Abstract
Intensive research over the past several years has demonstrated (or predicted) that pathological perturbations in copper homeostasis may contribute to the development of ischemic heart disease and neurodegenerative and connective tissue disorders in humans. Copper was also shown to facilitate the host response to bacterial infection. Emerging evidence links copper to common lipid-related pathologies such as nonalcoholic fatty liver disease. Also, research on copper chaperones continues to reveal novel roles for these intracellular proteins. Despite these major achievements, important issues remain unresolved. Sensitive and specific copper nutrition–related biomarkers need to be identified, to accelerate research on copper metabolism in humans. Moreover, recent experimental evidence suggests that frank copper deficiency in the United States is more common than traditionally thought and that the copper RDA for adults should be increased. These and other unresolved issues related to copper nutrition will undoubtedly be a focus for future investigation.
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