The molecular mechanisms underlying developmental programming of childhood obesity remain poorly understood. Here, the investigators address major questions about early childhood obesity programming by studying CD3+ T-cells from intrauterine growth restricted (IUGR) newborns who have an increased risk for obesity and other metabolic disorders in adult life.
Epidemiological studies of multiple cohorts suggest an increased risk for obesity, cardiovascular disease-related death and type 2 diabetes in low birth weight infants. However, the molecular mechanisms underlying developmental programming of childhood obesity remain poorly understood. Alterations in DNA methylation during fetal life have been proposed to be one of the mechanisms that regulate this phenotype. Here, the investigators address major questions about early childhood obesity programming by studying purified subpopulations of CD3+ T-cells from intrauterine growth restricted (IUGR) newborns who have an increased risk for obesity and other metabolic disorders in adult life. The investigators will correlate altered CD3+ T-cell DNA methylation profiles in cord and peripheral blood samples and functional changes in CD3+ T-cells with adiposity in childhood.
Study Type
OBSERVATIONAL
Enrollment
163
Jack D. Weiler Hospital
The Bronx, New York, United States
Growth velocity
Change in growth velocity based on DNA methylation marks and functional profiles of CD3+ T-cells
Time frame: Until 24 months of age
DNA methylation of CD3+ T-cells
Change in DNA methylation of CD3+ T-cells in the first 24 months of life in IUGR infants
Time frame: At birth and 24 months of age
T-cell function
Change in T-cell function in the first 24 months of life in IUGR infants
Time frame: At birth, 12 and 24 months of age
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