Vitamin E Induces Liver Iron Depletion and Alters Iron Regulation in Mice.


Journal

The Journal of nutrition
ISSN: 1541-6100
Titre abrégé: J Nutr
Pays: United States
ID NLM: 0404243

Informations de publication

Date de publication:
07 2023
Historique:
received: 08 03 2023
revised: 14 04 2023
accepted: 27 04 2023
pmc-release: 29 04 2024
medline: 10 7 2023
pubmed: 2 5 2023
entrez: 1 5 2023
Statut: ppublish

Résumé

Vitamin E (vit E) is an essential nutrient that functions as a lipophilic antioxidant and is used clinically to treat nonalcoholic fatty liver disease, where it suppresses oxidative damage and impedes the progression of steatosis and fibrosis. Mice lacking a critical liver iron-trafficking protein also manifest steatosis because of iron-mediated oxidative damage and are protected from liver disease by oral vit E supplements. We aimed to examine the role of dietary vit E supplementation in modulating iron-sensing regulatory systems and nonheme iron levels in mouse liver. C57Bl/6 male mice, aged 6 wk, were fed purified diets containing normal amounts of iron and either control (45 mg/kg) or elevated (450 mg/kg) levels of 2R-α-tocopherol (vit E) for 18 d. Mouse plasma and liver were analyzed for nonheme iron, levels and activity of iron homeostatic proteins, and markers of oxidative stress. We compared means ± SD for iron and oxidative stress parameters between mice fed the control diet and those fed the vit E diet. The Vit E-fed mice exhibited lower levels of liver nonheme iron (38% reduction, P < 0.0001) and ferritin (74% reduction, P < 0.01) than control-fed mice. The levels of liver mRNA for transferrin receptor 1 and divalent metal transporter 1 were reduced to 42% and 57% of the control, respectively. The mRNA levels for targets of nuclear factor erythroid 2-related factor (Nrf2), a major regulator of the oxidative stress response and iron-responsive genes, were also suppressed in vit E livers. Hepcidin, an iron regulatory hormone, levels were lower in the plasma (P < 0.05), and ferroportin (FPN), the iron exporter regulated by hepcidin, was expressed at higher levels in the liver (P < 0.05). Oral vit E supplementation in mice can lead to depletion of liver iron stores by suppressing the iron- and redox-sensing transcription factor Nrf2, leading to enhanced iron efflux through liver FPN. Iron depletion may indirectly enhance the antioxidative effects of vit E.

Sections du résumé

BACKGROUND
Vitamin E (vit E) is an essential nutrient that functions as a lipophilic antioxidant and is used clinically to treat nonalcoholic fatty liver disease, where it suppresses oxidative damage and impedes the progression of steatosis and fibrosis. Mice lacking a critical liver iron-trafficking protein also manifest steatosis because of iron-mediated oxidative damage and are protected from liver disease by oral vit E supplements.
OBJECTIVES
We aimed to examine the role of dietary vit E supplementation in modulating iron-sensing regulatory systems and nonheme iron levels in mouse liver.
METHODS
C57Bl/6 male mice, aged 6 wk, were fed purified diets containing normal amounts of iron and either control (45 mg/kg) or elevated (450 mg/kg) levels of 2R-α-tocopherol (vit E) for 18 d. Mouse plasma and liver were analyzed for nonheme iron, levels and activity of iron homeostatic proteins, and markers of oxidative stress. We compared means ± SD for iron and oxidative stress parameters between mice fed the control diet and those fed the vit E diet.
RESULTS
The Vit E-fed mice exhibited lower levels of liver nonheme iron (38% reduction, P < 0.0001) and ferritin (74% reduction, P < 0.01) than control-fed mice. The levels of liver mRNA for transferrin receptor 1 and divalent metal transporter 1 were reduced to 42% and 57% of the control, respectively. The mRNA levels for targets of nuclear factor erythroid 2-related factor (Nrf2), a major regulator of the oxidative stress response and iron-responsive genes, were also suppressed in vit E livers. Hepcidin, an iron regulatory hormone, levels were lower in the plasma (P < 0.05), and ferroportin (FPN), the iron exporter regulated by hepcidin, was expressed at higher levels in the liver (P < 0.05).
CONCLUSIONS
Oral vit E supplementation in mice can lead to depletion of liver iron stores by suppressing the iron- and redox-sensing transcription factor Nrf2, leading to enhanced iron efflux through liver FPN. Iron depletion may indirectly enhance the antioxidative effects of vit E.

