|Johnson Julie A|
|Reinhardt, Timothy - Tim|
|Beitz Donald C|
Submitted to: Archives Of Biochemistry and Biophysics
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/16/1995
Publication Date: N/A
Citation: Interpretive Summary: Vitamin D is required for the body to build strong healthy bones and teeth. In order to do its job, vitamin D must be "activated." The activated form of vitamin D, which is also known as 1,25- dihydroxyvitamin D, then acts at the intestine and kidney to cause calcium to enter the body. Formation of the 1,25-dihydroxyvitamin D takes place in the kidney, and can be increased in the blood by reducing the dietary calcium. The present experiment showed unexpectedly that we could prevent the increased formation of 1,25- dihydroxyvitamin D3 associated with reduced dietary calcium by feeding excess (100 times normal) vitamin D3. The depressed formation of the 1,25-dihydroxyvitamin D3 was the result of direct inhibition of its kidney-dependent synthesis, as well as its enhanced destruction by the intestine. These data further define the interactions between dietary vitamin D3 and calcium on the in vivo production of 1,25-dihydroxyvitamin D3.
Technical Abstract: We studied the effects of dietary calcium (Ca)4 restriction and excess vitamin D3 on tissue 25-hydroxyvitamin D-1-hydroxylase (1-OHase) and 1,25(OH)2D/25-OH-D-24-hydroxylase (24-OHase) activities in rats. Effects were studied in 4 groups of rats, with each group receiving one of the following diets: a control diet consisting of normal Ca and normal vitamin D3 (NC); NC plus excess (75,000 IU/wk) vitamin D3 (NCT); low Ca and normal vitamin D3 (LC); or LC diet with excess vitamin D3 (LCT). Rats fed the low Ca diets (LC and LCT) had elevated plasma parathyroid hormone (PTH) concentrations, increasing >3-fold relative to rats fed the normal Ca diets. The elevated concentrations of PTH in LCT rats did not result in increased plasma 1,25-dihydroxycholecalciferol [1,25(OH)2D3] (NC = 115 +/- 7 pg/ml; LCT = 99 +/- 11 pg/ml). Plasma 1,25(OH)2D in LC rats, however, was increased significantly (615 +/- 110, P = <0.01). There were no differences in either plasma Ca or phosphorus between the LC and LCT groups. Dietary Ca restriction led to an 18-fold stimulation in renal 1-OHase activity in LC rats (P = <0.01), while 1-OHase in the LCT rats was marginally but significantly elevated 2.3-fold (P = <0.05).