| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2846015 | Physiology & Behavior | 2007 | 7 Pages |
Leptin, which is produced in proportion to adiposity, has been reported to regulate feeding behaviors. Previous researchers reported that inhibition of nitric oxide (NO) synthase (NOS) decreased food intake, while L-arginine attenuated this effect. Recently, studies showed that NO plays an important role as a mediator of feeding behavior induced by a variety of neuropeptides. We investigated whether the anorectic effect of leptin is mediated by nitric oxide in broilers and Leghorns. In the first experiment, leptin was intracerebroventricularly (ICV) administered into the right lateral ventricle of broilers and food intake monitored at 15-min intervals through 180 min postinjection. L-arginine attenuated the decrease in food intake induced by leptin. In the second experiment, leptin was coinjected ICV with NG-nitro-arginine methyl ester HC1 (L-NNA), a NOS inhibitor. In the following study, we investigated whether the decreased feeding induced by leptin (10 μg/l0 μl) is mediated by nitric oxide in chickens. Three week old chickens were administered two levels of leptin (A = aCSF, B = 10 μg/l0 μl) into the right lateral ventricle, and nitrate and nitrite (nitric oxide metabolites) were monitored 30-min postinjection. The results showed leptin decreased NO formation significantly compared with the control group. These results suggest that NO interacts with leptin in the central nervous system to modulate feeding behavior in the chicken.
