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Title: ESSENTIALITY OF COPPER, ZINC, MAGNESIUM, BORON AND SILICON IN BONE DEVELOPMENT AND FUNCTION

Author

Submitted to: International Society For Trace Elements Research In Humans
Publication Type: Abstract Only
Publication Acceptance Date: May 31, 2004
Publication Date: December 1, 2004
Citation: Nielsen, F.H. 2004. Essentiality of copper, zinc, magnesium, boron and silicon in bone development and function [abstract]. The Journal of Trace Elements in Experimental Medicine. 17(4):263-4.

Technical Abstract: Among the nutritional factors that affect bone development and function are copper (Cu), zinc (Zn), magnesium (Mg), boron (B) and silicon (Si); this is confirmed by findings obtained in my laboratory. B deprivation (0.07 mg/kg diet) decreased femur strength in rats with the effect most marked in females fed a diet high in polyunsaturated fatty acids. B deprivation also altered femur shape and decreased tibia calcium (Ca) and phosphorus concentrations. B apparently has a function that affects bone development and is influenced by the fatty acid composition of the diet. Si deprivation (2 mg/kg diet) decreased plasma osteopontin, increased urinary helical peptide excretion, and altered femur shape in rats. Si deprivation did not affect femur Ca concentration, but decreased potassium and Zn, minerals associated with the organic matrix. Si may have a function that affects bone growth prior to bone crystal formation. In humans, a combination of low dietary Zn and Cu, or low dietary Zn alone, may be factors affecting bone health. In post menopausal women fed low Cu (1 mg/d), plasma osteocalcin was higher when dietary Zn was low (3 mg/day) than when it was high (53 mg/day). Regardless whether dietary Cu was low or luxuriant (3 mg/d), high compared to low dietary Zn increased the urinary excretion of N-telopeptides and decreased serum calcitonin. Mg deprivation (118 mg/d) decreased urinary Ca excretion, and increased Ca balance and intracellular Ca in postmenopausal women. Mg deprivation may affect bone health through changing cellular Ca such that inflammatory or oxidative processes result.

   
 
 
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