Objective

Rates of pediatric obesity are continuously rising and are likely to translate into a high incidence of metabolic disease later in life. Maternal exercise (ME) has been established as a useful non-pharmacological intervention to improve infant metabolic health; however, mechanistic insight behind these adaptations remains mostly confined to animal models. Infant mesenchymal stem cells (MSCs) give rise to infant tissues (e.g., skeletal muscle), and remain involved in mature tissue maintenance. Importantly, these cells maintain metabolic characteristics of an offspring donor and provide a model for the investigation of mechanisms behind infant metabolic health improvements.

Methods

We used undifferentiated MSC to investigate if ME affects infant MSC mitochondrial function and insulin action, and if these adaptations are associated with lower infant adiposity.

Results

We found that infants from exercising mothers have improvements in MSC insulin signaling are related to higher MSC respiration and fat oxidation, and expression and activation of energy-sensing and redox-sensitive proteins. Further, we found that infants exposed to exercise in utero were seemingly leaner at 1-month of age, with a significant inverse correlation between infant MSC respiration and infant adiposity at 6-months of age.

Conclusion

These data suggest that infants from exercising mothers are relatively leaner and this is associated with higher infant MSC mitochondrial respiration, fat use, and insulin action.