Pediatric obesity · 2025
Prenatal Exposure to Gestational Diabetes Mellitus Is Associated With Greater Pre-Pubertal BMI Growth and Faster Post-Pubertal Cortical Thinning During Peri-Adolescence.
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Hsu Eustace, Pickering Trevor A, Luo Shan
Аннотация
BACKGROUND: The longitudinal trajectory of body mass index (BMI) and brain structure development during peri-adolescence is not clearly defined in offspring prenatally exposed to gestational diabetes mellitus (GDM) versus unexposed offspring.
METHODS: Participants between age 9 and 10 years (N = 9583) were included from the Adolescent Brain and Cognitive Development (ABCD) Study and followed yearly through 4-year follow-up. GDM and puberty status were self-reported. BMI was calculated yearly, and MRI assessed brain structure biennially. Mixed-effects models analysed trajectories of BMI and brain structural measures between groups controlling for sociodemographic covariates, and linear spline was defined with a knot at the onset of puberty.
RESULTS: There was an interaction of exposure by age in change in BMI [β (95% CI) = 0.032 (0.008, 0.056), p = 0.009] and mean cortical thickness [β (95% CI) = -0.038 (-0.071, -0.004), p = 0.027]. The former was driven by greater pre-pubertal increases in BMI [β (95% CI) = 0.051 (0.002, 0.100), p = 0.043], whereas the latter was driven by faster post-pubertal declines in cortical thickness among GDM-exposed offspring [β (95% CI) = -0.051 (-0.095, -0.007), p = 0.046].
CONCLUSION: Prenatal GDM exposure is associated with greater pre-pubertal increases in BMI and faster post-pubertal cortical thinning in youth aged between 9 and 15.
METHODS: Participants between age 9 and 10 years (N = 9583) were included from the Adolescent Brain and Cognitive Development (ABCD) Study and followed yearly through 4-year follow-up. GDM and puberty status were self-reported. BMI was calculated yearly, and MRI assessed brain structure biennially. Mixed-effects models analysed trajectories of BMI and brain structural measures between groups controlling for sociodemographic covariates, and linear spline was defined with a knot at the onset of puberty.
RESULTS: There was an interaction of exposure by age in change in BMI [β (95% CI) = 0.032 (0.008, 0.056), p = 0.009] and mean cortical thickness [β (95% CI) = -0.038 (-0.071, -0.004), p = 0.027]. The former was driven by greater pre-pubertal increases in BMI [β (95% CI) = 0.051 (0.002, 0.100), p = 0.043], whereas the latter was driven by faster post-pubertal declines in cortical thickness among GDM-exposed offspring [β (95% CI) = -0.051 (-0.095, -0.007), p = 0.046].
CONCLUSION: Prenatal GDM exposure is associated with greater pre-pubertal increases in BMI and faster post-pubertal cortical thinning in youth aged between 9 and 15.