We propose that in obese patients, increased hepcidin production, at least partly leptin mediated, represents the missing link between obesity and disrupted iron metabolism.

Urinary hepcidin, inflammation, and iron metabolism were examined during the 24 hr after exercise. Eight moderately trained athletes (6 men, 2 women) completed a 60-min running trial (15-min warm-up at 75-80% HR(peak) + 45 min at 85-90% HR(peak)) and a 60-min trial of seated rest in a randomized, crossover design. Venous blood and urine samples were collected pretrial, immediately posttrial, and at 3, 6, and 24 hr posttrial. Samples were analyzed for interleukin-6 (IL-6), C-reactive protein (CRP), serum iron, serum ferritin, and urinary hepcidin. The immediate postrun levels of IL-6 and 24-hr postrun levels of CRP were significantly increased from baseline (6.9 and 2.6 times greater, respectively) and when compared with the rest trial (p < or = .05). Hepcidin levels in the run trial after 3, 6, and 24 hr of recovery were significantly greater (1.7-3.1 times) than the pre- and immediate postrun levels (p < or = .05). This outcome was consistent in all participants, despite marked variation in the magnitude of rise. In addition, the 3-hr postrun levels of hepcidin were significantly greater than at 3 hr in the rest trial (3.0 times greater, p < or = .05). Hepcidin levels continued to increase at 6 hr postrun but failed to significantly differ from the rest trial (p = .071), possibly because of diurnal influence. Finally, serum iron levels were significantly increased immediately postrun (1.3 times, p < or = .05). The authors concluded that high-intensity exercise was responsible for a significant increase in hepcidin levels subsequent to a significant increase in IL-6 and serum iron.

Dietary iron absorption is reduced by ≈ 40% in asymptomatic P. falciparum parasitemia, likely because of low-grade inflammation and its modulation of circulating hepcidin. Because asymptomatic parasitemia has a protracted course and is very common in malarial areas, this effect may contribute to IDA and blunt the efficacy of iron supplementation and fortification programs. This trial was registered at clinicaltrials.gov as NCT01108939.

We conclude that hepcidin levels were suppressed during the second and third trimester of pregnancy, which was likely determined by the occurrence of iron deficiency. These data give insight in iron homeostasis during normal pregnancy.

The effect of two running sessions completed within a 12-h period on hemolysis, inflammation, and hepcidin activity in endurance athletes was investigated. Ten males completed two experimental trials in a randomized, counterbalanced order. The two trials included (a) a one-running-session trial (T1) including 10 x 1 km interval repeats (90% peak VO2 velocity), and (b) a two-running-session trial (T2), comprising a continuous 10-km run (70% peak VO2 velocity), and a 10 x 1 km interval run (90% peak VO2 velocity) completed 12 h later. Interleukin-6 (IL-6), free hemoglobin (Hb), haptoglobin (Hp), iron, ferritin, and hepcidin were assessed post-exercise. After the T1 and T2 interval runs, free Hb was significantly increased and Hp significantly decreased (p