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The Journal of Clinical Endocrinology & Metabolism Vol. 84, No. 6 1949-1953
Copyright © 1999 by The Endocrine Society


Original Studies

High Serum Leptin Concentrations during Catch-Up Growth of Children Born with Intrauterine Growth Retardation1

D. Jaquet, J. Leger, M. D. Tabone, P. Czernichow and C. Levy-Marchal

INSERM U-457, Hôpital R. Debré (D.J., J.L., P.C., C.L.-M.), 75019 Paris; and Centre du Bilan de Santé de l’Enfant (M.D.T.), Paris, France

Address all correspondence and requests for reprints to: Delphine Jaquet, M.D., INSERM U-457, Hôpital Robert Debré, 48 boulevard Sérurier, 75019 Paris, France. E-mail: djacquet{at}infobiogen.fr

The aim of the study was to investigate how leptin could be involved in catch-up growth of children born with intrauterine growth retardation (IUGR). The study population was made up of 70 newborns with IUGR longitudinally studied during the first 2 yr of life and 35 newborns and 32, 66, and 61 children with normal birth weight aged 3 days, 12 months, and 24 months, respectively. Postnatal patterns of body mass index (BMI) were similar in the 2 groups, but BMI remained significantly lower in IUGR over the study period. In contrast, children born with IUGR aged 1 yr had significantly higher serum leptin levels than normal children (P < 0.0001) independently of BMI. The correlation observed between BMI and serum leptin at birth in both groups and in the control group thereafter disappeared in children born with IUGR. Similarly, sexual dimorphism observed in normal children over the study period was not observed in the IUGR group during the first 2 yr of life. In summary, serum leptin is effective and regulated during the first years of life as it is in older children. Children born with IUGR demonstrate high serum leptin values during the first year of life, with a loss of the regulatory effect of BMI and gender. We suggest that these children develop an adaptative leptin resistance beneficial for their catch-up growth. An alternative hypothesis is that these observations could reflect an adipocyte dysfunction, a consequence of the special time course of adipose tissue development in children born with IUGR.




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