Please use this identifier to cite or link to this item: https://hdl.handle.net/20.500.14279/1940
Title: Cord blood leptin and insulin-like growth factor levels are independent predictors of fetal growth
Authors: Papathanassoglou, Elizabeth 
Christou, Helen 
Connors, Jean Marie 
metadata.dc.contributor.other: Παπαθανάσογλου, Ελισάβετ
Major Field of Science: Medical and Health Sciences
Field Category: MEDICAL AND HEALTH SCIENCES
Keywords: Endocrinology;Metabolism;Insulin;Leptin;Fetus--Development;Hydrocortisone;Birth weight
Issue Date: Feb-2001
Source: Journal of Clinical Endocrinology and Metabolism, 2001, vol. 86, no. 2, pp. 935-938
Volume: 86
Issue: 2
Start page: 935
End page: 938
Journal: Journal of Clinical Endocrinology and Metabolism 
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
URI: https://hdl.handle.net/20.500.14279/1940
ISSN: 0021972X
DOI: 10.1210/jc.86.2.935
Rights: © Oxford University Press
Type: Article
Affiliation: Beth Israel Deaconess Medical Center 
Affiliation : Harvard University 
Publication Type: Peer Reviewed
Appears in Collections:Άρθρα/Articles

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