Male mice selected for rapid 3 to 6 wk postweaning gain (M16) and unselected controls (ICR) were ad libitum fed a stock diet containing 0, 50 or 200 ppm
cimaterol, a beta-agonist, from 4 to 7 or 4 to 10 wk of age. Mortality rate was higher in M16 than in ICR mice fed
cimaterol (12.5 vs 1.3%; P less than .01). No mortalities occurred in either line fed the control diet. Line M16 exceeded (P less than .01) ICR in growth rate, feed intake, feed efficiency and lean index. Line X
cimaterol level interactions (P less than .01) were found for the first three of these traits, although
cimaterol level did not change line ranking. Epididymal fat as a percentage of empty
body weight decreased at a faster rate in M16 than in ICR as
cimaterol level increased. At 0 and 50 ppm, M16 exceeded ICR (P less than .05), but at 200 ppm there was no line difference (P greater than .05). Line M16 exceeded (P less than .05) ICR in
blood glucose (5%),
nonesterified fatty acids (4%) and
lactate at 7 wk (9%), but
lactate was higher in ICR
at 10 wk (13%). Lines were not different in blood
urea-N. Compared to zero
cimaterol level, at 50 and 220 ppm
glucose decreased (14% and 23%; P less than .05),
nonesterified fatty acids decreased (3% and 29%; P less than .05),
lactate increased (9% and 11%; P less than .05) and blood
urea-N increased (3% and 16%; P less than .05). There were no line X
cimaterol level interactions for blood metabolites. Differences in mortality rate, growth, feed consumption, feed efficiency and epididymal fat pad percentage between the high-growth and control lines in response to
cimaterol may reflect genetic differences in mechanisms of metabolic regulation.