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Hyperphosphatemia, hypocalcemia and increased serum potassium concentration as distinctive features of early hypomagnesemia in magnesium-deprived mice Volume 28, issue 4, December 2015

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Authors
Department of Biology, The College at Brockport, State University of New York, 350 New Campus Drive, Brockport, NY 14420, USA
* Correspondence. Bernardo Ortega, Ph.D., Department of Biology, The College at Brockport, State University of New York, 350 New Campus Drive, Brockport, NY 14420-2973, USA

Magnesium-deficient patients show dysfunctional calcium (Ca2+) metabolism due to defective parathyroid hormone (PTH) secretion. In mice and rats, long-term magnesium (Mg2+) deprivation causes hyperphosphaturia and increases fibroblast growth factor 23 (FGF23) secretion, despite normal serum phosphate (Pi) and Ca2+. Electrolyte disturbances during early hypomagnesemia may explain the response of mice to long-term Mg2+ deprivation, but our knowledge of electrolyte homeostasis during this stage is limited. This study compares the effect of both short- and long-term Mg2+ restriction on the electrolyte balance in mice. Mice were fed control or Mg2+-deficient diets for one to three days, one week, or three weeks. Prior to killing the mice, urine was collected over 24 h using metabolic cages. Within 24 h of Mg2+ deprivation, hypomagnesemia, hypocalcemia and hyperphosphatemia developed, and after three days of Mg2+ deprivation, serum potassium (K+) was increased. These changes were accompanied by a reduction in urinary volume, hyperphosphaturia, hypocalciuria and decreased Mg2+, sodium (Na+) and K+ excretion. Surprisingly, after one week of Mg2+ deprivation, serum K+, Pi and Ca2+ had normalized, showing that mineral homeostasis is most affected during early hypomagnesemia. Serum Pi and K+ are known to stimulate secretion of FGF23 and aldosterone, which are usually elevated during Mg2+ deficiency. Thus, the hyperphosphatemia and increased serum K+ concentration observed during short-term Mg2+ deprivation may help our understanding of adaptation to chronic Mg2+ deficiency.