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Biochemical and Molecular Actions of Nutrients

Ferroportin-1 Is Not Upregulated in Copper-Deficient Mice¹

Department of Nutrition, Harvard School of Public Health, Boston, MA 02115 and ^* Department of Biochemistry and Molecular Biology, University of Minnesota, Duluth, MN 55812

²To whom correspondence should be addressed. E-mail: wessling{at}hsph.harvard.edu.

Body iron status regulates ferroportin-1 (FPN1) expression such that intestinal mRNA levels are enhanced by anemia, whereas liver transcripts are increased by iron overload. In vitro evidence suggests that copper also upregulates FPN1. To investigate whether copper deficiency affects FPN1 expression in vivo, starting at gestation d 17, pregnant mice were fed a modified AIN-76A diet low in copper (-Cu). Half of the mice were given copper in drinking water (+Cu). At 28 d, -Cu pups had significantly lower copper concentrations in duodenum, liver, and kidney (63, 50, and 27%, P < 0.01) and >95% loss of ceruloplasmin activity. -Cu mice also had reduced hemoglobin (81.8 vs. 124.4 g/L in +Cu mice) and hematocrits (0.35 vs. 0.46 in +Cu mice), and displayed hepatic iron-loading (2- to 3-fold relative to +Cu mice). Despite these changes in copper and iron status, FPN1 mRNA levels were not altered significantly in duodenum, liver, kidney, and spleen. Moreover, FPN1 protein levels were not altered in liver tissue from -Cu mice, despite hepatic iron-loading. These data indicate that tissue copper deficiency does not alter FPN1 expression but that copper adequacy may be required for appropriate regulation of FPN1 by iron status.

KEY WORDS: • copper deficiency • ferroportin-1 • iron export

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