Identifiants

pubmed: 37127137
pii: S0022-3166(23)37589-8
doi: 10.1016/j.tjnut.2023.04.018
pmc: PMC10375508
pii:
doi:

Substances chimiques

Iron E1UOL152H7
Vitamin E 1406-18-4
Hepcidins 0
NF-E2-Related Factor 2 0
Antioxidants 0
RNA, Messenger 0

Types de publication

Journal Article Research Support, N.I.H., Intramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

1866-1876

Informations de copyright

Published by Elsevier Inc.

Références

Cochrane Database Syst Rev. 2017 Apr 18;4:CD002854
pubmed: 28418065
PLoS One. 2013;8(4):e60534
pubmed: 23565256
PLoS Pathog. 2015 Aug 20;11(8):e1004998
pubmed: 26291319
Blood Cells Mol Dis. 2018 Mar;69:75-81
pubmed: 29032941
Semin Hematol. 2021 Jul;58(3):161-174
pubmed: 34389108
Int J Mol Sci. 2021 Jun 17;22(12):
pubmed: 34204327
Antioxidants (Basel). 2022 Jan 26;11(2):
pubmed: 35204118
Haematologica. 2010 Aug;95(8):1261-8
pubmed: 20179090
Antioxidants (Basel). 2021 Jan 26;10(2):
pubmed: 33530432
Curr Gastroenterol Rep. 2012 Feb;14(1):8-16
pubmed: 22124850
Bioresour Technol. 2008 Dec;99(18):8705-9
pubmed: 18550368
J Lipid Res. 2020 May;61(5):707-721
pubmed: 32086244
N Engl J Med. 2005 Jun 9;352(23):2379-88
pubmed: 15829527
Mol Cell Biol. 2006 Mar;26(6):2373-86
pubmed: 16508012
J Biochem Mol Toxicol. 2005;19(5):298-303
pubmed: 16292753
Free Radic Biol Med. 2021 Nov 1;175:18-27
pubmed: 34455040
Cochrane Database Syst Rev. 2017 Jul 31;7:CD000254
pubmed: 28756618
Haematologica. 2020 Feb 13;105(10):e493
pubmed: 33054090
Hepatology. 2021 Mar;73(3):1176-1193
pubmed: 32438524
Nat Metab. 2019 May;1(5):519-531
pubmed: 31276102
Blood. 2016 Jun 9;127(23):2809-13
pubmed: 27044621
Am J Hematol. 2017 Nov;92(11):1204-1213
pubmed: 28815688
Am Fam Physician. 1997 Jan;55(1):197-201
pubmed: 9012278
Nature. 2014 May 1;509(7498):105-9
pubmed: 24695223
Anal Biochem. 2009 Jun 15;389(2):124-9
pubmed: 19341701
Proc Natl Acad Sci U S A. 1988 Jul;85(14):5166-70
pubmed: 2839833
Br J Nutr. 2000 Sep;84(3):261-7
pubmed: 10967604
EMBO J. 2004 Jan 28;23(2):386-95
pubmed: 14726953
Metab Syndr Relat Disord. 2011 Aug;9(4):287-90
pubmed: 21417913
Am J Clin Nutr. 2007 Jan;85(1):293S-299S
pubmed: 17209213
Nat Cell Biol. 2014 Nov;16(11):1069-79
pubmed: 25327288
J Lipid Res. 2018 Sep;59(9):1597-1609
pubmed: 30084831
Molecules. 2019 Apr 07;24(7):
pubmed: 30959950
Nutrients. 2017 Sep 11;9(9):
pubmed: 28892009
Annu Rev Nutr. 2021 Oct 11;41:105-131
pubmed: 34115520
JAMA. 2013 May 15;309(19):2005-15
pubmed: 23644932
Antioxid Redox Signal. 2018 Dec 10;29(17):1727-1745
pubmed: 28899199
Am J Clin Nutr. 2019 Nov 1;110(5):1148-1167
pubmed: 31495886
Br J Haematol. 2021 Jun;193(5):882-893
pubmed: 33316086
JAMA. 2005 Jul 6;294(1):56-65
pubmed: 15998891
Curr Top Membr. 2012;70:169-214
pubmed: 23177986
Front Pharmacol. 2022 Apr 12;13:869794
pubmed: 35496274
N Engl J Med. 2000 Jun 22;342(25):1917-8
pubmed: 10877639
Cell Death Dis. 2019 Jun 18;10(6):449
pubmed: 31209199
JCI Insight. 2020 Jan 16;5(1):
pubmed: 31821172
Liver Int. 2018 Jan;38(1):164-173
pubmed: 28679028
N Engl J Med. 2010 May 6;362(18):1675-85
pubmed: 20427778
World J Gastroenterol. 2016 Jun 7;22(21):5096-103
pubmed: 27275102
J Clin Invest. 2017 May 1;127(5):1786-1797
pubmed: 28375153
JAMA. 2005 Mar 16;293(11):1338-47
pubmed: 15769967
J Biol Chem. 2017 Aug 4;292(31):12744-12753
pubmed: 28615439
J Lipid Res. 2015 Nov;56(11):2217-25
pubmed: 26351363
N Engl J Med. 1994 Apr 14;330(15):1029-35
pubmed: 8127329
Hepatology. 2020 Feb;71(2):495-509
pubmed: 30506586
Blood. 2011 Jul 21;118(3):747-56
pubmed: 21622652
Mol Med. 2018 Mar 15;24(1):5
pubmed: 30134796
Redox Biol. 2020 Oct;37:101710
pubmed: 32920226
JAMA. 2008 Nov 12;300(18):2123-33
pubmed: 18997197
Elife. 2015 Oct 05;4:
pubmed: 26436293
J Nutr. 2001 Feb;131(2):374S-7S
pubmed: 11160564
Blood. 2008 Nov 15;112(10):4292-7
pubmed: 18689548
JAMA. 2011 Oct 12;306(14):1549-56
pubmed: 21990298
IUBMB Life. 2019 Apr;71(4):411-415
pubmed: 30550633
Neuroscience. 2014 Feb 28;260:120-9
pubmed: 24342566
Free Radic Biol Med. 2021 Jan;162:592-602
pubmed: 33248265
Bone. 2020 Sep;138:115495
pubmed: 32585319

