{"id":1055,"date":"2017-10-27T16:47:06","date_gmt":"2017-10-27T16:47:06","guid":{"rendered":"https:\/\/courses.lumenlearning.com\/suny-nutrition\/?post_type=chapter&#038;p=1055"},"modified":"2017-11-02T13:18:21","modified_gmt":"2017-11-02T13:18:21","slug":"12-93-how-high-zinc-intake-can-lead-to-copper-iron-deficiencies","status":"publish","type":"chapter","link":"https:\/\/courses.lumenlearning.com\/suny-nutrition\/chapter\/12-93-how-high-zinc-intake-can-lead-to-copper-iron-deficiencies\/","title":{"raw":"12.93 How High Zinc Intake Can Lead to Copper &amp; Iron Deficiencies","rendered":"12.93 How High Zinc Intake Can Lead to Copper &amp; Iron Deficiencies"},"content":{"raw":"<div class=\"__UNKNOWN__\">\r\n\r\nAs you learned previously, thionein is the storage protein for zinc, but it more avidly binds copper. When it binds a mineral, it becomes metallothionein. High zinc intake results in increased thionein synthesis in the enterocyte. Thus, when an individual is consuming high zinc levels, the enterocyte will have high levels of thionein as shown below.\r\n\r\n\r\n\r\n\r\n<div>\r\n\r\n[caption id=\"\" align=\"aligncenter\" width=\"924\"]<img src=\"https:\/\/s3-us-west-2.amazonaws.com\/courses-images\/wp-content\/uploads\/sites\/2569\/2017\/10\/27164517\/100000000000039C0000022A64CFC5B3.png\" alt=\"\" width=\"924\" height=\"554\" \/> Figure 12.931 Zinc increases thionein production[\/caption]\r\n\r\n<\/div>\r\n\r\n\r\n\r\n\r\nThe high levels of thionein will bind any copper that is taken up into the enterocyte (as metallothionein), \"trapping\" the copper in the enterocyte and preventing it from being absorbed into circulation, as shown below.\r\n\r\n\r\n\r\n\r\n<div>\r\n\r\n[caption id=\"\" align=\"aligncenter\" width=\"1055\"]<img src=\"https:\/\/s3-us-west-2.amazonaws.com\/courses-images\/wp-content\/uploads\/sites\/2569\/2017\/10\/27164519\/100000000000041F0000029CF120E00B.png\" alt=\"\" width=\"1055\" height=\"668\" \/> Figure 12.932 Copper taken up into the enterocyte is bound to thionein forming metallothionein.[\/caption]\r\n\r\n<\/div>\r\n\r\n\r\n\r\n\r\nThe enterocytes containing the \"trapped\" copper move up the crypt and are sloughed off and excreted in feces. The copper consumed essentially is lost from the body through this process.\r\n\r\n\r\n\r\n\r\n<div>\r\n\r\n[caption id=\"\" align=\"aligncenter\" width=\"818\"]<img src=\"https:\/\/s3-us-west-2.amazonaws.com\/courses-images\/wp-content\/uploads\/sites\/2569\/2017\/10\/27164521\/1000000000000332000001731A5246AC.png\" alt=\"\" width=\"818\" height=\"371\" \/> Figure 12.933 Enterocytes are sloughed off and excreted in feces[\/caption]\r\n\r\n<\/div>\r\n\r\n\r\n\r\n\r\nWithout adequate copper being transported to the liver, no ceruloplasmin is produced and released into circulation.\u00a0The lack of copper further influences iron transport by decreasing ceruloplasmin in circulation and hephaestin (another copper-containing protein) on the membrane of the enterocyte. These 2 proteins normally convert Fe2+ to Fe3+ so that iron can bind to transferrin.