Effect of long-term vagal stimulation on food intake and body weight during diet induced obesity in rats.

Abstract

Regulation of food intake and body weight is accomplished by several mechanisms. CNS receives information from periphery and modifies food intake mainly by vagal nerves that provide the major neuroanatomical link between gastrointestinal sites stimulated during food intake and CNS sites that control feeding behavior and metabolism. Gastric mechanoreceptors and jejunal chemoreceptors activated by food or vagal nerve stimulation (VNS), which mimic the physiological input, suppress feeding within short-term regulation. Our research was aimed on determination the role of electrical VNS in long-term control of food intake and body weight in diet induced obesity fed rats. Food intake, body weight and epididymal fat pad were assessed in male Wistar rats divided into three groups (controls vs. VNS). Rats were implanted with microchip and kept during the whole study (100 days) on diet induced obesity. Vagal nerve was stimulated by electrical rectangular pulses duration 10 ms, amplitude 200 mV, frequency 0.05 Hz generated by microchip. In control group surgery produced no significant changes in meal size and body weight gain as compared to intact group. In contrast, significantly decreased epididymal fat pad weight, decreased meal size with effect on decreased weight gain was observed in VNS rats. Data support theory that VNS can increase vagal afferent signal conduct to CNS and mimics the satiety signals leading to reduce food intake and body weight gain.