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Submitted to: Biological Trace Element Research
Publication Type: Peer Reviewed Journal Publication Acceptance Date: 10/21/2008 Publication Date: 6/1/2009 Citation: Nielsen, F.H. 2009. Marginal Zinc Deficiency Increases Magnesium Retention and Impairs Calcium Utilization in Rats. Biological Trace Element Research. 128(3):220-231. Interpretive Summary: Animal studies show that a severe zinc-deficiency induces changes that adversely affect bone health, immune function, and the inflammatory response. Zinc supplementation studies with humans also indicate that a low zinc status impairs immune function and the inflammatory response. Evidence that a marginal or sub-clinical zinc deficiency induces biochemical changes to produce similar effects is lacking. Increased oxidative stress, which increases inflammatory stress, and altered magnesium and/or calcium metabolism, which regulate the inflammatory response, were hypothesized as mechanisms through which a marginal zinc deficiency would impair immune function and the inflammatory response and adversely affect bone health. Thus, an experiment with rats was conducted to determine whether magnesium retention is increased and calcium utilization is altered by, and whether increased oxidative stress induced by a marginal copper deficiency exacerbated responses to, a marginal zinc deficiency. Marginal zinc deficiency significantly decreased the urinary excretion of magnesium and calcium, increased the concentrations of magnesium and calcium in bone, increased the concentration of magnesium in kidney, and increased the urinary excretion of helical peptide (bone breakdown product). Marginal copper deficiency induced signs of increased oxidative stress but did not significantly change the response to marginal zinc deficiency. The findings indicate that marginal zinc deficiency may adversely affect bone health, immune function and the inflammatory response through increasing magnesium retention and impaired calcium utilization. These changes might be the result of an abnormal cellular uptake of magnesium and calcium because of a defect in membrane function. Technical Abstract: An experiment with rats was conducted to determine whether magnesium retention is increased and calcium utilization is altered by, and whether increased oxidative stress induced by a marginal copper deficiency exacerbated responses to, a marginal zinc deficiency. Weanling rats were assigned to six groups of 10 with dietary treatment variables of low zinc (5 mg/kg for 2 weeks and 8 mg/kg for 7 weeks), low copper (1.5 mg/kg), adequate zinc (15 mg/kg), and adequate copper (6 mg/kg). Two groups of rats were fed the adequate zinc diet with low or adequate copper and pair-fed with corresponding rats fed the low zinc diet. When compared to the pair-fed rats, marginal zinc deficiency significantly decreased the urinary excretion of magnesium and calcium, increased concentrations of magnesium and calcium in tibia, increased the concentration of magnesium in kidney, and increased the urinary excretion of helical peptide (bone breakdown product). Marginal copper deficiency decreased extracellular superoxide dismutase and glutathione, which suggests increased oxidative stress. None of the variables responding to the marginal zinc deficiency were significantly altered by the marginal copper deficiency. Findings in the present experiment suggest that increased magnesium retention and impaired calcium utilization are indicators of marginal zinc deficiency. |
