Differences in bone microarchitecture between genetic and secondary iron-overload mouse models suggest a role for hepcidin deficiency in iron-related osteoporosis.
Animals
Mice
Iron
/ metabolism
Hepcidins
/ genetics
Hemochromatosis
/ genetics
Alkaline Phosphatase
/ metabolism
Hemochromatosis Protein
/ genetics
Histocompatibility Antigens Class I
/ genetics
Iron Overload
/ complications
Liver
/ metabolism
Osteoporosis
/ genetics
Collagen
/ metabolism
Mice, Knockout
bone QCT/μCT
genetic animal models
hemochromatosis
iron overload
osteoporosis
Journal
FASEB journal : official publication of the Federation of American Societies for Experimental Biology
ISSN: 1530-6860
Titre abrégé: FASEB J
Pays: United States
ID NLM: 8804484
Informations de publication
Date de publication:
11 2023
11 2023
Historique:
revised:
04
09
2023
received:
03
07
2023
accepted:
25
09
2023
medline:
30
10
2023
pubmed:
24
10
2023
entrez:
24
10
2023
Statut:
ppublish
Résumé
Iron overload is one of the secondary osteoporosis etiologies. Cellular and molecular mechanisms involved in iron-related osteoporosis are not fully understood. The aim of the study was to investigate the respective roles of iron excess and hepcidin, the systemic iron regulator, in the development of iron-related osteoporosis. We used mice models with genetic iron overload (GIO) related to hepcidin deficiency (Hfe Despite an increase of bone iron concentration in all overloaded mice models, bone volume/total volume (BV/TV) and trabecular thickness (Tb.Th) only decreased significantly in GIO, at 12 months for Hfe Together, these data suggest that iron in excess alone is not sufficient to induce osteoporosis and that low hepcidin levels also contribute to the development of osteoporosis.
Identifiants
pubmed: 37874260
doi: 10.1096/fj.202301184R
doi:
Substances chimiques
Iron
E1UOL152H7
Hepcidins
0
Alkaline Phosphatase
EC 3.1.3.1
Hemochromatosis Protein
0
Histocompatibility Antigens Class I
0
Collagen
9007-34-5
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
e23245Informations de copyright
© 2023 Federation of American Societies for Experimental Biology.
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