Author
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Hunt, Curtiss |
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HERBEL, JO - 5450-20-00 |
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Submitted to: Trace Elements in Man and Animals International Symposium
Publication Type: Abstract Only Publication Acceptance Date: 5/19/1996 Publication Date: N/A Citation: N/A Interpretive Summary: 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 (43.9 vs 38.6 umol/g; p < 0.05; RMSE = 14.7), the three-carbon phosphorylated acid metabolic pool (glycerate-2-phosphate [G2P], 0.060 vs 0.051 umol/g; p < 0.0002; RMSE = 0.0002, and phosphoenolpyruvate, 0.120 vs 0.083 umol/g; p < 0.002; RMSE = 0.032), and lactate (1.01 vs 0.81 umol/g). Vitamin D deficiency increased the hexose phosphate metabolic pool (glucose-6-phosphate, 0.216 vs 0.251 umol/g; p < 0.005; RMSE = 0.080, and fructose-6-phosphate, 0.066 vs 0.073 umol/g). Boron deprivation increased hepatic content of G2P (0.052 vs 0.060; 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. |