This study was undertaken to investigate the effect of endogenous mu-receptor-selective peptide endomorphin 1, administered intracerebroventricularly, on oxygen consumption in mice. The intracerebroventricular injection of endomorphin 1 (3-30 nmol) significantly increased oxygen consumption in unrestrained mice. The effect of endomorphin 1 (30 nmol) was significantly antagonized by the simultaneous intraperitoneal administration of naloxone (100 nmol). These results suggest that endomorphin 1 stimulates oxygen consumption, and that the mu-opioid receptor influences energy balance in mice.