Ferroportin-Hepcidin Axis in Prepubertal Obese Children with Sufficient Daily Iron Intake

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.

Effects of Pubertal Status and Inflammation on the Use of Ferritin to Define Iron Deficiency in Children With Overweight or Obesity

“…9,28 In agreement, a recent study showed that obese pre-pubertal children presented higher hepcidin and lower ferroportin concentrations in comparison with normal-weight children. 29 Analysis of iron intakes suggests low iron absorption as an important contributor to ID in this cohort of children with OW/ OB. Accordingly, Cepeda-Lopez et al 14 found that CRP levels instead of iron intake were a major contributor to low serum iron and high total iron binding capacity in a Mexican Nutrition Survey which included 1174 children.…”

Iron Metabolism in Obesity and Metabolic Syndrome

“…Gajewska et al determined the iron status in a group of 80 children and found the obese ones to have a 40% increase in hepcidin levels, as well as a 30% reduction in FPN1 levels. However, soluble transferrin receptor (sTfR), ferritin, iron or hemoglobin levels were similar, as well as the mean corpuscular volume (MCV), a sign of an iron deficiency-independent alteration of the FPN-hepcidin axis [ 147 ]. In accordance, Park et al found HAMP mRNA to be lower in an HFD-induced murine model of obesity [ 148 ].…”

Elevated hepcidin, ferroportin associated with glucose metabolism disorder in midpregnancy

“…Hepcidin (Hepc) is a 25-amino-acid peptide secreted by the liver that is metabolized by the kidney and is considered a "core factor" in regulating iron metabolism [9] . Ferroportin (FPN)-the only iron exporter protein known to exist in mammals, is a 62.5-kDa protein consisting of 12 transmembrane domains [10].…”

“…Ferroportin (FPN)-the only iron exporter protein known to exist in mammals, is a 62.5-kDa protein consisting of 12 transmembrane domains [10]. Studies [9] [11,12]have shown that mice lacking the hepcidin gene as well as humans with hepcidin gene mutations suffer severe iron overload or other related diseases. Ganz T et al [13] found that inactivation of the FPN gene was associated with severe iron overload in the liver and the pancreas.…”