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Copper deficiency increases iron absorption in the rat.
Am J Physiol Gastrointest Liver Physiol. 2003 Nov; 285(5):G789-95.AJ

Abstract

Release of iron from enterocytes and hepatocytes is thought to require the copper-dependent ferroxidase activity of hephaestin (Hp) and ceruloplasmin (Cp), respectively. In swine, copper deficiency (CD) impairs iron absorption, but whether this occurs in rats is unclear. By feeding a diet deficient in copper, CD was produced, as evidenced by the loss of copper-dependent plasma ferroxidase I activity, and in enterocytes, CD reduced copper levels and copper-dependent oxidase activity. Hematocrit was reduced, and liver iron was doubled. CD reduced duodenal mucosal iron and ferritin, whereas CD increased iron absorption. Duodenal mucosal DMT1-IRE and ferroportin1 expression remained constant with CD. When absorption in CD rats was compared with that seen normally and in iron-deficient anemic animals, strong correlations were found among mucosal iron, ferritin, and iron absorption, suggesting that the level of iron absorption was appropriate given that the erythroid and stores stimulators of iron absorption are opposed in CD. Because CD reduced the activity of Cp, as evidenced by copper-dependent plasma ferroxidase I activity and hepatocyte iron accumulation, but iron absorption increased, it is unlikely that the ferroxidase activity of Hp is important and suggests another function for this protein in the export of iron from the enterocyte during iron absorption. Also, the copper-dependent ferroxidase activity of Cp does not appear important for iron efflux from macrophages, because Kupffer cells of the liver and nonheme iron levels of the spleen were normal during copper deficiency, suggesting another role for Cp in these cells.

Authors+Show Affiliations

Physiology School of Biomedical and Chemical Sciences, Univ. Of Western Australia, Crawley, 6009, Australia.No affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

12760904

Citation

Thomas, Carla, and Phillip S. Oates. "Copper Deficiency Increases Iron Absorption in the Rat." American Journal of Physiology. Gastrointestinal and Liver Physiology, vol. 285, no. 5, 2003, pp. G789-95.
Thomas C, Oates PS. Copper deficiency increases iron absorption in the rat. Am J Physiol Gastrointest Liver Physiol. 2003;285(5):G789-95.
Thomas, C., & Oates, P. S. (2003). Copper deficiency increases iron absorption in the rat. American Journal of Physiology. Gastrointestinal and Liver Physiology, 285(5), G789-95.
Thomas C, Oates PS. Copper Deficiency Increases Iron Absorption in the Rat. Am J Physiol Gastrointest Liver Physiol. 2003;285(5):G789-95. PubMed PMID: 12760904.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Copper deficiency increases iron absorption in the rat. AU - Thomas,Carla, AU - Oates,Phillip S, Y1 - 2003/05/21/ PY - 2003/5/23/pubmed PY - 2003/12/3/medline PY - 2003/5/23/entrez SP - G789 EP - 95 JF - American journal of physiology. Gastrointestinal and liver physiology JO - Am J Physiol Gastrointest Liver Physiol VL - 285 IS - 5 N2 - Release of iron from enterocytes and hepatocytes is thought to require the copper-dependent ferroxidase activity of hephaestin (Hp) and ceruloplasmin (Cp), respectively. In swine, copper deficiency (CD) impairs iron absorption, but whether this occurs in rats is unclear. By feeding a diet deficient in copper, CD was produced, as evidenced by the loss of copper-dependent plasma ferroxidase I activity, and in enterocytes, CD reduced copper levels and copper-dependent oxidase activity. Hematocrit was reduced, and liver iron was doubled. CD reduced duodenal mucosal iron and ferritin, whereas CD increased iron absorption. Duodenal mucosal DMT1-IRE and ferroportin1 expression remained constant with CD. When absorption in CD rats was compared with that seen normally and in iron-deficient anemic animals, strong correlations were found among mucosal iron, ferritin, and iron absorption, suggesting that the level of iron absorption was appropriate given that the erythroid and stores stimulators of iron absorption are opposed in CD. Because CD reduced the activity of Cp, as evidenced by copper-dependent plasma ferroxidase I activity and hepatocyte iron accumulation, but iron absorption increased, it is unlikely that the ferroxidase activity of Hp is important and suggests another function for this protein in the export of iron from the enterocyte during iron absorption. Also, the copper-dependent ferroxidase activity of Cp does not appear important for iron efflux from macrophages, because Kupffer cells of the liver and nonheme iron levels of the spleen were normal during copper deficiency, suggesting another role for Cp in these cells. SN - 0193-1857 UR - https://www.unboundmedicine.com/medline/citation/12760904/Copper_deficiency_increases_iron_absorption_in_the_rat_ L2 - https://journals.physiology.org/doi/10.1152/ajpgi.00509.2002?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -