Is the erythropoietin-erythroferrone-hepcidin axis intact in human neonates?
Erythroferrone
Erythropoietin
Hepcidin
Iron
RET-He
Supplementation
Journal
Blood cells, molecules & diseases
ISSN: 1096-0961
Titre abrégé: Blood Cells Mol Dis
Pays: United States
ID NLM: 9509932
Informations de publication
Date de publication:
05 2021
05 2021
Historique:
received:
03
12
2020
revised:
28
12
2020
accepted:
29
12
2020
pubmed:
16
1
2021
medline:
7
8
2021
entrez:
15
1
2021
Statut:
ppublish
Résumé
In a two-part process, we assessed elements of the principal hormonal pathway regulating iron homeostasis in human neonates. Part 1: Quantifying erythropoietin (Epo), erythroferrone (ERFE), hepcidin, and relevant serum and erythrocytic iron-related metrics in umbilical cord blood from term (n = 13) and preterm (n = 10) neonates, and from neonates born to mothers with diabetes and obesity (n = 13); Part 2: Quantifying serum Epo, ERFE, and hepcidin before and following darbepoetin administration. Part 1: We measured Epo, ERFE and hepcidin in all cord blood samples. Epo and ERFE levels did not differ between the three groups. Preterm neonates had the lowest hepcidin levels, while neonates born to diabetic women with a very high BMI had the lowest ferritin and RET-He levels. Part 2: Following darbepoetin dosing, ERFE levels generally increased (p < 0.05) and hepcidin levels generally fell (p < 0.05). Our observations suggest that the Epo/ERFE/hepcidin axis is intact in the newborn period.
Identifiants
pubmed: 33450539
pii: S1079-9796(21)00002-4
doi: 10.1016/j.bcmd.2021.102536
pmc: PMC9107158
mid: NIHMS1801396
pii:
doi:
Substances chimiques
EPO protein, human
0
Erfe protein, human
0
HAMP protein, human
0
Hepcidins
0
Peptide Hormones
0
Erythropoietin
11096-26-7
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Pagination
102536Subventions
Organisme : NIDDK NIH HHS
ID : U54 DK110858
Pays : United States
Informations de copyright
Copyright © 2021. Published by Elsevier Inc.
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