\r\n\r\n\r\n\r\n\r\n<div>\r\n\r\n[caption id=\"\" align=\"aligncenter\" width=\"981\"]<img src=\"https:\/\/s3-us-west-2.amazonaws.com\/courses-images\/wp-content\/uploads\/sites\/2569\/2017\/10\/27164524\/10000000000003D500000235A58EE7CE.png\" alt=\"\" width=\"981\" height=\"565\" \/> Figure 12.934 Lack of copper means that hephaestin and ceruloplasmin aren't available to oxidize Fe2+ to Fe3+[\/caption]\r\n\r\n<\/div>\r\n\r\n\r\n\r\n\r\nWithout hephaestin and ceruloplasmin, Fe3+ is not formed from Fe2+.\u00a0As a result Fe2+ is \"trapped\" in the enterocyte because it can't bind to transferrin as shown below.\r\n\r\n\r\n\r\n\r\n<div>\r\n\r\n[caption id=\"\" align=\"aligncenter\" width=\"1118\"]<img src=\"https:\/\/s3-us-west-2.amazonaws.com\/courses-images\/wp-content\/uploads\/sites\/2569\/2017\/10\/27164526\/100000000000045E000002BEFEE5ABE6.png\" alt=\"\" width=\"1118\" height=\"702\" \/> Figure 12.935 Fe2+ is trapped in the enterocyte[\/caption]\r\n\r\n<\/div>\r\n\r\n\r\n\r\n\r\nThe enterocytes containing the \"trapped\" iron move up the crypt and are also sloughed off and excreted in feces. The iron consumed essentially is lost from the body through this process.\r\n\r\n\r\n\r\n\r\n<div>\r\n\r\n[caption id=\"\" align=\"aligncenter\" width=\"818\"]<img src=\"https:\/\/s3-us-west-2.amazonaws.com\/courses-images\/wp-content\/uploads\/sites\/2569\/2017\/10\/27164521\/1000000000000332000001731A5246AC.png\" alt=\"\" width=\"818\" height=\"371\" \/> Figure 12.936\u00a0Enterocytes are sloughed off and excreted in feces[\/caption]\r\n\r\n<\/div>\r\n\r\n\r\n\r\n\r\nIn summary, high zinc intake increases thionein production, which traps all copper; the lack of copper decreases circulating ceruloplasmin and hephaestin, which causes all iron to be trapped as well. This example illustrates the interconnectedness of zinc, copper, and iron.\r\n\r\n\r\n\r\n<h3>No References<\/h3>\r\n\r\n<\/div>","rendered":"<div class=\"__UNKNOWN__\">\n<p>As you learned previously, thionein is the storage protein for zinc, but it more avidly binds copper. When it binds a mineral, it becomes metallothionein. High zinc intake results in increased thionein synthesis in the enterocyte. Thus, when an individual is consuming high zinc levels, the enterocyte will have high levels of thionein as shown below.<\/p>\n<div>\n<div style=\"width: 934px\" class=\"wp-caption aligncenter\"><img loading=\"lazy\" decoding=\"async\" src=\"https:\/\/s3-us-west-2.amazonaws.com\/courses-images\/wp-content\/uploads\/sites\/2569\/2017\/10\/27164517\/100000000000039C0000022A64CFC5B3.png\" alt=\"\" width=\"924\" height=\"554\" \/><\/p>\n<p class=\"wp-caption-text\">Figure 12.931 Zinc increases thionein production<\/p>\n<\/div>\n<\/div>\n<p>The high levels of thionein will bind any copper that is taken up into the enterocyte (as metallothionein), &#8220;trapping&#8221; the copper in the enterocyte and preventing it from being absorbed into circulation, as shown below.<\/p>\n<div>\n<div style=\"width: 1065px\" class=\"wp-caption aligncenter\"><img loading=\"lazy\" decoding=\"async\" src=\"https:\/\/s3-us-west-2.amazonaws.com\/courses-images\/wp-content\/uploads\/sites\/2569\/2017\/10\/27164519\/100000000000041F0000029CF120E00B.png\" alt=\"\" width=\"1055\" height=\"668\" \/><\/p>\n<p class=\"wp-caption-text\">Figure 12.932 Copper taken up into the enterocyte is bound to thionein forming metallothionein.