Longitudinal Trajectory and Early Life Determinant of Childhood Adipokines: Findings From a Racially Diverse Birth Cohort

Author:

Makker Kartikeya12ORCID,Zhang Mingyu34ORCID,Wang Guoying5,Hong Xiumei5ORCID,Aziz Khyzer12,Brady Tammy M2ORCID,Wang Xiaobin25ORCID

Affiliation:

1. Division of Neonatology, Department of Pediatrics, Johns Hopkins School of Medicine , Baltimore, MD 21287 , USA

2. Department of Pediatrics, Johns Hopkins School of Medicine , Baltimore, MD 21287 , USA

3. Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health , Baltimore, MD 21287 , USA

4. Department of Population Medicine, Harvard Medical School and Harvard Pilgrim Health Care Institute , Boston, MA 02115 , USA

5. Center on the Early Life Origins of Disease, Department of Population Family and Reproductive Health, Johns Hopkins Bloomberg School of Public Health , Baltimore, MD 21287 , USA

Abstract

Abstract Context Leptin and adiponectin play important roles in systemic metabolic homeostasis, beginning in utero. Limited data exist on the levels and trajectories of these 2 hormones at birth and in childhood and their biological and social determinants. Objective We examined the longitudinal trajectories of leptin and adiponectin from birth to early childhood, along with influential prenatal and infancy factors, and whether the trajectories and risk factors differ by preterm birth status. Methods We included mother-infant pairs in the Boston Birth Cohort, a predominantly Black, indigenous, and people of color (BIPOC) study population. We measured infant plasma leptin and adiponectin levels at birth and in early childhood. We examined longitudinal trajectories and the associated prenatal maternal and infancy factors. We analyzed 716 infants (158 preterm) who had leptin and adiponectin measured at birth and in early childhood (mean corrected age 2.18 years [interquartile range, 0.4-10.4]). Results Cord leptin was higher in term infants (40 230 vs 20 481 in preterm, P < 0.0001) but childhood leptin did not differ by prematurity (4123 in term vs 4181 in preterm, P = 0.92). Adiponectin was higher in term infants at birth (18 416 vs 11 223, P < 0.0001) and in childhood (12 108 vs 10532, P = 0.04). In stepwise regression, Black race was associated with higher childhood leptin and lower childhood adiponectin. Female sex was associated with higher childhood leptin levels and lower childhood adiponectin levels in multivariable regression models. Conclusion Our results highlight preterm status, race, and biological sex as predictors of adipokine trajectory throughout childhood. These findings raise the possibility that early life programming of adipokines may contribute to higher metabolic risk in life, especially among Black children born preterm.

Funder

National Institutes of Health

Publisher

The Endocrine Society

Subject

Biochemistry (medical),Clinical Biochemistry,Endocrinology,Biochemistry,Endocrinology, Diabetes and Metabolism

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