While metabolic disorders such as obesity and diabetes are costly and deadly to the current population, they are also extremely detrimental to the next generation. Much of the current literature focuses on the negative impact of poor maternal choices on offspring disease, while there is little work examining maternal behaviors that may improve offspring health. Research has shown that voluntary maternal exercise in mouse models improves metabolic function in offspring. In this study, we hypothesized that controlled maternal exercise in a mouse model will effect positive change on offspring obesity and glucose homeostasis. Female mice were separated into three groups: home cage, sedentary, and exercise. The sedentary home cage group was not removed from the home cage, while the sedentary wheel group was removed from the cage and placed in an immobile wheel apparatus. The exercise group was removed from the home cage and run on the same wheel apparatus but with the motor activated at 5-10 m/min for 1 h/d prior to and during pregnancy. Offspring were subjected to oral glucose tolerance testing and body composition analysis. There was no significant difference in offspring glucose tolerance or body composition as a consequence of the maternal exercise intervention compared to the sedentary wheel group. There were no marked negative consequences of the maternal controlled exercise intervention. Further research should clarify the potential advantages of the controlled exercise model and improve experimental techniques to facilitate translation of this research to human applications.
|Number of pages||8|
|Journal||Journal of Developmental Origins of Health and Disease|
|State||Published - Aug 10 2022|
Bibliographical noteFunding Information:
This study and core services for this study were supported by US NIH grant (National Center for Research Resources, 5P20 RR021954-05) as well as The National Institute of Diabetes and Digestive and Kidney Diseases, R01 DK090460, and the National Institute of Environmental Health Sciences, P42 ES007380. K.M.P. was supported by an NIH training grant (DK07778).
- Developmental programming
ASJC Scopus subject areas
- Medicine (miscellaneous)