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Cord Blood Leptin and Insulin-Like Growth Factor Levels are Independent Predictors of Fetal Growth

Division of Newborn Medicine, Children’s Hospital (H.C.) and Brigham and Women’s Hospital (H.C., S.A.R.), Hematology Division (J.M.C.), Department of Medicine, Brigham and Women’s Hospital and Division of Endocrinology (M.Z., V.H., E.P., C.S.M.), Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215

Address all correspondence and requests for reprints to: Christos S. Mantzoros, M.D., Division of Endocrinology, Beth Israel Deaconess Medical Center, 99 Brookline Avenue Boston, Massachusetts 02215. E-mail: cmantzor{at}caregroup.harvard.edu

Abstract

The insulin-like growth factor (IGF) system is the dominant endocrine regulator of fetal growth, whereas insulin has a permissive role. Although a role for leptin in fetal growth has been suggested recently, the mechanism by which leptin may be related to fetal growth is not known; but leptin may interact with the IGF system in utero as it does in the extrauterine life.

In the context of a hospital-based case control study, we collected anthropometric and demographic data and measured serum leptin, IGF-I, IGF-II, insulin, cortisol, and IGF binding protein 3 concentrations in 142 cord blood samples from full-term deliveries.

Cord leptin, IGF-I, and insulin levels correlated positively with birth weight (r = 0.46, r = 0.41, and r = 0.21, respectively, P < 0.01) by univariate analysis and were significantly higher in large-for-gestational-age (LGA) infants, compared with appropriate-for-gestational-age (AGA) infants. Cord leptin concentrations correlated with insulin levels (r = 0.36, P<0.01) but not with IGF-I levels (r = 0.20). Multiple linear and logistic regression analysis demonstrated an independent positive relationship of both leptin and IGF-I with birth weight and AGA/LGA status.

The positive association of leptin levels with birth weight and AGA/LGA status cannot be attributed to IGF-I. This suggests the existence of alternative mechanisms underlying leptin’s associations with fetal growth that should be further explored.

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