title: Nutritional manipulations in the perinatal period program adipose tissue in offspring.
abstract: Epidemiological studies demonstrated initially that maternal undernutrition results in low birth weight with increased risk for long-lasting energy balance disorders. Maternal obesity and diabetes associated with high birth weight, excessive nutrition in neonates, and rapid catchup growth also increase the risk of adult-onset obesity. As stated by the Developmental Origin of Health and Disease concept, nutrient supply perturbations in the fetus or neonate result in long-term programming of individual body weight set point. Adipose tissue is a key fuel storage unit involved mainly in the maintenance of energy homeostasis. Studies in numerous animal models have demonstrated that the adipose tissue is the focus of developmental programming events in a sex- and depot-specific manner. In rodents, adipose tissue development is particularly active during the perinatal period, especially during the last week of gestation and during early postnatal life. In contrast to rodents, this process essentially takes place before birth in bigger mammals. Despite these different developmental time windows, altricial and precocial species share several mechanisms of adipose tissue programming. Offspring from malnourished dams present adipose tissue with a series of alterations: impaired glucose uptake, insulin and leptin resistance, low-grade inflammation, modified sympathetic activity with reduced noradrenergic innervations, and thermogenesis. These modifications reprogram adipose tissue metabolism by changing fat distribution and composition and by enhancing adipogenesis, predisposing the offspring to fat accumulation. Subtle adipose tissue circadian rhythm changes are also observed. Inappropriate hormone levels, modified tissue sensitivity (especially glucocorticoid system), and epigenetic mechanisms are key factors for adipose tissue programming during the perinatal period.
authors.affiliation: Unité Environnement Périnatal et Croissance, UPRES EA 4489, Equipe Dénutritions Maternelles Périnatales, Université Lille-Nord de France, Villeneuve d'Ascq, France;
authors.forename: Marie-Amélie
authors.initials: MA
authors.lastname: Lukaszewski
authors.forename: Delphine
authors.initials: D
authors.lastname: Eberlé
authors.forename: Didier
authors.initials: D
authors.lastname: Vieau
authors.forename: Christophe
authors.initials: C
authors.lastname: Breton
mesh_terms: D000273:Adipose Tissue / Q000196:embryology* / Q000378:metabolism*; D000328:Adult; D000818:Animals; D001724:Birth Weight / Q000235:genetics / Q000502:physiology; D005260:Female; D018507:Gene Expression Regulation, Developmental; D006801:Humans; D007231:Infant, Newborn; D039382:Maternal Nutritional Physiological Phenomena / Q000502:physiology; D009765:Obesity / Q000209:etiology / Q000378:metabolism; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000235:genetics; D039401:Prenatal Nutritional Physiological Phenomena / Q000502:physiology*
keywords: adipogenesis; adipose tissue; epigenetics; gestation; lactation