Body Composition and Circulating High-Molecular-Weight Adiponectin and IGF-I in Infants Born Small for Gestational Age
Breast- Versus Formula-Feeding
- Francis de Zegher1,
- Giorgia Sebastiani2,3,
- Marta Diaz2,3,
- David Sánchez-Infantes2,3,
- Abel Lopez-Bermejo4,5 and
- Lourdes Ibáñez2,3⇓
- 1Department of Pediatrics, University of Leuven, Leuven, Belgium
- 2Hospital Sant Joan de Déu, University of Barcelona, Barcelona, Spain
- 3Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas, Instituto de Salud Carlos III, Madrid, Spain
- 4Department of Pediatrics, Dr. Josep Trueta Hospital, Girona, Spain
- 5Girona Institute for Biomedical Research, Girona, Spain
- Corresponding author: Lourdes Ibáñez, .
Prenatal growth restraint, if followed by postnatal overweight, confers risk for adult disease including diabetes. The mechanisms whereby neonatal nutrition may modulate such risk are poorly understood. We studied the effects of nutrition (breast-feeding [BRF] vs. formula-feeding [FOF]) on weight partitioning and endocrine state (as judged by high-molecular-weight [HMW] adiponectin and IGF-I) of infants born small for gestational age (SGA). Body composition (by absorptiometry), HMW adiponectin, and IGF-I were assessed at birth and 4 months in BRF infants born appropriate for gestational age (AGA; n = 72) and SGA infants receiving BRF (n = 46) or FOF (n = 56), the latter being randomized to receive a standard (FOF1) or protein-rich formula (FOF2). Compared with AGA-BRF infants, the catchup growth of SGA infants was confined to lean mass, independently of nutrition. Compared with AGA-BRF infants, SGA-BRF infants had normal HMW adiponectin and IGF-I levels at 4 months, whereas SGA-FOF infants had elevated levels of HMW adiponectin (particularly SGA-FOF1) and IGF-I (particularly SGA-FOF2). In conclusion, neonatal nutrition seems to influence endocrinology more readily than body composition of SGA infants. Follow-up will disclose whether the endocrine abnormalities in SGA-FOF infants can serve as early markers of an unfavorable metabolic course and whether they may contribute to design early interventions that prevent subsequent disease, including diabetes.
This article contains Supplementary Data online at http://diabetes.diabetesjournals.org/lookup/suppl/doi:10.2337/db11-1797/-/DC1.
- Received December 20, 2011.
- Accepted March 9, 2012.
- © 2012 by the American Diabetes Association.
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