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Mechanisms of hepatic iron accumulation with aging and environmental heat stress
Author(s) -
Bloomer Steven A.,
Kregel Kevin C.,
Brown Kyle E.
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1119.2
Subject(s) - hepcidin , hyperthermia , oxidative stress , medicine , endocrinology , inflammation , heat stress , homeostasis , chemistry , biology , zoology
Regulation of physiological iron stores is crucial for maintenance of homeostasis. Hepatic iron concentrations increase with aging and physiological challenges, which may result in oxidative injury after a stressor. The purpose of this study was to investigate mechanisms of iron regulation in these contexts. The iron regulatory hormone, hepcidin, is induced in response to increases in hepatic iron stores and inflammation; thus, we hypothesized that both aging and hyperthermia would be associated with elevated hepcidin. Young (6 mo) and old (24 mo) Fischer 344 rats were exposed to two bouts of environmental heat stress, and liver and blood samples were taken after the second heating. Hepatic hepcidin expression was evaluated using qPCR, and plasma iron was measured. Because hepcidin is induced by IL‐6, and heat stress is an inflammatory challenge, the plasma concentration of IL‐6 was also assayed. Heat stress was associated with significant hypoferremia in both age groups two hours after hyperthermia. IL‐6 was elevated in old compared to young rats, and was induced by heat stress in both age groups immediately (0 h) after hyperthermia. Hepcidin was induced only in old rats at the two‐hour timepoint. These results suggest that hepcidin may have a role in lowering plasma iron after hyperthermia in old rats, but that hypoferremia after heat stress in young rats involves a mechanism distinct from the IL‐6 – hepcidin axis.