Myélopathie postérieure par carence en cuivre acquise

Videt-Gibou, Dorothée; Belliard, Serge; Rivalan, Joseph; Ménard, D.; Edan, Gilles

doi:10.1016/j.neurol.2009.10.017

Cited by 6 publications

(1 citation statement)

References 14 publications

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“…For example, high iron intake perturbed copper absorption in infants and adults (32). Also, iron overload was postulated to interfere with copper utilization in humans with aceruloplasminemia (caused by mutation of the Cp gene) (35), and in those with acquired copper-deficiency myelopathy (36). Cp, an established biomarker of copper status, was also decreased in individuals with the genetic iron-loading disorder hereditary hemochromatosis (37), supporting the postulate that high iron impairs copper metabolism.…”

Section: Discussionmentioning

confidence: 95%

Progressive Increases in Dietary Iron Are Associated with the Emergence of Pathologic Disturbances of Copper Homeostasis in Growing Rats

Doguer

Flores

et al. 2018

The Journal of Nutrition

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Increasing dietary iron intakes to ∼9.5-fold above dietary recommendations caused copper deficiency. Importantly, human iron supplementation is common, and recommended intakes for at-risk individuals may be ≤10-fold above the RDA. Whether these iron intakes perturb copper metabolism is worth considering, especially since copper defi-ciency can impair iron utilization (e.g., by decreasing the ferroxidase activity of ceruloplasmin).

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Section: Discussionmentioning

confidence: 95%

Progressive Increases in Dietary Iron Are Associated with the Emergence of Pathologic Disturbances of Copper Homeostasis in Growing Rats

Doguer

Flores

et al. 2018

The Journal of Nutrition

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Intersection of Iron and Copper Metabolism in the Mammalian Intestine and Liver

Doguer

Collins

2018

Comprehensive Physiology

121

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Iron and copper have similar physiochemical properties; thus, physiologically relevant interactions seem likely. Indeed, points of intersection between these two essential trace minerals have been recognized for many decades, but mechanistic details have been lacking. Investigations in recent years have revealed that copper may positively influence iron homeostasis, and also that iron may antagonize copper metabolism. For example, when body iron stores are low, copper is apparently redistributed to tissues important for regulating iron balance, including enterocytes of upper small bowel, the liver, and blood. Copper in enterocytes may positively influence iron transport, and hepatic copper may enhance biosynthesis of a circulating ferroxidase, ceruloplasmin, which potentiates iron release from stores. Moreover, many intestinal genes related to iron absorption are transactivated by a hypoxia-inducible transcription factor, hypoxia-inducible factor-2α (HIF2α), during iron deficiency. Interestingly, copper influences the DNA-binding activity of the HIF factors, thus further exemplifying how copper may modulate intestinal iron homeostasis. Copper may also alter the activity of the iron-regulatory hormone hepcidin. Furthermore, copper depletion has been noted in iron-loading disorders, such as hereditary hemochromatosis. Copper depletion may also be caused by high-dose iron supplementation, raising concerns particularly in pregnancy when iron supplementation is widely recommended. This review will cover the basic physiology of intestinal iron and copper absorption as well as the metabolism of these minerals in the liver. Also considered in detail will be current experimental work in this field, with a focus on molecular aspects of intestinal and hepatic iron-copper interplay and how this relates to various disease states. © 2018 American Physiological Society. Compr Physiol 8:1433-1461, 2018.

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Copper

Collins

2020

Present Knowledge in Nutrition

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Myélopathie postérieure par carence en cuivre acquise

Cited by 6 publications

References 14 publications

Progressive Increases in Dietary Iron Are Associated with the Emergence of Pathologic Disturbances of Copper Homeostasis in Growing Rats

Progressive Increases in Dietary Iron Are Associated with the Emergence of Pathologic Disturbances of Copper Homeostasis in Growing Rats

Intersection of Iron and Copper Metabolism in the Mammalian Intestine and Liver

Copper

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