The pancreatic B-cell hormone amylin is known to be involved in the regulation of meal ending satiation and it also shares typical features of adiposity signals. Chronic amylin administration has recently been shown to increase energy expenditure under certain conditions. Here we investigate the acute effect of peripheral administration of amylin or its agonist salmon calcitonin (sCT) on energy expenditure and respiratory quotient (RQ). First, rats were injected with amylin (5 microg/kg IP) or saline just before dark onset. Despite significantly decreased food intake in amylin-treated rats compared to control until 2 h post-injection (p<0.05), amylin did not influence energy expenditure or RQ. Reduced food intake, which reduces energy expenditure, may have confounded a stimulatory effect of amylin on energy expenditure. Therefore, in the second experiment, amylin (1, 5 and 10 microg/kg IP) or saline was injected in the middle of the light phase (t=0 h) without access to food during 3 h post-injection. Amylin had no significant effects on energy expenditure or RQ. In a similar paradigm, the effect of sCT (0.1, 1.0 and 5.0 microg/kg IP) was tested. During food restriction, 5.0 microg/kg sCT significantly stimulated energy expenditure compared to control (p<0.05). Subsequent to refeeding at t=3 h, energy expenditure was decreased compared to control at t=8 h and t=10 h after 5.0 microg/kg sCT, probably due to sCT's strong anorectic action. Thus amylin may prevent the compensatory decrease in energy expenditure normally seen in animals that eat less. The longer acting sCT stimulated energy expenditure in animals without food access.