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Cord Blood Leptin and Insulin-Like Growth Factor Levels are Independent Predictors of Fetal Growth
Author(s) -
Helen Christou,
Jean M. Connors,
Mary Ziotopoulou,
Vassilia Hatzidakis,
Elizabeth Papathanassoglou,
Steven A. Ringer,
Christos S. Mantzoros
Publication year - 2001
Publication title -
the journal of clinical endocrinology and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.206
H-Index - 353
eISSN - 1945-7197
pISSN - 0021-972X
DOI - 10.1210/jcem.86.2.7217
Subject(s) - leptin , medicine , endocrinology , insulin , birth weight , fetus , insulin like growth factor , gestational age , context (archaeology) , cord blood , growth factor , biology , pregnancy , obesity , receptor , paleontology , genetics
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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