New developments in the regulation of intestinal copper absorption.
The transition metal copper is an essential trace element involved in many enzymatic processes that require redox-chemistry. The redox-activity of copper is potentially harmful. Severe imbalance of copper homeostasis can occur with some hereditary disorders of copper metabolism. Copper is acquired from the diet by intestinal absorption and is subsequently distributed throughout the body. The regulation of intestinal copper absorption to maintain whole-body copper homeostasis is currently poorly understood. This review evaluates novel findings regarding the molecular mechanism of intestinal copper uptake. The role of recently identified transporters in enterocyte copper uptake and excretion into the portal circulation is described, and the regulation of dietary copper uptake during physiological and pathophysiological conditions is discussed.
van den Berghe
Peter V  E
PV
Department of Metabolic and Endocrine Diseases, University Medical Center Utrecht, 3584 EA Utrecht, The Netherlands.
Klomp
Leo W J
LW
D001692:Biological Transport; D002570:Ceruloplasmin / Q000378:metabolism; D003300:Copper / Q000172:deficiency / Q000378:metabolism / Q000493:pharmacokinetics*; D020895:Enterocytes / Q000502:physiology*; D006527:Hepatolenticular Degeneration / Q000235:genetics; D006706:Homeostasis; D006801:Humans; D007408:Intestinal Absorption / Q000187:drug effects*; D007706:Menkes Kinky Hair Syndrome / Q000235:genetics; D008668:Metallothionein / Q000378:metabolism; D010084:Oxidation-Reduction; D014131:Trace Elements / Q000493:pharmacokinetics*
D014131:Trace Elements; D003300:Copper; D008668:Metallothionein; D002570:Ceruloplasmin