Effects of dietary boron on calcium and mineral metabolism in the streptozotocin-injected, vitamin D3-deprived rat.
Dietary boron, in concentrations similar to that found in human diets comprised mainly of fruits and vegetables, affects both mineral and energy metabolism. Therefore, the effects of boron on a model system with a perturbed metabolic insulin-vitamin D3 axis was examined. Weanling male rats were fed a ground corn-high protein casein-corn oil-based diet (0.06 mg B/kg; no supplemental vitamin D3) supplemented with B (as orthoboric acid) at 0 or 2.4 mg/kg. After 55 days, all rats were equilibrated in individual metabolic cages for 6 days. After another 6 days, one half of the rats in both dietary groups were injected intraperitoneally with streptozotocin (STZ). All rats were killed 3 days after STZ treatment. STZ affected many aspects of mineral metabolism as expected. Plasma ionized calcium concentrations fell by approximately 10% in STZ-treated rats. Brain and heart mineral metabolism was spared from the toxic effects of STZ whereas spleen mineral metabolism was especially vulnerable to STZ. Supplemental dietary boron increased urinary excretion of calcium in the non-STZ rats but did not affect the plasma concentrations of alkaline phosphatase, ionized calcium or the concentration of calcium in the brains, lungs, kidneys and spleens of those animals. Supplemental dietary boron temporarily reduced the abnormally elevated renal excretion of albumin, potassium and sodium during the acute phase of diabetes mellitus. On the other hand, physiological amounts of dietary boron exacerbated the abnormally elevated rate of collagen breakdown in the STZ animal. Finally, boron may have indirectly affected heart mineral metabolism because dietary boron did not affect cardiac boron concentrations but did affect cardiac copper, calcium, manganese, molybdenum and phosphorus concentrations, primarily in non-STZ rats. The findings suggest that dietary boron has both protective and regulatory roles in mineral metabolism.
Hunt
C D
CD
USDA, Grand Forks Human Nutrition Research Center, N. Dak.
Herbel
J L
JL
D000419:Albuminuria; D000818:Animals; D001895:Boron / Q000494:pharmacology*; D001921:Brain / Q000378:metabolism; D002118:Calcium / Q000378:metabolism; D002762:Cholecalciferol / Q000172:deficiency*; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism*; D007668:Kidney / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D008274:Magnesium / Q000378:metabolism; D008297:Male; D008903:Minerals / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism; D011188:Potassium / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D012964:Sodium / Q000378:metabolism; D013311:Streptozocin; D014131:Trace Elements / Q000378:metabolism; D014808:Vitamin D Deficiency / Q000378:metabolism*
D008903:Minerals; D014131:Trace Elements; D002762:Cholecalciferol; D013311:Streptozocin; D012964:Sodium; D008274:Magnesium; D001895:Boron; D011188:Potassium; D002118:Calcium