Date

May 2012

Document Type

Dissertation

Degree Name

Ph.D.

Institution

Oregon Health & Science University

Abstract

This study explores the relationship between leptin resistance (LR), as identified by elevated leptin levels, and cytokines, in obese children and adolescents. It is based on a conceptual framework that relates left ventricular hypertrophy (LVH) in obese children and adolescents to LR. LR is, perhaps, directly related to interleukin-1 receptor antagonist (IL-1RA), a potent anti-inflammatory cytokine. Regression analysis was performed with left ventricular mass (LVM) functioning as the dependent variable while age, sex, body mass index (BMI), mean arterial pressure (MAP), and serum levels of leptin, insulin, and IL1-RA as independent variables (R[superscript 2] = .41, F (7, 12) = 1.204, p = .37). Because statistical power was not achieved, Cohen’s guidelines for r were followed. Several correlations demonstrated moderate to large effects. The results showed that LVM correlated with BMI, suggesting a moderate effect (r = .46). Other moderate correlations with BMI were detected with age (r = .77), MAP (r = .50), leptin (r = .56), and insulin (r = .61). The MAP for the sample population yielded correlations of moderate effect with leptin (r = .50), insulin (r = .57), and correlated strongly with IL-1RA (r = .75). Insulin levels were also correlated with leptin (r = .64) and IL-1RA (r = .52), both moderate effects sizes. The findings supported previous studies in which elevated BMI was associated with LVH, elevated MAP, elevated leptin, and increased insulin levels. The moderately correlated effect between LVM and MAP contradicts results from some studies reporting that blood pressure in adults was not associated with LVH. Because no relationship was detected between leptin and IL-1RA, a mediator relationship could not be tested. No statistically significant interaction between LR and IL-1RA was detected. However, the findings support previous research suggesting that LVH in obese children is associated with an increase in MAP but not leptin. This suggests that changes in MAP may be related to increased IL1-RA.

Identifier

doi:10.6083/M4Q23X7G

School

School of Nursing

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