The effects of peptide YY on feeding behavior

　Obesity is becoming a growing health concern in the western world and developing countries because of the increasingly prevalent medical conditions such as diabetes and heart disease attributed to this state of increased adipose tissue. At present, insulin and leptin are the only two known long-term regulators of food intake. Peptide YY (PYY), its most common circulating form being PYY_3-36, is a short-term regulator of food consumption in concurrence with ghrelin, an orexigenic gut hormone. PYY_3-36 is released from the endocrine cells of the gastrointestinal tract initiated by gut distension after eating and exhibits anorexigenic effects.
　There have been reports of PYY_3-36 reducing the intake of food when administered intraperitoneally, though some groups have made contradictory claims. PYY_3-36 is postulated to activate the Y₂ receptor (Y₂R) localized in the arcuate nucleus of the hypothalamus to modulate feeding. When administered centrally, PYY_3-36 is known to have a potent orexigenic effect on feeding behavior.
　In order to examine the effects of peripheral PYY_3-36 on feeding behavior, male Sprague-Dawley rats that had been fasted overnight were given intraperitoneal injections of PYY_3-36 and re-fed directly following treatment. Food intake was measured along with a behavioral satiety sequence (BSS) study.
　In a different experiment, male Sprague-Dawley rats that had been fasted overnight were administered PYY_3-36 and/or a Y₂R antagonist intravenously and re-fed. Food intake was measured and the BSS studied.
　Food intake was not significantly decreased and the BSS was relatively unaltered when PYY_3-36 was injected intraperitoneally. However, intravenous administration of PYY_3-36 alone resulted in a significant reduction of food intake and a shift of the BSS to the left while maintaining its normality. The Y₂R antagonist blocked the anorexigenic effects of PYY_3-36 on food intake and did not cause the latency to rest in the BSS to occur at an earlier time point. These results give us reason to believe that when administered intravenously, PYY_3-36 acts as a natural satiety factor through the activation of Y₂ receptors.