boron and Vitamin-D-Deficiency

Topics: Animals; Arsenic; Bone and Bones; Boron; Bromine; Cadmium; Cholecalciferol; Connective Tissue; Fertility; Fluorine; Growth; Hematopoiesis; Humans; Lead; Lithium; Metalloproteins; Nickel; Nutritional Requirements; Silicon; Sleep; Tin; Trace Elements; Vanadium; Vitamin D Deficiency

Nutritional intakes of boron have been shown to lessen the adverse consequences of vitamin D deficiency in rodents. Pilot clinical studies suggest that this effect may be mediated, in whole or in part, by an increase in serum 25-hydroxyvitamin D. We propose that, in concentrations achievable with good diets, boron suppresses the activity of the microsomal enzyme 24-hydroxylase, chiefly responsible for catabolism of this steroid. This inhibition may reflect a direct interaction with the enzyme, or perhaps boron's ability to form a covalent complex with the product of its activity, 24,25-dihydroxyvitamin D. An up-regulatory impact of boron on 25-hydroxyvitamin D is potentially beneficial in light of the fact that the vitamin D status of many individuals is poor during winter months, and traditional supplemental doses of this vitamin are often too low to correct this problem. There is growing evidence that good vitamin D status -- as reflected by 25-hydroxyvitamin D levels -- may reduce risk for a host of prominent disorders; thus, boron may have the ability to potentiate this protection. Clinical studies also suggest that nutritional boron can up-regulate 17beta-estradiol levels in women, including postmenopausal women receiving hormone replacement therapy. The catabolism of this hormone is achieved by microsomal enzymes catalyzing vicinal hydroxylations -- a description that also applies to 24-hydroxylase. This suggests the more general hypothesis that nutritional boron can inhibit a range of microsomal enzymes which insert hydroxyl groups vicinal to existing hydroxyls in steroids -- including the enzymes which catabolize estradiol and 25-hydroxyvitamin D.

Topics: Administration, Oral; Boron; Clinical Trials as Topic; Cytochrome P-450 Enzyme Inhibitors; Cytochrome P-450 Enzyme System; Dietary Supplements; Enzyme Inhibitors; Gene Expression Regulation, Enzymologic; Humans; Steroid Hydroxylases; Up-Regulation; Vitamin D; Vitamin D Deficiency; Vitamin D3 24-Hydroxylase

Because dietary boron deprivation induces hyperinsulinemia in vitamin D-deprived rats, the influence of dietary boron on insulin metabolism as modified by nutritional stressors was examined in two animal models. Male weanling Sprague-Dawley rats were assigned to each of four (Experiment 1) or 8 (Experiment 2) dietary groups for 35 d: the basal diet (< 0.2 mg B; <1.0 mg Mg/kg) was supplemented with boron (as orthoboric acid) to contain <0.2 or 2.0 (a physiologic amount) mg B/kg; with magnesium (as magnesium acetate), at 100 (inadequate) or 360-400 (adequate) mg/kg; and with cholecalciferol [vitamin D-3; 25 microg/kg for study length (Experiment 2), or, depleted for 16-17 d then repleted until end of experiment (Experiments 1 and 2)]. In the rat model, boron reduced plasma insulin (Experiment 1, P < 0.002; Experiment 2, P < 0.03), but did not change glucose concentrations regardless of vitamin D-3 or magnesium status. Cockerels (1 d old) were fed a ground corn, high protein casein and corn oil-based basal diet (low boron; 0.3 mg B/kg) supplemented with boron as orthoboric acid to contain 0.3 or 1.65 mg/kg (a physiologic amount) and vitamin D-3 at 3.13 (inadequate) or 15.60 (adequate) microg/kg. In the chick model, boron decreased (P < 0.045) in situ peak pancreatic insulin release at 26-37 d of age regardless of vitamin D-3 nutriture. These results suggest that physiologic amounts of boron may help reduce the amount of insulin required to maintain plasma glucose.

Topics: Animals; Boron; Chickens; Diet; Insulin; Insulin Secretion; Islets of Langerhans; Magnesium; Male; Nutritional Requirements; Rats; Rats, Sprague-Dawley; Vitamin D; Vitamin D Deficiency

Although boron has long been known to be a required nutrient for plants, it was not until recently that there was any suggestion of a nutritional requirement for animals and humans. Addition of boron to the diet of vitamin D-deficient chicks indicated that boron may play a role in animal nutrition. Studies with rats have demonstrated that supplemental dietary boron has most marked effects when the diet is deficient in known nutrients. We observed higher apparent-balance values of calcium, magnesium, and phosphorus for rats fed a vitamin D-deprived diet with dietary supplemental boron (2.72 ppm), than for rats fed the same diet without added boron (0.16 ppm). The treatment group with dietary supplemental boron demonstrated a high degree of variability in response to boron. We hypothesize that relatively large and variable vitamin D stores in weanling rats from a colony supplemented with 3000 IU vitamin D/kg diet accounted for the observed variable response. A recent, unpublished study using weanling rats from a low-vitamin D colony appears to support this hypothesis.

Topics: Animals; Boron; Calcium; Dose-Response Relationship, Drug; Female; Magnesium; Male; Nutritional Requirements; Phosphorus; Rats; Rats, Sprague-Dawley; Tissue Distribution; Vitamin D Deficiency

The effects of different levels of dietary boron were determined in vitamin D deficient rats. Vitamin D deficient diets containing either 0.158 ppm or 2.72 ppm of boron were fed to rats for 11 w, and calcium, magnesium, and phosphorus apparent absorption and balance were measured in the twelfth week. Higher apparent absorption and balance values for calcium and phosphorus were observed in the rats with higher dietary boron, but very few differences were seen in body wt, organ wt, and bone parameters. Balance measurements represented the present status of the rats after 12 w on the diets, but other measurements represented an accumulation over the lifetime of the rat, including a suckling period with ample vitamin D and boron. The data demonstrated that when rats are vitamin D deficient, as indicated by hypocalcemia, the level of boron in the diet affects mineral balance.

Topics: Animals; Body Weight; Bone and Bones; Boron; Calcium; Diet; Feces; Hypocalcemia; Magnesium; Organ Size; Phosphorus; Rats; Rats, Inbred Strains; Vitamin D Deficiency

It has been hypothesized that boron (B) is an essential element for animals, but its action will vary greatly depending on the nutriture of the organism. One of the nutrients implicated as having an interaction with boron is cholecalciferol (Vit D3). This study was carried out to determine if such an interaction exists. The study was conducted utilizing vitamin D-deficient chicken embryos that were injected through the shell at 8 d of embryogenesis with carrier (NaCl and/or acetone), B (0.5 mg), B + Vit D3 (0.5 mg and 0.3 microgram, respectively), or Vit D3 (0.3 or 1.5 micrograms). The in ovo concomitant administration of boron and vitamin D enhanced (p less than 0.05) the hatchability of the vitamin D-deficient embryos. Furthermore, boron and/or vitamin D3 increased (p less than 0.05) the percent of bone ash and decreased (p less than 0.05) the exaggerated height of the proliferative zone of the epiphyseal growth plate normally observed in vitamin D deficiency, suggesting a more rapid bone formation. The results provide further evidence supporting the hypothesis that boron plays a role in bone mineralization through an interaction with vitamin D.

Topics: Analysis of Variance; Animals; Body Weight; Bone Density; Boron; Calcitriol; Chick Embryo; Chickens; Female; Osteogenesis; Vitamin D Deficiency