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COMPARATIVE STUDY
JOURNAL ARTICLE
High-sensitive C-reactive protein, tumor necrosis factor alpha, and cardiovascular risk factors before and after weight loss in obese children.
Metabolism: Clinical and Experimental 2005 September
To confirm the existence of obesity-induced inflammation and to clarify the association between such inflammation and other cardiovascular risk factors, we investigated the relationships between high-sensitive C-reactive protein (hsCRP), tumor necrosis factor alpha (TNF-alpha), obesity, blood pressure, lipids, and insulin resistance in a long-term follow-up of obese children. We compared the serum concentrations of hsCRP, TNF-alpha, high-density lipoprotein cholesterol, and triglycerides as well as blood pressure and the insulin resistance index (homeostasis model assessment [HOMA]) of 14 nonobese and 31 obese children. Furthermore, we studied the changes in these parameters in 16 obese children who lost weight and in 15 obese children without weight change over a 1-year period. In the obese children, blood pressure (P=.003), HOMA (P=.034), and triglyceride (P=.011), TNF-alpha (P=.015), and hsCRP (P<.001) levels were significantly higher, whereas high-density lipoprotein cholesterol concentrations were significantly (P=.015) lower compared with the nonobese children. Weight loss was associated with a significant decrease in hsCRP (P=.008) and triglyceride (P=.048) levels, HOMA (P<.001), and blood pressure (P=.019), whereas there were no significant changes in the children with stable weight status. The changes in hsCRP and TNF-alpha levels over the 1-year period were not significantly correlated to the changes in lipids, blood pressure, and HOMA. Obese children demonstrated significantly higher levels of hsCRP and TNF-alpha compared with nonobese children. The chronic inflammation markers TNF-alpha and hsCRP were independent of lipids, blood pressure, and insulin resistance index. Weight loss was associated with the significant decrease of hsCRP and triglyceride levels, and blood pressure.
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