Collards, turnip greens, leaf lettuce, and spinach, grown in nutrient solution so that their Mg content was 80 to 90% 26Mg, were tested in ambulant male volunteers stabilized on a constant metabolic diet. The freeze-dried vegetables were incorporated in bran muffins in which the vegetables replaced part of the bran. Bran muffins without vegetables were consumed for breakfast each day. They were also used as a standard test meal to which the vegetable muffins were compared. All subjects participated in three consecutive isotope absorption tests: one of the standard test meal and two of the vegetables. The standard test was carried out after at least 30 days on the controlled diet. Subsequent tests of vegetables followed at 4-wk intervals. Each test meal contained 30 microCi 28MgCl2 and 50 mg stable 26Mg, the latter either as the intrinsic label of a test vegetable or as 26MgCl2 in solution taken with the standard bran muffins. Net absorption of both isotopes was measured to establish exchangeability and to determine relative Mg absorption from the vegetables. Exchangeability was 90% or higher from all meals tested. Relative Mg absorption was highest from collards and least from the standard test meal. Net absorption values ranged from 40 to 60%.
Untreated diabetic (BB) rats exhibited compensatory intestinal growth which was associated with hyperplasia and was accompanied by an increase in unoccupied vitamin D receptors. Although vitamin D receptors were increased, low circulating 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] prevented amplification of the action of 1,25(OH)2D3, as evidenced by reductions in calbindin D-9K and alkaline phosphatase activity in the BB rat intestine compared to control. In the kidney, a lesser degree of compensatory growth was observed which was not associated with hyperplasia, and no significant effect of diabetes on vitamin D receptors or calbindin D-28K was observed. These studies suggest tissue-specific changes in 1,25(OH)2D3 metabolism during spontaneous diabetes which may be related to the hyperplasia which occurs during compensatory tissue growth.
Growing chicks fed magnesium-deficient (150 ppm Mg) diets for 14 or 21 days developed significant hypomagnesemia and hypocalcemia compared to control chicks fed 1,000 ppm Mg. The hypocalcemia was accompanied by significant parathyroid gland hyperactivity, suggesting that magnesium deficiency did not impair parathyroid gland function. Despite parathyroid gland hyperactivity, however, bone resorption was decreased in the magnesium-deficient chicks, although bone formation was not affected by magnesium depletion. The decrease in bone resorption in the magnesium-deficient chicks was correlated with significant bone magnesium depletion and resulted in increased bone calcium content. These findings suggested that the development of hypocalcemia in magnesium-deficient chicks was related to decreased bone resorption, due to impaired osteocytic function rather than parathyroid gland insufficiency. The results also offer an explanation for the decrease in skeletal responsiveness to PTH which has been reported during magnesium depletion.
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