What question did this study set out to answer?

This research aims to determine how gestational diabetes and maternal pre-pregnancy BMI affect fat distribution in children.

June 7, 2026

2165-P: Gestational Diabetes and Maternal Obesity Show Differential Associations with Childhood Fat Distribution

Key Points

This research aims to determine how gestational diabetes and maternal pre-pregnancy BMI affect fat distribution in children.
Examined 45 children with measures of total body fat percentage and abdominal MRI.
Used general linear models to analyze associations of GDM and maternal pre-pregnancy BMI with fat types.
Adjusted for age, sex, prenatal exposure, and other covariates in the analysis.
GDM exposure correlated with higher visceral adipose tissue (β=0.46, p=0.04) and marginally higher subcutaneous adipose tissue.
Maternal obesity was significantly linked with both visceral and subcutaneous fat (VAT: β=0.17, p=0.02; ASAT: β=0.19, p=0.01).
GDM increased visceral fat independent of overall adiposity, indicating a specific metabolic risk mechanism.

Abstract

Introduction and Objective: Prenatal exposure to GDM and maternal obesity are risk factors for offspring metabolic disease, but their independent effects on fat distribution remain unclear. We examined whether GDM and maternal pre-pregnancy BMI (mpBMI) differentially influence abdominal fat depots beyond overall adiposity. Methods: 45 children (mean age 11.3±1.2 yrs; 27 girls; 25 GDM-exposed; mpBMI range 19.2-49.3 kg/m2) had measures of total body fat % (% BF), and abdominal MRI to quantify visceral adipose tissue (VAT) and abdominal subcutaneous adipose tissue (ASAT). Data were log transformed as needed. General linear models tested associations of GDM exposure and mpBMI (per 5-unit increase) with VAT, ASAT, and % BF, adjusting sequentially for age, sex, alternate prenatal exposure, % BF, and all covariates. Results: GDM exposure was associated with higher VAT (β=0.46, p=0.04) and marginal ASAT (β=0.36, p=0.12); slightly attenuated after mpBMI adjustment (VAT: β=0.39, p=0.07; ASAT: β=0.28, p=0.21). Associations persisted after adjusting for % BF (VAT: β=0.23, p=0.05; ASAT: β=0.15, p=0.06), and all covariates (VAT: β=0.21, p=0.07; ASAT: β=0.135, p=0.08). GDM exposure was not associated with child total BF % (β=1.18, p=0.74). mpBMI was associated with VAT and ASAT (VAT: β=0.17, p=0.02; ASAT: β=0.19, p=0.01), persisting after GDM adjustment (VAT: β=0.15, p=0.04; ASAT: β=0.17, p=0.02), but attenuated after child % BF adjustment (VAT: β=0.039, p=0.30; ASAT: β=0.031, p=0.23) and all covariates (VAT: β=0.028, p=0.46; ASAT: β=0.024, p=0.35). mpBMI was associated with child total BF % (β=2.49, p=0.03). Conclusion: GDM exposure was associated with greater visceral adiposity independent of overall adiposity, suggesting a mechanism for metabolic risk. Maternal obesity may also contribute to metabolic risk, but this is likely explained by the child's overall adiposity. Disclosure K. Le: None. E.C. Morgan: None. T. Chow: None. J. Alves: None. B. Belcher: None. A. Xiang: None. K. Page: None. Funding American Diabetes Association (1-14-ACE-36), NIH (RO1DK116858, R01DK134079)

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