Hostname: page-component-586b7cd67f-2plfb Total loading time: 0 Render date: 2024-11-27T23:02:09.686Z Has data issue: false hasContentIssue false
  • English
  • Français

Leptin levels at birth and infant growth: the EPOCH study

Published online by Cambridge University Press:  26 March 2014

J. L. Kaar ,
J. T. Brinton ,
T. Crume ,
R. F. Hamman ,
D. H. Glueck  and
D. Dabelea
J. L. Kaar*
Affiliation:
Department of Pediatrics, Colorado School of Medicine, University of Colorado, Aurora, CO, USA
J. T. Brinton
Affiliation:
Department of Epidemiology, Colorado School of Public Health, University of Colorado, Aurora, CO, USA
T. Crume
Affiliation:
Department of Biostatistics and Informatics, Colorado School of Public Health, University of Colorado, Aurora, CO, USA
R. F. Hamman
Affiliation:
Department of Epidemiology, Colorado School of Public Health, University of Colorado, Aurora, CO, USA
D. H. Glueck
Affiliation:
Department of Biostatistics and Informatics, Colorado School of Public Health, University of Colorado, Aurora, CO, USA
D. Dabelea
Affiliation:
Department of Epidemiology, Colorado School of Public Health, University of Colorado, Aurora, CO, USA
*
*Address for correspondence: J. L. Kaar, PhD, Department of Pediatrics, Colorado School of Medicine, University of Colorado, Aurora, CO 80045, USA. Email: [email protected]
Get access Rights & Permissions [Opens in a new window]

Abstract

Objective: To examine the association of cord blood leptin with body mass index (BMI) growth velocity from birth to 12 months of age among infants exposed and not exposed to over-nutrition in utero (defined as maternal overweight/obesity or presence of gestational diabetes). Methods: 185 infants enrolled in the Exploring Perinatal Outcomes among Children study (76 exposed and 109 not exposed) had leptin and insulin measured in cord blood. Longitudinal weight and length measures in the first 12 months of life (average 4 per participant) obtained from medical records were used to compute BMI growth rates. Mixed models were used to examine associations of cord blood leptin with growth. Results: Compared with unexposed infants, those exposed had significantly higher cord blood insulin (8.64 v. 6.97 uU/ml, P<0.01) and leptin levels (8.89 v. 5.92 ng/ml, P=0.05) as well as increased birth weights (3438.04 v. 3306.89 g, P=0.04). There was an inverse relationship between cord leptin levels and BMI growth from birth to 12 months of age (P=0.005); however, exposure to over-nutrition in utero did not significantly modify this association (P=0.59). Conclusion: We provide support of a possible operational feedback mechanism by which lower cord blood leptin levels are associated with faster infant growth in the first year of life. Our data do not tend to support the hypothesis that this mechanism is altered in infants exposed to over-nutrition in utero; however our sample is too small to provide sufficient evidence. Larger epidemiological studies are needed to elucidate the mechanisms responsible for increased propensity for obesity in exposed offspring.

Keywords

childhood obesitydiabetesfetal overnutritioninsulinleptinmaternal obesity
Type
Original Article
Information
Journal of Developmental Origins of Health and Disease , Volume 5 , Issue 3 , June 2014 , pp. 214 - 218
Copyright
© Cambridge University Press and the International Society for Developmental Origins of Health and Disease 2014 

