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Abstract
The purpose of the three studies within this dissertation were to investigate the influence that ‘normal-weight’ obesity, characterized by a normal BMI in the presence of excess relative adiposity, exerts on the increased cardiometabolic risk observed in children with cerebral palsy (CP), and to improve the measurement of this risk. The adipose-tissue derived hormone leptin and the development of ‘leptin-resistance’ was proposed as a possible mediator between altered body composition and cardiometabolic risk in children with CP. The first aim was to determine whether children with CP had elevated leptin levels. Children with CP had higher leptin than typically developing control children, and the difference remained significant when controlling for BMI (p < 0.05). The second aim was to investigate the relationship between leptin and traditional biomarkers of cardiometabolic risk in children with CP. Leptin was significantly related to markers of prediabetes and dyslipidemia in children with CP (all p < 0.05). The third aim was to determine whether there were differences between a single initial blood pressure (BP) measurement and the average of 3 subsequent measurements. There were no differences between the two methods of BP measurement (p < 0.05). The fourth aim was to determine the reliability of a single initial BP measurement and the average of 3 subsequent measurements. The average of the 3 subsequent BP measurements exhibited superior reliability relative to the single initial measurement (intraclass correlation coefficient range = 0.44 to 0.61 vs 0.80 to 0.92). The fifth aim was to investigate the relationship between increased leptin and elevated BP in children with CP. Leptin was significantly related to all BP measurements in children with CP (r range = 0.34 to 0.40, all p < 0.05). Children with CP have higher leptin levels than their typically developing peers, and this difference is not explained by BMI. Increased leptin is related to biomarkers of prediabetes and dyslipidemia, as well as elevated BP in children with CP. These findings are consistent with the development of leptin resistance, and provide further insight into the consequences of normal-weight obesity as it pertains to cardiometabolic risk.