ESPE Abstracts (2018) 89 P-P2-172

University of Chieti, Chieti, Italy

Background: Childhood obesity is associated with non-alcoholic fatty liver disease (NAFLD). Previous studies in obese adult and pubertal children with NAFLD have shown that chronic inflammation/oxidative stress and insulin resistance might induce iron metabolism disorders, characterized by increased Hepcidin and Ferritin levels and decreased serum Iron levels. However, data evaluating these findings in a well selected population of obese prepubertal children are still missing.

Methods: Therefore we aimed to characterize iron metabolism in a group of 40 obese prepubertal children with (11 Male/9 Female) and without (12 Male/8 Female) NAFLD defined by ultrasonography, compared to 40 healthy prepubertal age- and gender matched peers (22 Male/18 Female). We also investigated correlations between iron metabolism and both oxidative stress and metabolic markers. Anthropometric measurements were determined. Fasting blood samples were collected for measurement of insulin, glucose, lipid profile, ALT, AST and iron profile including iron concentration, ferritin and hepcidin. Lag-phase and MDA were evaluated as markers of oxidative stress. Differences across the three groups were evaluated by One-way Anova test and post-hoc assessment was calculated by Bonferroni test. In obese subjects a Pearson’s correlation was used for searching correlations between Hepcidin and other parameters.

Results: A significant increase of total cholesterol, triglycerides, Insulin, HOMA-IR and ALT values were higher in obese prepubertal children with and without NAFLD compared to controls, while only ALT were significantly higher in those with NAFLD compared to those without NAFLD. A significant increase of Ferritin and hepcidin values were documented across the three groups (all P<0.05). In particular, significant higher values were shown between obese prepubertal children with NAFLD compared to those without NAFLD and controls, while only ferritin but not hepcidin was significantly different in those without NAFLD compared to controls. Similarly, compared to controls MDA and Lag-phase were increased and decreased respectively in the two groups of obese without and with NAFLD, showing the last one significant differences compared to those without NAFLD. In addition, Iron values were lower in obese with NAFLD compared to controls, while no differences were found between those without NAFLD and the other two groups. In obese prepubertal children Hepcidin levels inversely correlated with oxidative stress activity (lag-phase).

Conclusions: Obese prepubertal children show impaired iron metabolism disorders, especially in those subjects with NAFLD. The correlation between Hepcidin levels and increased oxidative stress activity in obese prepubertal children suggest a role of these components in the early pathogenesis of NAFLD in prepubertal children.

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