A series of experiments was conducted to test the hypothesis that vita
min D utilization may not be as efficient in chicks with tibial dyscho
ndroplasia (TD). The basal diet contained 1.0% Ca and 0.45% available
P with no supplemental cholecalciferol (D-3) Chicks from low TD (LTD)
and high TD (HTD) selected lines were fed diets supplemented with vari
ous levels of vitamin D compounds and examined for rickets and TD. Whe
n chicks were fed a D-3-deficient diet containing only 1.25 mu g/kg ad
ded D-3, HTD chicks had a greater incidence of severe rickets than LTD
chicks (P < 0.05). The LTD chicks did not exhibit TD when fed a diet
containing adequate (20 mu g/kg) Dg. The LTD chicks fed a diet supplem
ented with 5 mu g/kg D-3, however, had 22% incidence of TD. When HTD c
hicks were fed diets supplemented with 5 mu g/kg Dg [control diet that
meets NRC (1994) requirement for D-3], 20 mu g/kg D-3, 5 mu g/kg 1,25
-dihydroxycholecalciferol [1,25-(OH)(2)D-3] or the combination of both
D-3 (20 mu g/kg) and 1,25-(OH)(2)D-3 (5 mu g/kg), TD incidence was hi
ghest in HTD chicks fed the control diet. When HTD chicks were fed die
ts with an increased dietary level of 1,25-(OH)(2)D-3 (10 mu g/kg) fur
ther reduction of TD incidence (P < 0.05) occurred. A potentially toxi
c level (Soares et al., 1983) of 1,25-(OH)(2)D-3 (15 mu g/kg) fed to H
TD chicks resulted in still greater suppression of incidence of TD eve
n though growth and feed intake in HTD chicks was greater than those o
f LTD chicks. It is concluded that the development of TD in HTD chicks
is associated with subnormal ability to metabolize vitamin D.