<\/p>\n<\/div>\n<\/div>\n<p>The enterocytes containing the &#8220;trapped&#8221; copper move up the crypt and are sloughed off and excreted in feces. The copper consumed essentially is lost from the body through this process.<\/p>\n<div>\n<div style=\"width: 828px\" class=\"wp-caption aligncenter\"><img loading=\"lazy\" decoding=\"async\" src=\"https:\/\/s3-us-west-2.amazonaws.com\/courses-images\/wp-content\/uploads\/sites\/2569\/2017\/10\/27164521\/1000000000000332000001731A5246AC.png\" alt=\"\" width=\"818\" height=\"371\" \/><\/p>\n<p class=\"wp-caption-text\">Figure 12.933 Enterocytes are sloughed off and excreted in feces<\/p>\n<\/div>\n<\/div>\n<p>Without adequate copper being transported to the liver, no ceruloplasmin is produced and released into circulation.\u00a0The lack of copper further influences iron transport by decreasing ceruloplasmin in circulation and hephaestin (another copper-containing protein) on the membrane of the enterocyte. These 2 proteins normally convert Fe2+ to Fe3+ so that iron can bind to transferrin.<\/p>\n<div>\n<div style=\"width: 991px\" class=\"wp-caption aligncenter\"><img loading=\"lazy\" decoding=\"async\" src=\"https:\/\/s3-us-west-2.amazonaws.com\/courses-images\/wp-content\/uploads\/sites\/2569\/2017\/10\/27164524\/10000000000003D500000235A58EE7CE.png\" alt=\"\" width=\"981\" height=\"565\" \/><\/p>\n<p class=\"wp-caption-text\">Figure 12.934 Lack of copper means that hephaestin and ceruloplasmin aren&#8217;t available to oxidize Fe2+ to Fe3+<\/p>\n<\/div>\n<\/div>\n<p>Without hephaestin and ceruloplasmin, Fe3+ is not formed from Fe2+.\u00a0As a result Fe2+ is &#8220;trapped&#8221; in the enterocyte because it can&#8217;t bind to transferrin as shown below.<\/p>\n<div>\n<div style=\"width: 1128px\" class=\"wp-caption aligncenter\"><img loading=\"lazy\" decoding=\"async\" src=\"https:\/\/s3-us-west-2.amazonaws.com\/courses-images\/wp-content\/uploads\/sites\/2569\/2017\/10\/27164526\/100000000000045E000002BEFEE5ABE6.png\" alt=\"\" width=\"1118\" height=\"702\" \/><\/p>\n<p class=\"wp-caption-text\">Figure 12.935 Fe2+ is trapped in the enterocyte<\/p>\n<\/div>\n<\/div>\n<p>The enterocytes containing the &#8220;trapped&#8221; iron move up the crypt and are also sloughed off and excreted in feces. The iron consumed essentially is lost from the body through this process.<\/p>\n<div>\n<div style=\"width: 828px\" class=\"wp-caption aligncenter\"><img loading=\"lazy\" decoding=\"async\" src=\"https:\/\/s3-us-west-2.amazonaws.com\/courses-images\/wp-content\/uploads\/sites\/2569\/2017\/10\/27164521\/1000000000000332000001731A5246AC.png\" alt=\"\" width=\"818\" height=\"371\" \/><\/p>\n<p class=\"wp-caption-text\">Figure 12.936\u00a0Enterocytes are sloughed off and excreted in feces<\/p>\n<\/div>\n<\/div>\n<p>In summary, high zinc intake increases thionein production, which traps all copper; the lack of copper decreases circulating ceruloplasmin and hephaestin, which causes all iron to be trapped as well. This example illustrates the interconnectedness of zinc, copper, and iron.