Nitric oxide mediates hyperphagia of obese zucker rats: Relation to specific changes in the microstructure of feeding behavior

• Published in: Life sciences (1973) 1996, Vol.58 (1), p.PL9-PL15
• Main Authors: Stricker-Krongrad, A., Beck, B., Burlet, C.
• Format: Article
• Language: English
• Subjects: Animals; Arginine - analogs & derivatives; Arginine - pharmacology; Body Weight - physiology; Dose-Response Relationship, Drug; Eating - drug effects; Enzyme Inhibitors - pharmacology; feeding behavior; Feeding Behavior - drug effects; Feeding Behavior - physiology; hyperphagia; Hyperphagia - drug therapy; Hyperphagia - enzymology; Hyperphagia - physiopathology; Male; meal duration; NG-Nitroarginine Methyl Ester; nitric oxide; Nitric Oxide - physiology; Nitric Oxide Synthase - antagonists & inhibitors; Obesity - drug therapy; Obesity - enzymology; Obesity - physiopathology; Rats; Rats, Zucker
• ISSN: 0024-3205; 1879-0631
• DOI: 10.1016/0024-3205(95)02260-0

The presence of a nitric oxide synthetase (NOS) was demonstrated in the rat brain. It has been demonstrated recently that NOS-inhibitors reduce food intake in mammals and this suggest that nitric oxide (NO) might be a physiological mediator involved in the mechanisms controlling feeding behavior. Actually, there is no information about the acute central and peripheral effects of NOSinhibitors on feeding behavior in obese an lean Zucker rats. That is why we investigated the acute dose-dependent activity of N G-Nitro-Arginine-Methyl-Ester (L-NAME) on food intake and feeding behavior in these rats. When given peripherally in the obese rats, L-NAME produced a dosedependent decrease in food intake (p < 0.001). The calculated MED and the ED 50 were 0.50 mg/kg IP and 3.46 mg/kg IP, respectively. These effects could not be reproduced in the lean Zucker rats whatever the dose used (p = 0.59). The anorectic properties of L-NAME were wery well translated into the microstructure of the feeding behavior. Time spent to eat (p < 0.001), meal duration (p < 0.01) and meal number (p < 0.001) were reduced in the obese rats. Interestingly, L-NAME produced the same effects in the lean rats, but meal size increased in a compensatory manner. Central administration of L-NAME reproduced the same effects in the obese rats, but lean rats still remained insensitive. Central aminergic and/or peptidergic defects associated with the expression of hyperphagia might explain the differences observed between these lean and the obese animals. These results indicate a role of nitric oxide in the expression of hyperphagia and show that it might be a physiological mediator involved in the mechanisms controlling feeding behavior.