Three experiments were conducted to examine the efficacy of dietary
1,25-dihydroxycholecalciferol [(
1,25-(OH)2D3)] on the development of tibial
dyschondroplasia (TD) in chickens divergently selected for high (HTD) and low (LTD) incidences of TD. In Experiment 1, chickens from the two lines were fed two
calcium levels (0.75 and 1.0%), with and without 5 micrograms/ kg dietary 1,25-(OH)2D3. In Experiment 2, both lines were fed diets containing 1.0%
calcium and 0, 5, 10, or 15 micrograms/kg 1,25-(OH)2D3. The addition of 1,25-(OH)2D3 did not reduce the overall incidence of TD in Experiment 1, but did reduce the incidence of severe TD from 69 to 48% in the chickens receiving the 0.75%
calcium diet. In this experiment, LTD chickens had higher plasma
phosphorus and
bone ash. No line differences were noted between plasma
vitamin D metabolites or intestinal
vitamin D receptors. In Experiment 2, 5 micrograms/kg of 1,25-(OH)2D3 decreased the incidence of TD from 94 to 76% and number three scores from 69 to 44% (P < or = 0.001). Higher amounts of 1,25-(OH)2D3 further decreased TD, but there was a reduction in
body weight above 5 micrograms/kg. Plasma
25-hydroxycholecalciferol [25-(
OH)D3] and 1,25-(OH)2D3 were higher and intestinal
vitamin D receptors were lower in HTD chickens than in LTD chickens. Plasma 1,25-(OH)2D3 was not affected by dietary treatment, but 25-(OH)D3 was reduced by dietary 1,25-(OH)2D3. Experiment 3 was conducted to examine effects of line and dietary 1,25-(OH)2D3 on plasma
vitamin D metabolites and intestinal and growth plate receptors. No effect of genetic line or dietary 1,25-(OH)2D3 was observed for
vitamin D receptors concentration or plasma 1,25-(OH)2D3 levels. Plasma 25-(OH)D3 was reduced when 1,25-(OH)2D3 was fed. These results indicate that HTD chickens are somewhat responsive to dietary 1,25-(OH)2D3, but this treatment failed to prevent the lesion in a large portion of the population.