<\/p>\n<h3>No References<\/h3>\n<\/div>\n\n\t\t\t <section class=\"citations-section\" role=\"contentinfo\">\n\t\t\t <h3>Candela Citations<\/h3>\n\t\t\t\t\t <div>\n\t\t\t\t\t\t <div id=\"citation-list-1055\">\n\t\t\t\t\t\t\t <div class=\"licensing\"><div class=\"license-attribution-dropdown-subheading\">CC licensed content, Shared previously<\/div><ul class=\"citation-list\"><li>Kansas State University Human Nutrition Flexbook. <strong>Authored by<\/strong>: Brian Lindshield. <strong>Provided by<\/strong>: Kansas State University. <strong>Located at<\/strong>: <a target=\"_blank\" href=\"http:\/\/goo.gl\/vOAnR\">http:\/\/goo.gl\/vOAnR<\/a>. <strong>License<\/strong>: <em><a target=\"_blank\" rel=\"license\" href=\"https:\/\/creativecommons.org\/licenses\/by\/4.0\/\">CC BY: Attribution<\/a><\/em><\/li><\/ul><\/div>\n\t\t\t\t\t\t <\/div>\n\t\t\t\t\t <\/div>\n\t\t\t <\/section>","protected":false},"author":311,"menu_order":37,"template":"","meta":{"_candela_citation":"[{\"type\":\"cc\",\"description\":\"Kansas State University Human Nutrition Flexbook\",\"author\":\"Brian Lindshield\",\"organization\":\"Kansas State University\",\"url\":\"goo.gl\/vOAnR\",\"project\":\"\",\"license\":\"cc-by\",\"license_terms\":\"\"}]","CANDELA_OUTCOMES_GUID":"","pb_show_title":"on","pb_short_title":"","pb_subtitle":"","pb_authors":[],"pb_section_license":""},"chapter-type":[],"contributor":[],"license":[],"class_list":["post-1055","chapter","type-chapter","status-publish","hentry"],"part":883,"_links":{"self":[{"href":"https:\/\/courses.lumenlearning.com\/suny-nutrition\/wp-json\/pressbooks\/v2\/chapters\/1055","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/courses.lumenlearning.com\/suny-nutrition\/wp-json\/pressbooks\/v2\/chapters"}],"about":[{"href":"https:\/\/courses.lumenlearning.com\/suny-nutrition\/wp-json\/wp\/v2\/types\/chapter"}],"author":[{"embeddable":true,"href":"https:\/\/courses.lumenlearning.com\/suny-nutrition\/wp-json\/wp\/v2\/users\/311"}],"version-history":[{"count":3,"href":"https:\/\/courses.lumenlearning.com\/suny-nutrition\/wp-json\/pressbooks\/v2\/chapters\/1055\/revisions"}],"predecessor-version":[{"id":1448,"href":"https:\/\/courses.lumenlearning.com\/suny-nutrition\/wp-json\/pressbooks\/v2\/chapters\/1055\/revisions\/1448"}],"part":[{"href":"https:\/\/courses.lumenlearning.com\/suny-nutrition\/wp-json\/pressbooks\/v2\/parts\/883"}],"metadata":[{"href":"https:\/\/courses.lumenlearning.com\/suny-nutrition\/wp-json\/pressbooks\/v2\/chapters\/1055\/metadata\/"}],"wp:attachment":[{"href":"https:\/\/courses.lumenlearning.com\/suny-nutrition\/wp-json\/wp\/v2\/media?parent=1055"}],"wp:term":[{"taxonomy":"chapter-type","embeddable":true,"href":"https:\/\/courses.lumenlearning.com\/suny-nutrition\/wp-json\/pressbooks\/v2\/chapter-type?post=1055"},{"taxonomy":"contributor","embeddable":true,"href":"https:\/\/courses.lumenlearning.com\/suny-nutrition\/wp-json\/wp\/v2\/contributor?post=1055"},{"taxonomy":"license","embeddable":true,"href":"https:\/\/courses.lumenlearning.com\/suny-nutrition\/wp-json\/wp\/v2\/license?post=1055"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}