Copper supplementation reverses dietary iron overload-induced pathologies in mice

Basit Öğe Kaydı
dc.authorid0000-0003-0059-1819
dc.authorid0000-0001-9665-4292
dc.authorid0000-0001-5282-531X
dc.authorscopusid56155484400
dc.authorscopusid57202704036
dc.authorscopusid55934188600
dc.authorscopusid57206601483
dc.authorscopusid57190974099
dc.authorscopusid56767690300
dc.authorscopusid7402784605
dc.authorwosidDoguer, Caglar/ABA-3152-2020
dc.contributor.authorWang, Tao
dc.contributor.authorXiang, Ping
dc.contributor.authorHa, Jung-Heun
dc.contributor.authorWang, Xiaoyu
dc.contributor.authorDoğuer, Çağlar
dc.contributor.authorFlores, Shireen R. L.
dc.contributor.authorCollins, James F.
dc.date.accessioned2022-05-11T14:48:42Z
dc.date.available2022-05-11T14:48:42Z
dc.date.issued2018
dc.departmentYüksekokullar, Sağlık Yüksekokulu, Beslenme ve Diyetetik Bölümü
dc.description.abstractDietary iron overload in rodents impairs growth and causes cardiac hypertrophy, serum and tissue copper depletion, depression of serum ceruloplasmin (Cp) activity and anemia. Notably, increasing dietary copper content to similar to 25-fold above requirements prevents the development of these physiological perturbations. Whether copper supplementation can reverse these high-iron-related abnormalities has, however, not been established. The current investigation was thus undertaken to test the hypothesis that supplemental copper will mitigate negative outcomes associated with dietary iron loading. Weanling mice were thus fed AIN-93G-based diets with high (>100-fold in excess) or adequate (similar to 80 ppm) iron content. To establish the optimal experimental conditions, we first defined the time course of iron loading, and assessed the impact of supplemental copper (provided in drinking water) on the development of high-iron-related pathologies. Copper supplementation (20 mg/L) for the last 3 weeks of a 7-week high-iron feeding period reversed the anemia, normalized serum copper levels and Cp activity, and restored tissue copper concentrations. Growth rates, cardiac copper concentrations and heart size, however, were only partially normalized by copper supplementation. Furthermore, high dietary iron intake reduced intestinal Cu-64 absorption (similar to 60%) from a transport solution provided to mice by oral, intragastric gavage. Copper supplementation of iron-loaded mice enhanced intestinal Cu-64 transport, thus allowing sufficient assimilation of dietary copper to correct many of the noted high-iron-related physiological perturbations. We therefore conclude that high- iron intake increases the requirement for dietary copper (to overcome the inhibition of intestinal copper absorption). (C) 2018 Elsevier Inc. All rights reserved.
dc.description.sponsorshipNational Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)United States Department of Health & Human ServicesNational Institutes of Health (NIH) - USANIH National Institute of Diabetes & Digestive & Kidney Diseases (NIDDK) [R01 DK074867]; NIDDKUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USANIH National Institute of Diabetes & Digestive & Kidney Diseases (NIDDK) [R01 DK109717]; Office of Dietary SupplementsUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USA; China Scholarship CouncilChina Scholarship Council [201506240036]; NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASESUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USANIH National Institute of Diabetes & Digestive & Kidney Diseases (NIDDK) [R01DK074867, R01DK109717] Funding Source: NIH RePORTER
dc.description.sponsorshipThis investigation was funded by grants R01 DK074867 from the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) and R01 DK109717 from NIDDK and the Office of Dietary Supplements (to JFC). T.W. was supported by an award from the China Scholarship Council (No. 201506240036).
dc.identifier.doi10.1016/j.jnutbio.2018.05.006
dc.identifier.endpage63
dc.identifier.issn0955-2863
dc.identifier.issn1873-4847
dc.identifier.pmid29960117
dc.identifier.scopus2-s2.0-85049091253
dc.identifier.scopusqualityQ1
dc.identifier.startpage56
dc.identifier.urihttps://doi.org/10.1016/j.jnutbio.2018.05.006
dc.identifier.urihttps://hdl.handle.net/20.500.11776/10674
dc.identifier.volume59
dc.identifier.wosWOS:000444664900007
dc.identifier.wosqualityQ1
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.institutionauthorDoğuer, Çağlar
dc.language.isoen
dc.publisherElsevier Science Inc
dc.relation.ispartofJournal of Nutritional Biochemistry
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectAnemia
dc.subjectCardiac hypertrophy
dc.subjectCeruloplasmin
dc.subjectIntestine
dc.subjectCopper absorption
dc.subjectDietary iron loading
dc.subjectPeroxidation In-Vivo
dc.subjectStable-Isotope Cu-65
dc.subjectYoung Men
dc.subjectDeficiency
dc.subjectRats
dc.subjectMetabolism
dc.subjectAbsorption
dc.subjectRetention
dc.subjectCells
dc.titleCopper supplementation reverses dietary iron overload-induced pathologies in mice
dc.typeArticle

Dosyalar

Orijinal paket
Listeleniyor 1 - 1 / 1
Küçük Resim
İsim:
10674.pdf
Boyut:
905.42 KB
Biçim:
Adobe Portable Document Format
Açıklama:
Tam Metin / Full Text
İndir

Koleksiyon

WoS İndeksli Yayınlar Koleksiyonu
PubMed İndeksli Yayın Koleksiyonu
Sağlık Yüksekokulu Koleksiyonu
Scopus İndeksli Yayınlar Koleksiyonu