Studies were carried out to evaluate the mechanism of
hypocalcemia in
magnesium depletion. Day old chicks fed a
magnesium deficient diet developed marked
hypocalcemia, with a direct relation between serum
calcium (y) and
magnesium (x): y = 2.68 x + 4.24, r = 0.84 (both in mg/100 ml).
Injections of parathyroid extract that increased serum
calcium 2-3 mg/100 ml in normals had no effect in Mg-depleted birds. Very large dietary supplements of
calcium or
vitamin D(3) increased mean serum
calcium only from 5.3 to 7.7 and 7.8 mg/100 ml, respectively, while a normal
magnesium diet for 3 days increased
calcium from 5.3 to 9.9 mg/100 ml despite absence of
dietary calcium. Intestinal
calcium transport, studied in vitro, and the
calcium concentration of the carcass was significantly increased in
magnesium-depleted chicks, making it unlikely that reduced intestinal absorption of
calcium caused the
hypocalcemia. In
magnesium-deficient chicks, the bone content of
magnesium was decreased by 74%, the
calcium content was unchanged, and the cortical thickness of bone was markedly increased. After 3 days of
magnesium-repletion, cortical thickness was reduced with increased endosteal resorption. There was an increase in unmineralized osteoid tissue in the
magnesium-depleted chicks. Parathyroid gland size and histology did not differ in
magnesium-depleted and control birds. The results suggest that
hypocalcemia develops due to altered equilibrium of
calcium between extracellular fluid and bone, favoring increased net movement into the latter. Failure of parathyroid gland function could also exist, and unresponsiveness to
parathyroid hormone (PTH) may also contribute to the
hypocalcemia. However, failure of PTH action is probably due to the presence of excess osteoid tissue rather than a primary event leading to
hypocalcemia.