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Ferroportin-Hepcidin Axis in Prepubertal Obese Children with Sufficient Daily Iron Intake
Joanna Gajewska1, Jadwiga Ambroszkiewicz2, Witold Klemarczyk3
1Screening Department and Metabolic Diagnostics, Institute of Mother and Child, Kasprzaka 17a, 01-211 Warsaw, Poland. joanna.gajewska@imid.med.pl.
Insights
Obese children show altered iron regulation (ferroportin/hepcidin axis) despite adequate iron intake and normal iron status. This suggests micronutrient interactions may influence iron metabolism in childhood obesity.
Area of Science:
- Pediatric Endocrinology
- Nutritional Science
- Hematology
Background:
- Obesity can disrupt iron metabolism.
- The ferroportin-hepcidin axis is crucial for iron regulation.
- Understanding iron status in obese children is important.
Purpose of the Study:
- To assess iron status, focusing on ferroportin and hepcidin.
- To investigate the ferroportin-hepcidin axis in prepubertal obese children.
- To explore associations between iron markers and dietary intake.
Main Methods:
- Compared serum ferroportin, hepcidin, ferritin, sTfR, and iron in 40 obese and 40 normal-weight children.
- Analyzed hematological parameters and daily dietary intake.
- Used correlation and multivariate regression analyses.
Main Results:
- Obese children had significantly lower ferroportin/hepcidin and ferritin/hepcidin ratios.
- No significant differences in iron concentration, sTfR/ferritin index, or hematological parameters were observed.
- The ferroportin/hepcidin ratio correlated with energy, iron, and vitamin B12 intake in obese children.
Conclusions:
- Obese children may exhibit an altered ferroportin-hepcidin axis without overt iron deficiency.
- Iron status in obese children might be influenced by factors beyond dietary iron.
- Further research into micronutrient roles in childhood obesity iron metabolism is warranted.
Abstract:
Iron metabolism may be disrupted in obesity, therefore, the present study assessed the iron status, especially ferroportin and hepcidin concentrations, as well as associations between the ferroportin-hepcidin axis and other iron markers in prepubertal obese children. The following were determined: serum ferroportin, hepcidin, ferritin, soluble transferrin receptor (sTfR), iron concentrations and values of hematological parameters as well as the daily dietary intake in 40 obese and 40 normal-weight children. The ferroportin/hepcidin and ferritin/hepcidin ratios were almost two-fold lower in obese children (p = 0.001; p = 0.026, respectively). Similar iron concentrations (13.2 vs. 15.2 µmol/L, p = 0.324), the sTfR/ferritin index (0.033 vs. 0.041, p = 0.384) and values of hematological parameters were found in obese and control groups, respectively. Iron daily intake in the obese children examined was consistent with recommendations. In this group, the ferroportin/hepcidin ratio positively correlated with energy intake (p = 0.012), dietary iron (p = 0.003) and vitamin B12 (p = 0.024). In the multivariate regression model an association between the ferroportin/hepcidin ratio and the sTfR/ferritin index in obese children (β = 0.399, p = 0.017) was found. These associations did not exist in the controls. The results obtained suggest that in obese children with sufficient iron intake, the altered ferroportin-hepcidin axis may occur without signs of iron deficiency or iron deficiency anemia. The role of other micronutrients, besides dietary iron, may also be considered in the iron status of these children.
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