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U.S. Department of Agriculture, Agricultural Research Service, Grand Forks Human Nutrition Research Center, Grand Forks, ND 58202 and
* University of North Dakota, Department of Anatomy and Cell Biology, Grand Forks, ND 58203
5To whom correspondence should be addressed. E-mail: chunt{at}gfhnrc.ars.usda.gov.
Because dietary boron deprivation induces hyperinsulinemia in vitamin Ddeprived 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 360400 (adequate) mg/kg; and with cholecalciferol [vitamin D-3; 25 µg/kg for study length (Experiment 2), or, depleted for 1617 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 oilbased 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) µg/kg. In the chick model, boron decreased (P < 0.045) in situ peak pancreatic insulin release at 2637 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.
KEY WORDS: boron vitamin D insulin chicks rats
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