31 Swarnali das 2007 Food intake, anti- Obesity, signal of satiety, Y2 receptor, gut hormone, inhibitory effect Obesity is one of the greatest threats to the health of the developed world. In order to design effective drugs to treat the alarming increase in obesity, it is essential to understand the physiology of normal appetite control and the pathophysiology of obesity. This obesity epidemic is caused by both biological and environmental factors. The environmental factors include the over consumption of food due to its increased availability, lower prices, high calorie density and good taste. In addition the trend towards a less active lifestyle results in the reduction of energy expenditure. Recent evidence suggests that certain gut hormones – ghrelin, Peptide YY3-36 (PYY(3-36)) , pancreatic polypeptide, glucagon-like-peptide 1, cholecystokinin (CCK) and oxyntomodulin,– have a physiological role in governing satiety via the hypothalamus.Gut hormone appetite-regulatory systems represent a potential target for the design of antiobesity drugs.2 A combination of drugs that decrease preprandial appetite (ghrelin antagonist) and increase post-prandial satiety (gut hormone fragment peptide YY 3–36) might have a chance of achieving sustained weight loss. The hormone, PYY (for peptide YY 3-36), is of particular interest because it appears to be the intestine's signal of satiety and because overweight people normally make less of it than thin people.12 It is the anti-ghrelin because this hormone makes one feel full. The gastrointestinal peptide hormone ghrelin stimulates appetite in rodents and humans via hypothalamic actions. Within the hypothalamus, ghrelin bound mostly on presynaptic terminals of NPY neurons. Ghrelin stimulated the activity of arcuate NPY neurons and mimicked the effect of NPY in the paraventricular nucleus of the hypothalamus (PVH).16 PYY inhibits Neuropeptide Y and Agouti-related peptide, leading to a lower appetite because these molecules increase appetite and decrease metabolism.3-5. Peripheral administration of full length PYY increase fluid and electrolyte absorption from ileum and inhibit gut motility, meal induced pancreatic and gastric secretion, and emptying8-9. It also act as a vasoconstrictor. The action of peripheral PYY 3-36 on satiety appear to be mediated by a direct action on the accurate Y2 receptor, a presynaptic inhibitory receptor of neuropeptideY neurone.2 PYY released postprandially in proportion to the amount of calories ingested 17 .