Insulin-like growth factor I (IGF-I) plays a pivotal role in pediatric muscle and bone development. Whereas IGF-I acts directly upon the bone-forming osteoblasts, the tropic effect of IGF-I on skeletal muscle is suspected to, at least in part, facilitate its effect on bone. Insulin and IGF-I act at the level of the muscle and bone through a similar downstream signaling process. Animal and cell culture studies have shown that biological factors that contribute to insulin resistance moderate IGF-I function. Thus, it is plausible that the potentially adverse influence of insulin resistance on pediatric bone health involves IGF-I. The objective of this dissertation is to utilize existing data in order to examine the relationships between insulin resistance and pediatric bone outcomes, in addition to the potential influence of insulin resistance on the IGF-I-bone relationship in children. For all studies, total body bone mass, lean mass, and fat mass were measured via dual-energy X-ray absorptiometry; cortical bone geometry was assessed via peripheral quantitative computed tomography; and insulin resistance was measured via the homeostasis model assessment of insulin resistance. In Manuscript #1, which is a cross-sectional study of black and white girls (N = 147; 50% black, ages 9-11 years), insulin resistance had a significant and negative influence on the lean mass-dependent relationships between IGF-I and bone mass. In Manuscript #2, which is a cross-sectional study of black and white boys and girls (N = 315; 50% female, 50% black, ages 9-13 years), children with higher insulin resistance had lower cortical bone size and estimated bending strength. In addition, insulin resistance moderated the relationship between IGF-I and lean mass as well as cortical bone size and strength. Our data are the first to implicate a suppression of IGF-I-dependent lean mass accretion as a contributor to the smaller cortical bone in children with insulin resistance. As such, insulin resistance-related deficits in cortical bone size and subsequent bending strength, which might involve IGF-I, could help explain the greater propensity for skeletal fracture in obese youth.