185-OR: Effects of Exposure to Maternal Obesity In Utero on White Matter Connections between the Hypothalamus and Hippocampus in Children

Abstract

Exposure to maternal obesity in utero is associated with a greater risk for obesity and cognitive deficits in children. The mechanisms are not yet established, but rodent studies suggest that disruption of connectivity between the hypothalamus and hippocampus might be involved. We tested the hypothesis that exposure to maternal overweight/obesity (OW/OB) is associated with reduced integrity of the fornix, a tract connecting the hippocampus and hypothalamus, in children. Seventy-four children (42 girls, 32 boys) ages 7 to 11 years who were born at Kaiser Permanente Southern California participated. Maternal pre-pregnancy BMI was obtained from electronic medical records. Child’s height and weight were measured directly. Diffusion tensor imaging (DTI) was used to measure left and right fornix fractional anisotropy (FA), a measure from zero to one that reflects white matter integrity in coherent fiber bundles. Intracranial volume (ICV) was measured with an anatomical scan. Linear regression was used to compare FA in the fornix of children born to normal-weight (NW) mothers vs. children born to OW/OB mothers without and with adjustment for potential confounding variables. Seventeen mothers were NW (BMI <25 kg/m2) and 57 were OW/OB (BMI ≥25 kg/m2) prior to pregnancy. Children’s mean (±SD) BMI was 18.6±4 kg/m2. FA in the fornix ranged from 0.25 to 0.34. Children born to OW/OB mothers had lower FA in both left and right fornix than children born to NW mothers, with the difference for the right fornix statistically significant (p=0.01). Results remained after adjusting for child ICV, age, sex, BMI (p=0.04) and further adjusting for maternal GDM and socioeconomic status (p=0.02). Results show that in utero exposure to maternal OW/OB is associated with reduced integrity of the hypothalamic-hippocampal pathway in children and suggest a possible mechanism linking maternal obesity to metabolic and cognitive deficits in offspring. Disclosure K.A. Page: None. S. Luo: None. T. Chow: None. R.P. Cabeen: None. K. Clark: None. J. Alves: None. M.P. Martinez: None. T.A. Buchanan: Research Support; Self; Allergan, Apollo EndoSurgery. A. Xiang: None. Funding American Diabetes Association (1-14-ACE-36 to K.A.P.)