Children exposed to gestational diabetes mellitus (GDM) in utero have an increased propensity of developing obesity. Little is known about the mechanisms underlying this propensity. Here we examine the relationship between GDM exposure and its timing on energy intake (EI) and brain reward responses to food cues in children. Participants were 142 children (39% boys; 56% GDM-exposed) aged from 7 to 11 years old. GDM status was extracted from EMR. Adiposity measurements were collected. Repeated 24-hour recalls were conducted to assess mean daily EI (kcal/day). A subset (n=89) of children completed an MRI session where they viewed food and non-food cues. %signal change in the orbital frontal cortex (OFC), insula and amygdala for food vs. non-food contrast was measure of interest. GDM exposure was modeled by: 1) yes vs. no at any time in pregnancy and 2) GDM diagnosed at <= 26 weeks (early exposed), > 26 weeks (late exposed) and unexposed. GDM exposure (vs. unexposed) was associated with greater EI (mean difference ±SE: 169 ±65, P=0.01) and OFC food cue reactivity (0.19±0.09, P=0.04). Results were strengthened after adjusting for age, sex, physical activity, SES and pre-pregnancy BMI (EI: P=0.008; OFC: P=0.024). In the adjusted models, both subgroups (early exposed(N=27): 178 ± 92, P=0.055; late exposed (N=53): 173±72, P=0.018) had greater EI than controls. Early exposed group had greater OFC food cue reactivity than controls (0.30±0.15, P=0.048) and the difference between late exposed and controls was marginally significant (0.20±0.11, P=0.07). Children exposed to GDM (vs. unexposed) had larger WHR (0.02±0.01, P=0.03), and this was driven by the difference between early exposed vs. controls (0.04±0.01, P=0.006). Exposure to GDM in utero, in particular before 26 weeks gestation, is associated with increased energy intake, enhanced OFC food cue reactivity and increased WHR. Whether these changes predict development of obesity remains to be determined.
S.H. Luo: None. B.C. Angelo: None. T. Chow: None. J. Alves: None. T.A. Buchanan: None. A. Xiang: None. K.A. Page: None.
National Institutes of Health (K01DK11563)