hydroxysteroid Dehydrogenase Type 2 / Q000378:metabolism; D000273:Adipose Tissue / Q000378:metabolism / Q000503:physiopathology; D000818:Animals; D005260:Female; D005938:Glucocorticoids / Q000378:metabolism*; D006801:Humans; D007030:Hypothalamo-Hypophyseal System / Q000378:metabolism / Q000503:physiopathology; D044342:Malnutrition / Q000150:complications* / Q000378:metabolism / Q000503:physiopathology; D039382:Maternal Nutritional Physiological Phenomena; D009752:Nutritional Status; D009765:Obesity / Q000209:etiology* / Q000378:metabolism / Q000503:physiopathology; D010913:Pituitary-Adrenal System / Q000378:metabolism / Q000503:physiopathology; D010920:Placenta / Q000378:metabolism / Q000503:physiopathology; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D011965:Receptors, Glucocorticoid / Q000378:metabolism; D015398:Signal Transduction
chemical_list: D005938:Glucocorticoids; D011965:Receptors, Glucocorticoid; D043205:11-beta-Hydroxysteroid Dehydrogenase Type 1; D043209:11-beta-Hydroxysteroid Dehydrogenase Type 2
keywords: fetal developmental programming; glucocorticoids; maternal undernutrition; metabolic syndrome