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

1. Dabelea, D, Pettitt, DJ. Intrauterine diabetic environment confers risks for type 2 diabetes mellitus and obesity in the offspring, in addition to genetic susceptibility. J Pediatr Endocrinol Metab. 2001; 14, 1085–1091.CrossRefGoogle ScholarPubMed
2. Pettitt, DJ, Bennett, PH, Knowler, WC, Baird, HR, Aleck, KA. Gestational diabetes mellitus and impaired glucose tolerance during pregnancy. Long-term effects on obesity and glucose tolerance in the offspring. Diabetes. 1985; 34, 119–122.CrossRefGoogle Scholar
3. Crume, TL, Ogden, L, Daniels, S, et al. The impact of in utero exposure to diabetes on childhood body mass index growth trajectories: the EPOCH study. J Pediatr. 2011; 158, 941–946.CrossRefGoogle ScholarPubMed
4. Freinkel, N. Banting Lecture 1980. Of pregnancy and progeny. Diabetes. 1980; 29, 1023–1035.CrossRefGoogle ScholarPubMed
5. Lawlor, DA, Smith, GD, O’Callaghan, M, et al. Epidemiologic evidence for the fetal overnutrition hypothesis: findings from the mater-university study of pregnancy and its outcomes. Am J Epidemiol. 2007; 165, 418–424.CrossRefGoogle ScholarPubMed
6. Dabelea, D, Crume, T. Maternal environment and the transgenerational cycle of obesity and diabetes. Diabetes. 2011; 60, 1849–1855.CrossRefGoogle ScholarPubMed
7. Koistinen, HA, Koivisto, VA, Andersson, S, et al. Leptin concentration in cord blood correlates with intrauterine growth. J Clin Endocrinol Metab. 1997; 82, 3328–3330.Google ScholarPubMed
8. Silverman, BL, Rizzo, T, Green, OC, et al. Long-term prospective evaluation of offspring of diabetic mothers. Diabetes. 1991; 40(Suppl. 2), 121–125.CrossRefGoogle ScholarPubMed
9. Schwartz, R, Teramo, KA. Effects of diabetic pregnancy on the fetus and newborn. Sem Perinatol. 2000; 24, 120–135.CrossRefGoogle ScholarPubMed
10. Ong, KK, Ahmed, ML, Sherriff, A, et al. Cord blood leptin is associated with size at birth and predicts infancy weight gain in humans. ALSPAC Study Team. Avon Longitudinal Study of Pregnancy and Childhood. J Clin Endocrinol Metab. 1999; 84, 1145–1148.CrossRefGoogle Scholar
11. Jaquet, D, Leger, J, Levy-Marchal, C, Oury, JF, Czernichow, P. Ontogeny of leptin in human fetuses and newborns: effect of intrauterine growth retardation on serum leptin concentrations. J Clin Endocrinol Metab. 1998; 83, 1243–1246.CrossRefGoogle ScholarPubMed
12. Kieffer, TJ, Habener, JF. The adipoinsular axis: effects of leptin on pancreatic beta-cells. Am J Physiol Endocrinol Metab. 2000; 278, E1–E14.CrossRefGoogle ScholarPubMed
13. Seufert, J, Kieffer, TJ, Leech, CA, et al. Leptin suppression of insulin secretion and gene expression in human pancreatic islets: implications for the development of adipogenic diabetes mellitus. J Clin Endocrinol Metab. 1999; 84, 670–676.Google ScholarPubMed
14. Parker, M, Rifas-Shiman, SL, Belfort, MB, et al. Gestational glucose tolerance and cord blood leptin levels predict slower weight gain in early infancy. J Pediatr. 2011; 158, 227–233.CrossRefGoogle ScholarPubMed
15. Mantzoros, CS, Rifas-Shiman, SL, Williams, CJ, et al. Cord blood leptin and adiponectin as predictors of adiposity in children at 3 years of age: a prospective cohort study. Pediatrics. 2009; 123, 682–689.CrossRefGoogle ScholarPubMed
16. National Diabetes Data Group. Classification and diagnosis of diabetes mellitus and the other categories of glucose intolernance. Diabetes. 1979; 28, 1039–1057.CrossRefGoogle Scholar
17. Simmons, D, Breier, BH. Fetal overnutrition in polynesian pregnancies and in gestational diabetes may lead to dysregulation of the adipoinsular axis in offspring. Diabetes Care. 2002; 25, 1539–1544.CrossRefGoogle ScholarPubMed