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Pediatric and Adolescent Endocrinology

MON-222 - Maternal Diet-Driven Changes in Milk Bile Acids Regulate Neonatal Growth via TGR5 and IGF-1 Signaling

Monday, June 15, 2026
9:00 AM - 2:00 PM CT
Location: ENDOExpo; Poster Floor
Disclosure(s):
Haley Wilt: No financial relationships to disclose
Early life exposures during breastfeeding strongly program metabolic health and body weight, with maternal diet playing a central role. In high resource settings, maternal consumption of a high fat diet during lactation promotes excess weight gain and obesity in offspring through alterations in milk composition, whereas in low resource settings breastfeeding protects against growth failure and stunting. Defining the nutritional components of milk that drive these divergent growth outcomes is essential for developing strategies to optimize infant nutrition and growth across diverse global contexts. One potential mediator of these effects is bile acids—bioactive metabolites present in breast milk that are shaped by maternal diet and gut microbiota—whose role in early-life metabolic programming remains poorly understood. In adults, bile acids facilitate dietary lipid digestion and function as signaling molecules that regulate energy balance through receptors such as TGR5 and FXR. TGR5 activation has been associated with enhanced energy expenditure and weight regulation, and altered bile acid profiles are observed in obesity. These observations raise the possibility that milk bile acids may influence neonatal growth. Using a mouse model, we demonstrate that maternal HFD increases bile acid levels in breast milk, correlating with increased weight gain and elevated circulating insulin-like growth factor-1 (IGF-1) in nursing pups. Sequestration of bile acids in lactating HFD dams normalizes offspring weight gain and prevents the HFD-associated increase in IGF-1, indicating a mechanistic link between milk bile acids and IGF-1 regulation. Our preliminary findings support a model whereby milk bile acids regulate IGF-1 levels through neonatal TGR5. Overall, this work establishes that milk bile acids can act as active metabolic regulators during lactation through TGR5 and IGF-1 signaling.

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