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. 2010:2010:892081.
doi: 10.1155/2010/892081. Epub 2010 Oct 31.

Adiponectin and leptin metabolic biomarkers in chinese children and adolescents

Affiliations

Adiponectin and leptin metabolic biomarkers in chinese children and adolescents

Jie Mi et al. J Obes. 2010.

Abstract

Objective. To evaluate leptin and adiponectin as biomarkers of metabolic syndrome (MS) risk factors even in nonobese children/adolescents. Methods. Serum leptin, adiponectin, leptin:adiponectin ratio, lipids, glucose, and insulin concentrations as well as body size parameters and pubertal development were evaluated in a large population of Chinese children/adolescents (n = 3505, 6-18 years, 1722 girls and 1783 boys). Results. Leptin concentration increased while adiponectin decreased with obesity, both were influenced by pubertal development. Central obesity had an additive effect on leptin levels (above obesity alone). Leptin/adiponectin increased 8.4-fold and 3.2-fold in overweight/obesity, and 15.8- and 4.5-fold with obesity plus MS, in early and late puberty, respectively. Even in normal weight children/adolescents, higher leptin and lower adiponectin concentrations associated with increased risk profile. Conversely, overweight/obese with lower leptin or higher adiponectin concentrations had a less compromised metabolic profile. Conclusion. Leptin, adiponectin, and leptin:adiponectin ratio are informative biomarkers for obesity, central obesity, MS, and abnormal metabolic profile even in normal weight children/adolescents.

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Figures

Figure 1
Figure 1
Leptin and adiponectin versus body size and central fat. Children were separated according to Tanner (puberty) and body size into non-overweight (NonOwt), overweight, and obese (Owt/Ob) ± central obesity. Values are reported as leptin for girls (a), and boys (b), and mean adiponectin for girls (c) and boys (d). One way ANOVA is **P < .01, ***P < .001 versus NonOwt, P < .01, ∆∆∆P < .001 Owt/Ob.
Figure 2
Figure 2
Leptin and adiponectin in overweight/obese children/adolescents ± metabolic syndrome (MS) versus non-overweight (NonOwt) children. Children were separated according to early puberty (Tanner I + II) and late puberty (Tanner stage IV + V) and body size NonOwt and overweight/obese groups (Owt/Ob) ± MS. Mean ± SD for leptin (a), adiponectin (b) and leptin/adiponectin (c) were analyzed using general linear model gender-adjusted (P < .001), where **P < .01, ***P < .001 versus NonOwt and ∆∆P < .01, ∆∆∆P < .001 versus OWt/Ob − MS.

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