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.

Abstract. Chronic, systemic inflammation, which is associated with obesity and numerous other diseases, impairs iron status by increasing hepcidin concentration. Inflammation also decreases the concentration of transferrin, the main iron transport protein and a negative acute phase protein, which is indirectly assessed by measuring total iron binding capacity (TIBC). However, the contribution of diet-induced inflammation has not been studied. Data from two studies, namely Diet and Inflammation and Selenium and Inflammation Studies (total n=98) were used to assess the associations among Dietary Inflammatory Index (DII®) scores derived from three-day dietary records, body mass index (BMI=weight[kg]/height[m]2), inflammatory and hematological markers among young adults with normal-weight, overweight or obesity. Subjects’ diets were also categorized as less inflammatory diets (LID) and inflammatory diets (ID) using cluster analysis. Independent t-test and regression analyses were used to assess associations in the data. Intakes of iron, proteins, fat, fiber, and calories were higher in the LID group compared to the ID group (p<0.05). Demographic characteristics and concentrations of C-reactive protein (CRP) and iron status biomarkers did not differ significantly between the two groups (p>0.05). Higher DII score was associated with increasing CRP (β+SE=0.23+0.07, p=0.002) and lower TIBC (β+SE=−8.46+3.44, p=0.02), independent of BMI category. The LID diet was associated with higher TIBC (β+SE=29.87+10.75, p=0.007) compared to the ID diet. In conclusion, inflammatory diets may impair iron status by reducing the iron binding capacity of transferrin.

Objectives Selenium deficiency is considered a risk factor for anemia of chronic inflammation, which is mediated by hepcidin. However, there are no 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 obesity compared with their normal weight counterparts, since obesity presents with low-grade chronic inflammation Methods A total of 59 college students (18–40y) consisting of 27 individuals with normal weight and 32 individuals with overweight/obesity were recruited for this study. Fasting blood samples were collected for the analysis of iron status biomarkers, plasma selenoproteins (glutathione peroxidase (GPX) activity and selenoprotein P) and plasma hepcidin concentration. Subjects completed 3-day dietary records to determine average daily nutrient intakes. Regression analysis, independent t-test and Wilcoxon rank sum tests were used to determine the relationships among variables. Statistical significance was set at P ≤ 0.05. Results There were no significant differences in nutrient intakes between subjects with overweight/obesity and those with normal weight (P > 0.05). Selenoprotein P 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 the relationship between hepcidin concentration and transferrin saturation depended on body weight status with an inverse relationship in subjects with overweight/obesity compared with their normal weight counterparts (P = 0.046). GPX activity (β = −0.018, P = 0.008) and selenoprotein P concentration (β = −1.24, P = 0.03) were inversely associated with hepcidin concentration (P < 0.001). Conclusions Our study showed an inverse association between selenium status and hepcidin concentration which highlights the importance of selenium in addressing inflammation-related anemia. Intervention studies on the effect of selenium supplementation on hepcidin concentration and iron status in individuals with anemia of inflammation are needed to support these findings. Funding Sources None.

Objectives Several studies have investigated the role of hepcidin in hypoferremia of obesity, but findings are mixed. In this study we examined the interrelationships among inflammatory markers, hepcidin and circulating iron, and investigated the contribution of hepcidin to iron status among subjects with overweight or obesity compared to those with normal weight. Methods This study combined data from two different cross-sectional studies in which inflammatory and iron status markers and hepcidin concentrations were measured from fasting blood samples for a total of 98 subjects with either normal weight (n = 28), overweight (n = 39) or obesity (n = 31). Associations among variables were investigated using ANOVA, correlation and regression analyses. Statistical significance was set at P ≤ 0.05. Mean ± SEM were reported for continuous variables except for skewed variables in which case geometric means (geometric mean ± 1SEM interval) were reported. Results Subjects with obesity had lower serum iron concentration compared to those with normal weight [(72 ± 6 µg/dL vs. 103 ± 10 µg/dL; P = 0.01)]. C-reactive protein concentration was highest in subjects with obesity [3.63 (2.98, 4.43) mg/L], followed by those with overweight [0.80 (0.66, 0.98) mg/L] and lowest among those with normal weight [(0.40 (0.32, 0.48) mg/L) (P < 0.05 for all). Ferritin concentration did not differ among groups (P > 0.05). Hepcidin concentration was positively correlated with BMI, hemoglobin, serum iron and serum ferritin, and transferrin saturation. Regression analyses adjusting for confounding variables showed that the association between plasma hepcidin concentration and both serum iron and transferrin saturation depended on the BMI category (P-values for interactions <0.05) with an inverse relationship among subjects with obesity compared to a positive association among those with normal weight. Conclusions The results of our study contribute to evidence of the role of elevated hepcidin in hypoferremia among individuals with obesity compared to those with normal weight. Funding Sources none.

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I would also like to thank Lauren Haldeman and Steven Fordahl for serving on my thesis committee. Dr. Fordahl's wisdom and guidance kept me motivated throughout the project. I am especially grateful for Dr. Haldeman who was the first to encourage me to earn a Master of Science degree in Nutrition. Her leadership will always inspire me. Additionally, I am thankful for my early science professors Bruce Banks, PhD and Maulik Trivedi, PhD for dispelling my fears of chemistry through their inspiring and fascinating lectures and for every instructor in the Nutrition department for the expertise and knowledge they share daily. I would also like to recognize the ongoing support of Paula Cooney, the departmental research coordinator, and Sherry Ritter, the department's administrative assistant who makes everything possible in the Department of Nutrition. Lastly, I would like to express my deepest appreciation for my husband, Timothy and children, Jack and Katy, my parents and my sister for encouraging me in every way while I pursued learning about food and nutrition. Their love, care and support are truly boundless.