Auteurs

Ethan Baratz (E)

Genetics and Metabolism Section, NIDDK, NIH, Bethesda, MD, United States.

Olga Protchenko (O)

Genetics and Metabolism Section, NIDDK, NIH, Bethesda, MD, United States.

Shyamalagauri Jadhav (S)

Genetics and Metabolism Section, NIDDK, NIH, Bethesda, MD, United States.

Deliang Zhang (D)

Section on Human Iron Metabolism, NICHD, NIH, Bethesda, MD, United States.

Pierre-Christian Violet (PC)

Molecular and Clinical Nutrition Section, NIDDK, NIH, Bethesda, MD, United States.

Samantha Grounds (S)

Genetics and Metabolism Section, NIDDK, NIH, Bethesda, MD, United States.

Minoo Shakoury-Elizeh (M)

Genetics and Metabolism Section, NIDDK, NIH, Bethesda, MD, United States.

Mark Levine (M)

Molecular and Clinical Nutrition Section, NIDDK, NIH, Bethesda, MD, United States.

Caroline C Philpott (CC)

Genetics and Metabolism Section, NIDDK, NIH, Bethesda, MD, United States. Electronic address: carolinep@mail.nih.gov.

Articles similaires

Smoking Cessation and Incident Cardiovascular Disease.

Jun Hwan Cho, Seung Yong Shin, Hoseob Kim et al.
1.00
Humans Male Smoking Cessation Cardiovascular Diseases Female
Humans United States Aged Cross-Sectional Studies Medicare Part C
1.00
Humans Yoga Low Back Pain Female Male
Humans Meals Time Factors Female Adult

Classifications MeSH