Background
Declines in iron status are frequently reported in those who regularly engage in strenuous physical activity. A possible reason for the declines in iron status with physical activity is increases in the iron regulatory hormone hepcidin, which functions to inhibit dietary iron absorption and can be induced by the inflammatory cytokine interleukin-6 (IL-6).
Objective
The current study aimed to determine the impact of a prolonged bout of running on hepcidin and dietary iron absorption in trained female and male runners.
Methods
Trained female and male collegiate cross country runners (n=28; age: 19.7±1.2 y; VO2max: 66.1±6.1 mL‧kg–1‧min–2; serum ferritin: 21.9±13.3 ng/mL) performed a prolonged run (98.8±14.7 min, 21.2±3.8 km, 4.7±0.3 min/km) during a team practice. Participants consumed a stable iron isotope with a standardized meal 2 h post-run and blood was collected 1 h later. The protocol was repeated 2 weeks later except participants abstained from exercise (rest). Red blood cells were collected 15 d after exercise and rest to determine isotope enrichment. Differences between exercise and rest were assessed by paired t-tests and Wilcoxon matched-pairs signed rank tests. Data are means±SD.
Results
Plasma hepcidin increased 52% after exercise (45.8±34.4 ng/mL) compared to rest (30.3±27.2 ng/mL, P=0.0011). Fractional iron absorption was reduced by 36% after exercise (11.8±14.6%) compared to rest (18.5±14.4%, P=0.025). Plasma IL-6 was greater after exercise (0.660±0.354 pg/mL) compared to rest (0.457±0.212 pg/mL, P<0.0001). Exploratory analyses revealed that the increase in hepcidin with exercise may be driven by a response in males but not females.
Conclusions
A prolonged bout of running increases hepcidin and decreases dietary iron absorption compared to rest in trained runners with low iron stores. The current study supports that IL-6 contributes to the increase in hepcidin with prolonged physical activity, though future studies should explore potential sex differences in the hepcidin response.
Background
Short-term starvation and severe food deprivation (FD) reduce dietary iron absorption and restricts iron to tissues, thereby limiting the amount of iron available for erythropoiesis. These effects may be mediated by increases in the iron regulatory hormone hepcidin; however, whether mild-to-moderate FD has similar effects on hepcidin and iron homeostasis is not known.
Objective
To determine the effects of varying magnitudes and durations of FD on hepcidin and indicators of iron status in male and female mice.
Methods
Male and female C57BL/6 mice (14 wk old; n = 170) were randomized to consume AIN-93 M diets ad libitum (AL) or varying magnitudes of FD (10, 20, 40, 60, 80, or 100% FD). FD was calculated based on the average amount of food consumed by the AL males or females, respectively, and food was split into morning and evening meals. Mice were euthanized at 48 h and 1, 2, and 3 wk and hepcidin and indicators of iron status were measured. Data were analyzed by Pearson correlation and one-way ANOVA.
Results
Liver hepcidin mRNA was positively correlated with the magnitude of FD at all timepoints (P < 0.05). At 3 wk, liver hepcidin mRNA increased 3-fold with 10% and 20% FD compared to AL and was positively associated with serum hepcidin (R = 0.63, P < 0.0001). Serum iron was reduced by ∼65% (P ≤ 0.01) and liver non-heme iron concentrations were ∼75% greater (P ≤ 0.01) with 10% and 20% FD for 3 wk compared to AL. Liver hepcidin mRNA at 3 wk was positively correlated with liver Bmp6 (R = 0.765, P < 0.0001) and liver gluconeogenic enzymes (R = >0.667, P < 0.05), but not markers of inflammation (P > 0.05).
Conclusion
FD increases hepcidin in male and female mice and results in hypoferremia and tissue iron sequestration. These findings suggest that increased hepcidin with FD may contribute to the disturbances in iron homeostasis with undernutrition.
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