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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

1,25-dihydroxycholecalciferol supplementation prevents hypocalcemia in magnesium-deficient chicks.

To determine the relevance of circulating 1,25-dihydroxycholecalciferol [1,25(OH)2D3] to the pathogenesis of hypocalcemia during magnesium deficiency, growing chicks were pair fed control or Mg-deficient diets with or without 1,25(OH)2D3 supplementation. Within 14 d, chicks fed the Mg-deficient diet without 1,25(OH)2D3 supplementation exhibited hypomagnesemia and hypocalcemia compared to control chicks. 1,25-Dihydroxycholecalciferol supplementation in Mg-deficient chicks elevated plasma 1,25(OH)2D3 twofold and increased plasma calcium to control levels. Supplementation with 1,25(OH)2D3 did not increase plasma Mg concentration in Mg-deficient chicks, indicating that exogenous 1,25(OH)2D3 prevented hypocalcemia in the absence of greater Mg availability. Magnesium-deficient chicks supplemented with 1,25(OH)2D3 had more intestinal calbindin D-28K relative to Mg-deficient nonsupplemented chicks, suggesting that increased absorption of dietary Ca may have contributed to the greater plasma Ca concentration in 1,25(OH)2D3 supplemented Mg-deficient chicks. Although clinical hypomagnesemia has been associated with vitamin D resistance, our data indicate that primary Mg deficiency did not impair target tissue responsiveness to 1,25(OH)2D3, at least at the level of the intestine. Supplementation with 1,25(OH)2D3 did not increase bone Mg concentration and did not alter the characteristic skeletal morphology. It also did not increase bone Ca concentration in Mg-deficient chicks. The data suggest that skeletal alterations during Mg deficiency result from hypomagnesemia per se, rather than hypocalcemia or insufficient 1,25(OH)2D3.[1]


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