Injection of 2-deoxy-D-glucose (2DG) elicits both analgesic and hyperphagic responses in rats. While pituitary dysfunction, decreased dopamine availability, or neonatal monosodium glutamate treatment decreases 2DG hyperphagia, they increase 2DG analgesia. In contrast, 2-DG analgesia alone is decreased by repeated 2-DG injections, while 2-DG hyperphagia alone is decreased following naloxone pretreatment. The present four experiments examined further mechanisms subserving these two induced responses. In the first experiment, rats were deprived of food for 6 h following 2-DG (600 mg/kg). While 2-DG hyperphagia persisted in the absence of glucoprivation, 2-DG analgesia failed to occur after this delay. In the second experiment, acute exposure to inescapable foot shock (4 mA, 0.5 s/5 s for 1 h) preceded administration of 2-DG (600 mg/kg). While 2-DG hyperphagia was eliminated by this procedure, 2-DG analgesia was significantly potentiated. In the third experiment, repeated morphine (10 mg/kg) injections over 14 days eliminated 2-DG analgesia on the fifteenth day, but failed to affect 2-DG hyperphagia. In the fourth experiment, lesions placed in either the lateral hypothalamus or zona incerta decreased 2-DG hyperphagia, but failed to affect 2-DG analgesia. These results are discussed in terms of common and dissociative mechanisms mediating both responses.