Abstract
Selenium deficiency has been linked to anemia of inflammation, which is mediated by hepcidin. However, there are few studies providing evidence of the role of hepcidin in this relationship. In this study, we investigated the interrelationships among selenium biomarkers, hepcidin concentration, and iron status among individuals with overweight/obesity compared to their normal weight counterparts, since obesity is associated with chronic inflammation. A total of 59 college students were recruited for this study. Fasting blood samples were collected for the analysis of iron status, plasma selenoproteins (glutathione peroxidase (GPX) activity and selenoprotein P (SEPP1)), and plasma hepcidin. Subjects completed three-day dietary records to determine average daily nutrient intakes. SEPP1 concentration, GPX activity, and iron status biomarkers (serum iron, transferrin saturation, and hemoglobin concentration) were lower among individuals with overweight/obesity compared with individuals with normal weight, but these differences were not significant (p > 0.05). Regression analysis showed that GPX activity (β = −0.018, p = 0.008) and SEPP1 concentration (β = −1.24, p = 0.03) were inversely associated with hepcidin concentration. The inverse association between selenoproteins and hepcidin concentration supports a potential role of hepcidin as a mediator between selenium and iron status and warrants further studies to better understand this relationship.
Highlights
Anemia affects a third of the world’s population [1]
A few studies have reported significantly higher concentrations of serum iron, transferrin saturation, and hemoglobin in obese adolescents compared to their non-obese counterparts (20,21), most studies have demonstrated that obesity is associated with iron deficiency, hypoferremia, and hyperferritinemia [29,30]
While the results of this study showed the expected trends in serum iron, hemoglobin, transferrin saturation and ferritin, it is likely that the differences were not significant because there were no individuals with morbid obesity in the overweight/obese group, with most of them having overweight status
Summary
Anemia affects a third of the world’s population [1]. In the US, the prevalence increased by3% from years 2003 to 2012 [2]. Anemia results from a homeostatic iron imbalance with increased destruction and/or impaired synthesis of erythrocytes [1]. Iron deficiency is the most common cause of anemia accounting for about half of all cases, followed by inflammation [3,4]. Inflammation accounts for about a fifth of anemia cases in older adults in the US and, among individuals with obesity, the observed chronic low-grade inflammation is implicated to result in hypoferremia [1,3,4,7]. Anemia caused by inflammation is associated with alterations in iron metabolism, erythrocyte life span and production, lowered transferrin saturation and serum iron, and increased ferritin concentrations [8]. The link between inflammation and anemia has been explained by the iron regulatory protein, hepcidin. Hepcidin is a 25-amino-acid (disulfide-rich) peptide that plays a critical role in iron metabolism by acting as a signaling molecule, and in immunity
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