title: Circulating Hepcidin-25 Is Reduced by Endogenous Estrogen in Humans.
abstract: OBJECTIVE
  Hepcidin 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.
  
  
  METHODS
  We 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.
  
  
  RESULTS
  In 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.
  
  
  CONCLUSIONS
  In 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.
authors: Department of Endocrinology, Metabolism and Diabetes, Departments of Medicine and Molecular Medicine and Surgery, Karolinska Institutet at Karolinska University Hospital, S-141 86 Stockholm, Sweden.
authors: Mikael
authors: M
authors: Lehtihet
authors: Department of Endocrinology, Metabolism and Diabetes, Departments of Medicine and Molecular Medicine and Surgery, Karolinska Institutet at Karolinska University Hospital, S-141 86 Stockholm, Sweden.|Molecular Nutrition Unit, Center for Innovative Medicine, Department of Biosciences and Nutrition, Karolinska Institutet at Karolinska University Hospital, S-141 86 Stockholm, Sweden.
authors: Ylva
authors: Y
authors: Bonde
authors: Department of Endocrinology, Metabolism and Diabetes, Departments of Medicine and Molecular Medicine and Surgery, Karolinska Institutet at Karolinska University Hospital, S-141 86 Stockholm, Sweden.|Molecular Nutrition Unit, Center for Innovative Medicine, Department of Biosciences and Nutrition, Karolinska Institutet at Karolinska University Hospital, S-141 86 Stockholm, Sweden.
authors: Lena
authors: L
authors: Beckman
authors: Department of Endocrinology, Metabolism and Diabetes, Departments of Medicine and Molecular Medicine and Surgery, Karolinska Institutet at Karolinska University Hospital, S-141 86 Stockholm, Sweden.
authors: Katarina
authors: K
authors: Berinder
authors: Department of Endocrinology, Metabolism and Diabetes, Departments of Medicine and Molecular Medicine and Surgery, Karolinska Institutet at Karolinska University Hospital, S-141 86 Stockholm, Sweden.
authors: Charlotte
authors: C
authors: Hoybye
authors: Department of Endocrinology, Metabolism and Diabetes, Departments of Medicine and Molecular Medicine and Surgery, Karolinska Institutet at Karolinska University Hospital, S-141 86 Stockholm, Sweden.|Molecular Nutrition Unit, Center for Innovative Medicine, Department of Biosciences and Nutrition, Karolinska Institutet at Karolinska University Hospital, S-141 86 Stockholm, Sweden.
authors: Mats
authors: M
authors: Rudling
authors: Lilly Research Laboratories, Eli Lilly & Co, Indianapolis, Indiana, United States of America.
authors: John H
authors: JH
authors: Sloan
authors: Lilly Research Laboratories, Eli Lilly & Co, Indianapolis, Indiana, United States of America.
authors: Robert J
authors: RJ
authors: Konrad
authors: Department of Endocrinology, Metabolism and Diabetes, Departments of Medicine and Molecular Medicine and Surgery, Karolinska Institutet at Karolinska University Hospital, S-141 86 Stockholm, Sweden.|Molecular Nutrition Unit, Center for Innovative Medicine, Department of Biosciences and Nutrition, Karolinska Institutet at Karolinska University Hospital, S-141 86 Stockholm, Sweden.
authors: Bo
authors: B
authors: Angelin
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000740:Anemia / Q000097:blood* / Q000378:metabolism; D002097:C-Reactive Protein / Q000096:biosynthesis / Q000378:metabolism; D018491:Dopamine Agonists / Q000737:chemistry; D004967:Estrogens / Q000502:physiology*; D005260:Female; D005293:Ferritins / Q000096:biosynthesis / Q000378:metabolism; D005307:Fertilization in Vitro; D064451:Hepcidins / Q000097:blood*; D019382:Human Growth Hormone / Q000172:deficiency / Q000378:metabolism; D006801:Humans; D006966:Hyperprolactinemia / Q000150:complications; D006980:Hyperthyroidism / Q000150:complications; D007118:Immunoassay; D007501:Iron / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D015175:Prolactinoma / Q000097:blood; D014168:Transferrin / Q000096:biosynthesis / Q000378:metabolism; D055815:Young Adult
chemical_list: D018491:Dopamine Agonists; D004967:Estrogens; D064451:Hepcidins; D014168:Transferrin; C545475:hepcidin 25, human; D019382:Human Growth Hormone; D002097:C-Reactive Protein; D005293:Ferritins; D007501:Iron