Dietary 1,25-dihydroxycholecalciferol has variable effects on the incidences of leg abnormalities, plasma vitamin D metabolites, and vitamin D receptors in chickens divergently selected for tibial dyschondroplasia.
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.
Mitchell
R D
RD
Department of Poultry Science, University of Georgia, Athens 30602, USA.
Edwards
H M
HM
McDaniel
G R
GR
Rowland
G N
GN
D000821:Animal Feed; D000818:Animals; D001835:Body Weight / Q000187:drug effects; D002112:Calcifediol / Q000097:blood; D002117:Calcitriol / Q000008:administration & dosage / Q000097:blood / Q000494:pharmacology*; D002645:Chickens / Q000002:abnormalities* / Q000235:genetics*; D000013:Congenital Abnormalities / Q000453:epidemiology / Q000235:genetics / Q000662:veterinary*; D004305:Dose-Response Relationship, Drug; D005260:Female; D005527:Food, Fortified; D006132:Growth Plate / Q000187:drug effects / Q000378:metabolism; D006614:Hindlimb / Q000002:abnormalities*; D015994:Incidence; D007413:Intestinal Mucosa / Q000187:drug effects / Q000378:metabolism; D008297:Male; D010009:Osteochondrodysplasias / Q000453:epidemiology / Q000235:genetics / Q000517:prevention & control / Q000662:veterinary*; D011201:Poultry Diseases; D018167:Receptors, Calcitriol / Q000378:metabolism*; D013977:Tibia
D018167:Receptors, Calcitriol; D002117:Calcitriol; D002112:Calcifediol