What question did this study set out to answer?

The study aims to assess the relationship between higher maternal pre-pregnancy BMI and satiety hormone responses in children.

June 7, 2026

1076-OR: Blunted Satiety Hormone Responses in Children Prenatally Exposed to Maternal Obesity

Puntos clave

The study aims to assess the relationship between higher maternal pre-pregnancy BMI and satiety hormone responses in children.
Analyzed data from 19 children aged 7-14 in the BrainChild Study.
Measured fasting and post-glucose plasma concentrations of GLP-1, GIP, and PYY after glucose ingestion.
Used linear regression adjusted for child age, sex, and BMI with maternal pre-pregnancy BMI as a primary predictor.
Maternal pre-pregnancy BMI was linked to reduced GLP-1 (β=−0.33, p=0.04), GIP (β=−0.29, p=0.002), and PYY (β=−0.23, p=0.01) secretion.
After adjusting for child BMI, GIP (β=−0.24, p=0.02) and PYY (β=−0.24, p=0.03) showed statistical significance.
GLP-1 secretion was attenuated (β=−0.26, p=0.14) after adjustment.

Resumen

Introduction and Objective: Children prenatally exposed to higher maternal pre-pregnancy BMI face increased risk for obesity and type 2 diabetes. Post-nutrient dysregulation of satiety hormones may contribute to metabolic dysfunction in exposed offspring. We hypothesized that prenatal exposure to higher maternal pre-pregnancy BMI is associated with impaired satiety hormone responses to glucose ingestion. Methods: We analyzed data from 19 children (68% female; ages 7-14; maternal pregnancy BMI 18.9-42.0 kg/m2) in the BrainChild Study. Maternal pre-pregnancy BMI was obtained from electronic health records. Pre-pregnancy weight was the weight measured closest to last menstrual period before or in 1st trimester. Child anthropometrics, fasting and 30-minute post-glucose (1.75 g/kg body weight) plasma concentrations of glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), and peptide YY (PYY) were measured. Hormonal responses (Δ=30 min − baseline) were examined using linear regression, adjusted for child age and sex, and then further adjusted for child BMI, with maternal pre-pregnancy BMI as the primary predictor. Results: Maternal pre-pregnancy BMI was associated with reduced secretion of GLP-1 (β=−0.33, p=0.04), GIP (β=−0.29, p=0.002), and PYY (β=−0.23, p=0.01) in response to glucose challenge. After further adjustment for child BMI, GIP (β=−0.24, p=0.02) and PYY (β=−0.24, p=0.03) remained significant; GLP-1 was attenuated (β=−0.26, p=0.14). Conclusion: Higher maternal pre-pregnancy BMI is associated with blunted satiety hormone responses in children, independent of child BMI. Impaired post-nutrient satiety signaling may represent a mechanism linking prenatal exposure to increased metabolic disease risk in offspring. Disclosure J. Smith: None. E.C. Morgan: None. J. Alves: None. K. Page: None. A. Xiang: None. T. Chow: None. M. Sidell: None. Funding American Diabetes Association (1-14-ACE-36), NIH (R01 DK134079, RO1 DK116858)

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