The Role of Copper as a Modifier of Lipid Metabolism

Abstract

Copper homeostasis in mammals Dietary copper enters the body largely through the small intestine. Two membrane transporters are essential for this process. The high affinity copper uptake protein Ctr1 is responsible for making copper that enters via the apical membrane available in the cytosol for further utilization [1], whereas the copper-transporting ATPase ATP7A facilitates copper exit from the enterocytes into circulation [2] (Figure 1). Complete genetic inactivation of either transporter in experimental animals is embryonically lethal [3-5]. However, partial inactivation or tissue specific inactivation of ATP7A or Ctr1, respectively, in either case is associated with copper accumulation in the intestine, impaired copper entry into the bloodstream, and severe copper deficiency in many organs and tissues [1]. Copper deficiency, in turn, produces distinct metabolic changes that are discussed in detail in the following sections.