Author
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Reeves, Phillip |
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Submitted to: Federation of American Societies for Experimental Biology Conference
Publication Type: Abstract Only Publication Acceptance Date: 4/6/1997 Publication Date: N/A Citation: N/A Interpretive Summary: Technical Abstract: Feeding high-zinc diets to humans or animals lowers their copper (Cu) status. It is hypothesized that the mechanism involves the binding of Cu to zinc (Zn)-induced intestinal metallothionein (iMT), which in turn reduces Cu absorption. Previous studies in my laboratory, using normal rats, suggested that this hypothesis is not true. The recent development of a mouse without a functional MT gene offers an excellent model to test this hypothesis. Two groups of adult male mice, MT-null and control, were divided into two groups each and fed a diet (Reeves et al., Nutr. Res., 14: 897, 1994) with either 35 or 350 ug Zn/kg for eight weeks. Each diet contained only 1.5 ug Cu/kg. Plasma Zn concentrations were significantly lower in MT-null mice than controls regardless of dietary Zn concentration, but plasma Zn was elevated by the same degree in both types of mice as a result of consuming the high-Zn diet. Liver Zn also was lower r in MT-null mice than in controls, and was significantly elevated by high dietary Zn in MT-null mice but not in the controls. High-Zn significantly elevated iMT in the control mice, but as expected, not in the MT-null mice. Plasma Cu was the most sensitive indicator of Cu status, and was significantly lower in MT-null mice than in controls, and lower in those fed high-Zn than in those fed normal Zn, regardless of genotype. Plasma ceruloplasmin activity was not affected by high-Zn in the control mice, but was slightly but significantly depressed in the MT-null mice. This study suggests that the induction of intestinal MT by high dietary Zn is not responsible for low Cu status in this strain of mice. |
