Early Childhood Obesity Programming by Intrauterine Growth Restriction

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.

Inclusion Criteria:

- Healthy singleton term IUGR and AGA infants whose mothers are followed by the
Obstetric Department of Montefiore Medical Center and who deliver at the Weiler
Division of Montefiore Medical Center.

Exclusion Criteria:

- Multiple gestation, maternal depression, maternal renal disease, infants in extremis,
Apgar score <7 at 5 min and umbilical artery pH ≤7.25, chromosomal/ congenital
abnormalities, congenital infections and inborn errors of metabolism. We will also
exclude infants born to mothers with a history of maternal smoking in the 2nd and 3rd
trimester of pregnancy and maternal gestational diabetes/T2D.