3.8 Article

Plasma leptin, fatty acids, and tumor necrosis factor-receptor and insulin resistance in children

Journal

OBESITY RESEARCH
Volume 11, Issue 4, Pages 532-540

Publisher

NORTH AMER ASSOC STUDY OBESITY
DOI: 10.1038/oby.2003.75

Keywords

leptin; nonesterified fatty acid; tumor necrosis factor-receptor; insulin resistance; children

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Objective: To evaluate the effect of plasma leptin, nonsterified fatty acids (NEFAs), and tumor necrosis factor-receptor 1 (TNFR1) on plasma insulin and insulin-resistance status in children. Research Methods and Procedures: One thousand thirty-two children (521 boys and 511 girls) were included in this study. We measured plasma insulin and leptin levels by radioimmunoassay, plasma NEFA levels by enzymatic acyl-coenzyme A synthase-acyl-coenzyme A oxidase spectrophotometric methods, and TNFR1 levels by enzyme-linked immunosorbent assay. We calculated insulin resistance index (IRI) using homeostasis model assessment and calculated insulin-resistance syndrome summary score (IRS) by adding the quartile ranks from the distribution of systolic blood pressure (BP), serum triglyceride, high-density lipoprotein-cholesterol (inverse), and insulin levels. Results: Overweight children had higher BP, plasma leptin, and insulin levels and higher IRI and IRS than normal-weight children. Plasma leptin and TNFR1 were positively correlated with insulin levels, IRI, and IRS. The correlation coefficients of leptin and TNFR1 in IRI were 0.53 and 0.12, respectively, for boys and 0.25 and 0.18, respectively, for girls. In multivariate regression analyses, TNFR1 was positively associated with insulin level and IRI in girls; NEFA was positively associated only with IRS. Plasma leptin levels were significantly positively associated with insulin levels, IRI, and IRS, even after adjusting for BMI and other potential confounders. Discussion: Overweight children had higher BP, plasma insulin, and leptin levels and adverse insulin-resistance status than normal-weight children. Plasma leptin levels, rather than NEFA and TNFR1, may play a significant role in the development of hyperinsulinemia and insulin resistance in children.

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