Background: Hepcidin is a hormone that regulates iron flow in plasma, its production is induced by an iron overload and by inflammation. Some studies conducted in children and adolescents report an iron deficiency secondary to obesity-related to elevated levels of hepcidin. Although it is know hepcidin rises when IL6 increases, the relationship between hepcidin, dyslipidemia, IR, visceral adiposity index (VAI) and endothelial dysfunction in adolescents with obesity is unclear. Aims: We set out to explore the difference of hepcidin, iron metabolism markers and IL-6 between obese and no obese adolescents, and identify associations of with inflammation, dyslipidemia, insulin resistance, and endothelial dysfunction. Methods: Cross-sectional study of 29 obese adolescents and 30 controls subjects (normal BMI) from Guanajuato, Mexico. Anthropometric measurements and blood pressure were conducted using standard methods, VAI was calculated. Iron metabolism markers (hepcidin, transferrin, ferritin, soluble transferrin receptor -sTFR) were assayed by ELISA, as well as IL-6. Lipid profile and insulin were measured by standard auto-analyzer methods. We calculated HOMA index. sdLDL was analyzed by gradient electrophoresis using the Lipoprint LDL method from Quantimetrix. Flow-mediated vasodilation (FMD) and arterial stiffness were measured by ultrasound. The Ethical Committee of the University of Guanajuato approved this study and informed consent was obtained from the participant adolescents and their parents. Results: The obesity group showed significantly higher levels of hepcidin 14070.8 ± 7113.5 vs 8419.1 ± 4826.8c; IL-6 2.0 (1.0-4.9) vs 0.9 (0.5-1.3)c and ferritin 94.4 ± 82.4 vs 55.1 ± 39.6a. No significant difference was found for transferrin, sTFR and sTFR index. Obese adolescents showed significantly lower HDL-C (58.2 ± 9.6 vs 63.6 ± 5.0a mg/dl and higher levels of TG 139.3 ± 64.2 vs 83.2 ± 42.9c; mg/dl, sdLDL% 3.78 ± 4 vs 1.85 ±2.7a; HOMA (3.34 (2.4-5.5) vs 1.8 (1.2-2.2)d; VAI 1.6 ± 0.8 vs 0.9 ± 0.5c. FMD was significantly lower in obese adolescents 20.64 ± 7.1 vs 27.7 ± 9.3b. Hepcidin correlated positively with VAI r=0.29a; IL-6 r=0.35b; TG r=0.38b; sdLDL3% r=0.31a; HOMA r=0.29a; SBP r=0.36b; arterial stiffness r=0.29a; and negatively with FMD r=-0.29a. IL-6 correlated positively with VAI r=0.30 a and HOMA r=0.36 b ap<0.05; bp<0.01, cp<0.001; dp<0.0001 Conclusions: Adolescents with obesity show higher hepcidin levels that are associated with cardiometabolic risk markers such as IR, VAI, atherogenic dyslipidemia and endothelial dysfunction, while IL-6 was only associated with IR, and VAI. This suggests that hepcidin is a valuable marker of inflammation regardless of changes in iron metabolism and total body iron (TBI) as demonstrated by unchanged sTFR and TBI as sTFR/ferritin index. Long term effects of higher hepcidin levels on iron status should be explored.