Abstract

Organ copper is conserved in response to dietary copper restriction. In organs such as brain and heart, conservation is highly efficient, resulting in the loss of little organ copper. In contrast, conservation of copper in liver is induced only after a significant amount of organ copper is lost. Thus, the conservation of copper during dietary restriction is highly organ specific. Although the long-term pattern of organ copper conservation in rats has now been described through use of the continuous feeding of a single stable isotope, the mechanisms responsible for this conservation have not been identified or studied. These mechanisms may include copper-regulated changes in gene expression as well as other mechanisms. We now have the molecular tools that will permit the isolation of copper-regulated genes that may play a role in the conservation of organ copper. Identification of these mechanisms will allow the exploration of the effects of mild short-term and long-term copper deficiency and the role of copper in other physiologic and biochemical systems.

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