The objective was to determine the effect of a mouse metallothionein/bovine
growth hormone transgene on resting metabolic rate (RMR), cold-induced the
rmogenesis, and beta-agonist stimulated nonshivering thermogenesis in mice.
Non-transgenic littermates were used as controls. Open-circuit indirect ca
lorimetry was used to assess RMR and cold-induced thermogenesis in 64 mice.
Air temperature in the chamber was set at 31 degrees C for RMR and was dec
reased to 28, 25, 21, or 17 degrees C to determine cold-induced thermogenes
is. Response to the beta-agonist isoproterenol was evaluated by monitoring
changes in colonic temperature of 34 mice upon injection of the drug or sal
ine. Despite the fact that RMR tended to be lower in transgenics than in no
ntransgenics, at 31 degrees C transgenic mice were able to regulate colonic
temperature at the same level as nontransgenics, but colonic temperature d
ecreased in transgenics relative to nontransgenics as air temperature was r
educed. For each degree decrease in air temperature between 31 and 17 degre
es C, nontransgenic mice increased heat production by 1.03 +/- .10 watt/kg,
whereas transgenic mice increased it by only .56 +/- .08 watt/kg, indicati
ng that the thermogenic response of transgenics to cold was inferior. The m
agnitude of the maximal increase in colonic temperature after isoproterenol
injection was similar for both groups, but the response was slower in tran
sgenics. We suggest that lean body mass and substrate availability for shiv
ering thermogenesis are reduced in transgenics relative to total body weigh
t, and that they allow colonic temperature to decrease to conserve energy.