The aim of this cross-sectional study was to investigate the relationship between soluble form of receptor for advanced glycation end products (sRAGE), obesity, and metabolic syndrome (MetS) in adolescents. A total of 522 male and 561 female adolescents were enrolled into the final analyses. Anthropometric parameters, blood pressure, blood biochemistry, fasting insulin, and plasma sRAGE levels were measured. In males, sRAGE was significantly and inversely correlated with waist circumference (WC), body mass index (BMI), systolic blood pressure, triglyceride (TG), low density lipoprotein cholesterol (LDL-C), and homeostasis model assessment-insulin resistance (HOMA-IR). Only WC and BMI were significantly and inversely correlated with sRAGE in females. Using linear regression analysis adjusting for age and gender, significant association was found between sRAGE and WC, BMI, TG, LDL-C, and HOMA-IR in adolescents of either gender ( ). This association was abolished when further adjusting BMI. In addition, sRAGE was significantly and inversely correlated with the increasing number of components of MetS in males ( for trend？=？0.006) but not in females ( for trend？=？0.422). In conclusion, plasma sRAGE is associated with obesity and MetS among adolescents. BMI may be the most important determinant of sRAGE levels in adolescents. 1. Introduction The metabolic syndrome (MetS), which includes abdominal obesity, dyslipidemia, hypertension, and hyperglycemia, all documented risk factors for cardiovascular disease (CVD), has become one of the major public health challenges in developed and developing countries. The increasing prevalence of the syndrome is associated with the global epidemic of obesity and diabetes [1]. The International Diabetes Federation (IDF) identifies central obesity, measured by waist circumference, as an obligatory finding for the diagnosis of MetS [2]. The causes of the MetS are multifactorial, stemming from complex genetic and environmental influences. Insulin resistance is believed to play a major role in the underlying pathophysiology of the MetS, possibly contributing to atherosclerosis and increasing the risk of glucose intolerance and diabetes [3]. However, the cellular and molecular bases for the pathologic phenomena occurring in the MetS have not been fully elucidated. Advanced glycation end products (AGE) are formed from proteins and peptides by nonenzymatic glycoxidation after contact with aldose sugars [4, 5]. AGEs are known to accumulate in the vessel wall, where they may act to alter the extracellular matrix, cell surface
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