
Vol. 65, Suppl. 3, 2006
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Understanding the Biology and Therapeutic Consequences of Being Born SGA. Editor(s): Czernichow, P. (Paris), Dunger, D. (Cambridge), Lévy-Marchal, C. (Paris)
Early Postnatal Growth
Size at Birth, Postnatal Growth and Risk of Obesity
K.K. Onga, b
aMRC Epidemiology Unit, Strangeways Research Laboratory, Cambridge, and bDepartment of Paediatrics, University of Cambridge, Addenbrooke's Hospital, Cambridge, UK
Address of Corresponding Author
Horm Res 2006;65 (Suppl. 3):65-69 (DOI: 10.1159/000091508)
Key Words
- Birth weight
- Catch-up
- Diabetes
- Obesity
- Weight gain
Abstract
Epidemiological studies over the last 15 years have shown that size at birth, early postnatal catch-up growth and excess childhood weight gain are associated with an increased risk of adult cardiovascular disease and type 2 diabetes. At the same time, rising rates of obesity and overweight in children, even at pre-school ages, have shifted efforts towards the identification of very early factors that predict risk of subsequent obesity, which may allow early targeted interventions. Overall, higher birth weight is positively associated with subsequent greater body mass index in childhood and later life; however, the relationship is complex. Higher birth weight is associated with greater subsequent lean mass, rather than fat mass. In contrast, lower birth weight is associated with a subsequent higher ratio of fat mass to lean mass, and greater central fat and insulin resistance. This paradoxical effect of lower birth weight is at least partly explained by the observation that infants who have been growth restrained in utero tend to gain weight more rapidly, or 'catch up', during the early postnatal period, which leads to increased central fat deposition. There is still debate as to whether there are critical early periods for obesity: does excess weight gain during infancy, childhood or even very early neonatal life have a greater impact on long-term fat deposition and insulin resistance? Early identification of childhood obesity risk will be aided by identification of maternal and fetal genes that regulate fetal nutrition and growth, and postnatal genes that regulate appetite, energy expenditure and the partitioning of energy intake into fat or lean tissue growth. Copyright © 2006 S. Karger AG, Basel
Author Contacts
K.K. Ong MRC Epidemiology Unit, Strangeways Research Laboratory Wort's Causeway Cambridge CB1 8RN (UK) Tel. +44 1223 740 003, Fax +44 1223 740 050, E-Mail ken.ong@mrc-epid.cam.ac.uk
Article Information
Published online: April 10, 2006
Number of Print Pages : 5
Number of Figures : 0, Number of Tables : 1, Number of References : 32 |
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