Recent studies have suggested that the tridecapeptide, neurotensin, may be an endogenous satiety factor. The present study was undertaken to examine the effects of neurotensin on multiple paradigms known to stimulate feeding. Following a 30 hour starvation period, neurotensin suppressed feeding at the 20 μg and 10 μg dose, but not at the 1 μg dose when compared to saline controls. Norepinephrine (20 μg ICV) induced feeding was suppressed at the 20 μg neurotensin dose but not at the 10 μg or 1 μg dose. In contrast, neurotensin did not suppress muscimol induced feeding at any of the doses. Insulin induced feeding (10 units SC) also was not suppressed by neurotensin. Neurotensin suppressed dynorphin induced feeding at the 20 μg and 10 μg but not at the 1 μg dose. Neurotensin suppressed spontaneous feeding (p<0.01) in vagotomized rats (2.5±0.3 g/2 hr) when compared with saline controls (4.2±0.5 g/2 hr) suggesting that an intact vagus is not necessary for neurotensin's anorectic effect. We conclude that neurotensin may play a role in short-term appetite regulation by a complex interaction with monoamines and neuropeptides, particularly norepinephrine and the kappa opiate agonist, dynorphin.
- Multiple feeding paradigms