Abstract
ObjectiveHepcidin reduces iron absorption by binding to the intestinal iron transporter ferroportin, thereby causing its degradation. Although short-term administration of testosterone or growth hormone (GH) has been reported to decrease circulating hepcidin levels, little is known about how hepcidin is influenced in human endocrine conditions associated with anemia.Research design and methodsWe used a sensitive and specific dual–monoclonal antibody sandwich immunoassay to measure hepcidin-25 in patients (a) during initiation of in vitro fertilization when endogenous estrogens were elevated vs. suppressed, (b) with GH deficiency before and after 12 months substitution treatment, (c) with hyperthyroidism before and after normalization, and (d) with hyperprolactinemia before and after six months of treatment with a dopamine agonist.ResultsIn response to a marked stimulation of endogenous estrogen production, median hepcidin levels decreased from 4.85 to 1.43 ng/mL (p < 0.01). Hyperthyroidism, hyperprolactinemia, or GH substitution to GH-deficient patients did not influence serum hepcidin-25 levels.ConclusionsIn humans, gonadotropin-stimulated endogenous estrogen markedly decreases circulating hepcidin-25 levels. No clear and stable correlation between iron biomarkers and hepcidin-25 was seen before or after treatment of hyperthyroidism, hyperprolactinemia or growth hormone deficiency.
Highlights
Hepcidin-25 plays a key role in the regulation of iron metabolism in humans by controlling the absorption of iron from the intestine [1]
Our findings indicate that changes in endogenous estrogen levels induced with gonadotropins influence the levels of circulating hepcidin-25, whereas no changes were seen in chronic growth hormone (GH) deficiency, hyperthyroidism or hyperprolactinemia before or after restoration to physiological conditions
31 healthy females were studied during suppression and stimulation of endogenous estrogen levels as part of pretreatment for in vitro fertilization (IVF) (Table 2)
Summary
Hepcidin-25 plays a key role in the regulation of iron metabolism in humans by controlling the absorption of iron from the intestine [1]. It is mainly synthesized in the liver as an 84 amino acid preprohormone which is converted to an active 25-amino acid peptide hormone detectable in serum and urine [2, 3]. Hepcidin-25 binds to the iron transporter ferroportin, present on the basolateral plasma membrane of intestinal enterocytes [4, 5]. Through a mechanism that is still incompletely understood, this binding causes the internalization and subsequent degradation of ferroportin, which leads to enterocytes becoming unable to transport iron across their basolateral plasma membranes [2, 3]. Mammalian iron homeostasis is concertedly regulated through hepcidin and ferroportin that fundamentally govern iron absorption, transport, storage and utilization [2, 3, 5]
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