Author
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Hunt, Curtiss |
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Submitted to: Trace Elements in Man and Animals International Symposium
Publication Type: Proceedings Publication Acceptance Date: 5/19/1996 Publication Date: N/A Citation: N/A Interpretive Summary: There is now evidence that boron, when fed at concentrations similar to that found in human diets containing ample amounts of fruits and vegetables affects blood biochemical markers of energy metabolism. Vitamin D3 helps to regulate the use of glucose and current research indicates that boron modifies that regulatory function. For example, groups of chicks receiving inadequate amounts of both boron and vitamin D3 had a change in blood sugar similar to that described for animals with glucose intolerance. Adding boron to the diet substantially alleviated most of that change. Therefore, an experiment was conducted with chicks to find out more how boron influences the use of glucose in the body, especially during times of poor vitamin D nutrition. We found that both boron and vitamin D in the diet affect the way glucose is stored and used in the liver. In addition, we found that boron and vitamin D had opposite effects on glucose storage and usage. For example, adding vitamin D to the diet increased the amounts of certain glucose products whereas adding boron to the diet decreased the amounts of these glucose products. Adding normal amounts of either vitamin D or boron to the diet was beneficial for the chick because either addition improved body growth. Technical Abstract: To characterize further the influence of boron on energy substrate utilization, especially pronounced during concomitant vitamin D deficiency, hepatic glycolytic metabolite concentrations were determined in three experiments with the same fully crossed two-factor design. Day- old cockerel chicks (18 per group) were fed a ground corn, high protein casein, and corn oil based diet (approx 0.20 mg B/kg) supplemented with boron at 0 or 1.3 mg/kg and vitamin D3 at 125 (inadequate) or 625 (adequate) IU/kg. At 28 d of age, moderate vitamin D deficiency decreased hepatic content of glycogen (38.6 vs 43.9 umol/g; p < 0.05; RMSE = 14.7), the three-carbon phosphorylated acid metabolic pool (glycerate-2-phosphate [G2P], 0.051 vs 0.060 umol/g; p < 0.0002; RMSE = 0.0002, and phosphoenolpyruvate, 0.083 vs 0.120 umol/g; p < 0.002; RMSE = 0.032), and lactate (0.81 vs 1.01 umol/g). Vitamin D deficiency increased the hexose phosphate metabolic pool (glucose-6-phosphate, 0.251 vs 0.216 umol/g; p < 0.005; RMSE = 0.080, and fructose-6-phosphate, 0.073 vs 0.066 umol/g). Boron deprivation increased hepatic content of G2P (0.060 vs 0.052 umol/g; p < 0.003; RMSE = 0.013). The opposite effects of vitamin D and boron on hepatic G2P concentrations suggest that boron does not act directly on vitamin D to modify the glycolytic pathway. |