This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. The overall objective of this proposal is to examine the role of AMP-activated protein kinase (AMPK) in fetal and neonatal skeletal muscle development that occurs in the setting of maternal obesity. Maternal obesity negatively affects fetal muscle development including increase in the number of intramuscular adipocytes, pre-disposing offspring muscle to insulin resistance, a key event leading to type II diabetes. AMPK has crucial roles in energy metabolism. In this project, we will study the role of AMPK in cell differentiation during fetal skeletal muscle development, focusing on the formation of adipocytes. Meanwhile, we will define the underlying mechanisms regulating adipogenesis as affected by maternal obesity. Knowledge obtained will provide targets for interventions to ensure proper fetal SM development in fetuses of the increasing number of obese pregnant women in this country, allowing them to deliver healthy children.