Author(s): Roth CL, Kratz M, Ralston MM, Reinehr T
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Abstract Obesity has been associated with low-grade chronic systemic inflammation, potentially leading to insulin resistance. This study was designed to examine relationships between cardiovascular risk factors, insulin resistance, and simultaneously measured inflammatory parameters in obese children. We examined serum inflammatory parameters in 115 obese children and 30 normal-weight controls; 62 obese children were followed longitudinally in a 1-year obesity intervention study. Serum concentrations of adipose tissue hormones adiponectin and resistin as well as adipocytokines were assessed. Cross-sectional analysis showed significant correlations between standard deviation score body mass index and resistin (P = .0004) as well as monocyte chemoattractant protein-1 (MCP-1, P = .04). Increased homeostasis model assessment of insulin resistance index greater than 95th percentile was present in 32\% of obese patients, correlating with adiponectin (r = -0.40, P = .0007). Significant correlations were found between adiponectin and several mediators of inflammation (interleukins [ILs] IL-1β, IL-6, and IL-8 and tumor necrosis factor-α). In longitudinal analysis, substantial weight loss (change standard deviation score body mass index >0.5) observed after intervention in 29 children was associated with a significant decrease in blood pressure, homeostasis model assessment of insulin resistance index, and serum concentrations of insulin and IL-1β, IL-8, and MCP-1, but increase of adiponectin (all Ps < .05). In 33 children without substantial weight loss, resistin and MCP-1 levels increased after 1 year. Changes in IL-1β correlated positively with changes of weight status, interferon-γ, IL-6, IL-8, and tumor necrosis factor-α (all Ps < .01). Our study demonstrates significant correlations between different metabolic risk factors at baseline and after changes of weight status and that weight loss in obese children reduces low-grade inflammation, insulin resistance, and blood pressure. Copyright © 2011 Elsevier Inc. All rights reserved.
This article was published in Metabolism
and referenced in Journal of Diabetes & Metabolism