A Decrease in Maternal Iron Levels Is the Predominant Factor Suppressing Hepcidin during Pregnancy in Mice.

Autor: Helman SL; Molecular Nutrition Laboratory, QIMR Berghofer Medical Research Institute, Herston, QLD 4006, Australia., Wilkins SJ; Iron Metabolism Laboratory, QIMR Berghofer Medical Research Institute, Herston, QLD 4006, Australia., Chan JCJ; Molecular Nutrition Laboratory, QIMR Berghofer Medical Research Institute, Herston, QLD 4006, Australia., Hartel G; Statistics Unit, QIMR Berghofer Medical Research Institute, Herston, QLD 4006, Australia.; School of Public Health, The University of Queensland, Herston, QLD 4006, Australia.; School of Nursing, Queensland University of Technology, Kelvin Grove, QLD 4059, Australia., Wallace DF; School of Biomedical Sciences and Centre for Genomics and Personalised Health, Queensland University of Technology, Kelvin Grove, Brisbane, QLD 4059, Australia., Anderson GJ; Iron Metabolism Laboratory, QIMR Berghofer Medical Research Institute, Herston, QLD 4006, Australia., Frazer DM; Molecular Nutrition Laboratory, QIMR Berghofer Medical Research Institute, Herston, QLD 4006, Australia.; School of Biomedical Sciences, Queensland University of Technology, Gardens Point, QLD 4000, Australia.; School of Biomedical Sciences, The University of Queensland, St. Lucia, QLD 4067, Australia.
Jazyk: angličtina
Zdroj: International journal of molecular sciences [Int J Mol Sci] 2023 Sep 21; Vol. 24 (18). Date of Electronic Publication: 2023 Sep 21.
DOI: 10.3390/ijms241814379
Abstrakt: In order to supply adequate iron during pregnancy, the levels of the iron regulatory hormone hepcidin in the maternal circulation are suppressed, thereby increasing dietary iron absorption and storage iron release. Whether this decrease in maternal hepcidin is caused by changes in factors known to regulate hepcidin expression, or by other unidentified pregnancy factors, is not known. To investigate this, we examined iron parameters during pregnancy in mice. We observed that hepatic iron stores and transferrin saturation, both established regulators of hepcidin production, were decreased in mid and late pregnancy in normal and iron loaded dams, indicating an increase in iron utilization. This can be explained by a significant increase in maternal erythropoiesis, a known suppressor of hepcidin production, by mid-pregnancy, as indicated by an elevation in circulating erythropoietin and an increase in spleen size and splenic iron uptake. Iron utilization increased further in late pregnancy due to elevated fetal iron demand. By increasing maternal iron levels in late gestation, we were able to stimulate the expression of the gene encoding hepcidin, suggesting that the iron status of the mother is the predominant factor influencing hepcidin levels during pregnancy. Our data indicate that pregnancy-induced hepcidin suppression likely occurs because of reductions in maternal iron reserves due to increased iron requirements, which predominantly reflect stimulated erythropoiesis in mid-gestation and increased fetal iron requirements in late gestation, and that there is no need to invoke other factors, including novel pregnancy factor(s), to explain these changes.
Databáze: MEDLINE
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