Measuring intake of nutrients and their effects: the case of copper 127 5.9 Functional copper status The bodys total copper content is the end result of a balance achieved between absorption and biliary excretion. In comparison to other trace elements, relatively little copper is present in the body, usually about 100 mg. The largest tissue pool of copper is in the skeleton, followed by the muscle, however, the major site for storage of exchangeable copper is the liver, which contains 4-6ugg wet weight. This is followed by the brain, kidney and heart. Functional copper status, however, is not dependent only on the absolute copper content of the body. Utilisation of absorbed copper is also modulated by the interactions of copper with a number of other factors, deriving from the general status and requirements of the body. Furthermore, individual organs have the potential to modulate copper status by retaining copper in response to dietary restriction. This capacity is highly organ-specific, being stronger and/or more sen- sitive in some tissues than in others. Depletion studies in animals have found plasma to possess almost no copper conservation mechanisms, whereas and brain were shown to conserve most of their endogenous copper periods of restriction. Liver copper conservation mechanisms, while induced only after levels had dropped to around 60% of normal, were thereafter found to operate so strictly that almost no copper was exported into the plasma, and biliar copper excretion was also significantly reduced 5.10 Mechanisms of copper absorption Copper absorption in humans has been found to depend on a number of factors, of which the most important is probably dietary copper intake. The efficiency of copper absorption is regulated to maintain body copper status, with levels of uptake rising to 70% during periods of deficiency, and falling to 12% in high-copper diets. This modulation of absorption, which provides a means of dapting to changing dietary intake, appears to develop during childhood, wit copper absorption in infants operating at a lower level than in adults. While low level of copper absorption occurs in the stomach, the main site of absorption is the duodenum. Copper absorption from the gut lumen by enterocytes involves both passive and active carrier-mediated systems, which uptake copper across e brush-border, and transport it across the basolateral membrane into the Most of the copper in foods is found as a component of macromolecules In organic mineral salts are present in dietary supplements but otherwise probably do not contribute substantially to dietary copper intake. 6 In the UK only 1-2% of adults report taking supplements containing copper although in the US the figure may be as high as 15%.The sulphate, nitrate, chloride and acetate are easily absorbed, but copper oxide and copper porphyrin are unavailable. Gastric acid can solubilise the carbonate and facilitate the release of copper from5.9 Functional copper status The body’s total copper content is the end result of a balance achieved between absorption and biliary excretion. In comparison to other trace elements, relatively little copper is present in the body, usually about 100 mg. The largest tissue pool of copper is in the skeleton, followed by the muscle;60 however, the major site for storage of exchangeable copper is the liver,61 which contains 4–6mg/g wet weight.60 This is followed by the brain, kidney and heart. Functional copper status, however, is not dependent only on the absolute copper content of the body. Utilisation of absorbed copper is also modulated by the interactions of copper with a number of other factors, deriving from the general status and requirements of the body. Furthermore, individual organs have the potential to modulate copper status by retaining copper in response to dietary restriction. This capacity is highly organ-specific, being stronger and/or more sen￾sitive in some tissues than in others. Depletion studies in animals have found plasma to possess almost no copper conservation mechanisms, whereas the heart and brain were shown to conserve most of their endogenous copper during periods of restriction.62 Liver copper conservation mechanisms, while induced only after levels had dropped to around 60% of normal, were thereafter found to operate so strictly that almost no copper was exported into the plasma, and biliary copper excretion was also significantly reduced. 5.10 Mechanisms of copper absorption Copper absorption in humans has been found to depend on a number of factors, of which the most important is probably dietary copper intake.6 The efficiency of copper absorption is regulated to maintain body copper status, with levels of uptake rising to 70% during periods of deficiency,63 and falling to 12% in high-copper diets.61 This modulation of absorption, which provides a means of adapting to changing dietary intake, appears to develop during childhood, with copper absorption in infants operating at a lower level than in adults.38 While a low level of copper absorption occurs in the stomach, the main site of absorption is the duodenum. Copper absorption from the gut lumen by enterocytes involves both passive and active carrier-mediated systems, which uptake copper across the brush-border, and transport it across the basolateral membrane into the plasma. Most of the copper in foods is found as a component of macromolecules. In￾organic mineral salts are present in dietary supplements but otherwise probably do not contribute substantially to dietary copper intake.64 In the UK only 1–2% of adults report taking supplements containing copper65 although in the US the figure may be as high as 15%.17 The sulphate, nitrate, chloride and acetate are easily absorbed, but copper oxide and copper porphyrin are unavailable.63 Gastric acid can solubilise the carbonate and facilitate the release of copper from macromolecules.64 Measuring intake of nutrients and their effects: the case of copper 127