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Appetite Signals

Appetite, the urge to seek food, is controlled by a complex interplay between endocrine, neural, and metabolic signals from multiple body organs and neurons (nerve cell) and neuropeptides (molecules made by nerve cells) in the brain.

Sight, taste, and smell of food are important signals for regulating food intake. There are receptors in the mouth that recognize the taste, texture, and temperature of ingested food, and taste plays an important role in the selection of foods. There are several peptides (molecules made of short chains of amino acids) that are important for perception of taste, three of which are: substance P, opioids, and cholecystokinin (CCK). Substance P, found in the nerve fibers of taste buds in the tongue, released on ingestion of foods such as chili peppers, reduces intake of water compared to sweet solutions containing sucrose. Opioid peptides seem to stimulate ingestion of sweet-tasting foods. CCK modulates taste preferences through the gastrointestinal tract.

Gut Hormones

The next set of appetite signals come from various gastrointestinal organs. CCK is released from the duodenum (first part of the small bowel) in response to ingestion of proteins and fats and helps their digestion by stimulating secretion of digestive enzymes and bile. CCK, upon release, inhibits appetite via two mechanisms.

It acts via the vagus nerve to send signals to areas in the brainstem (lower part of the brain, just above the spinal cord). It also acts locally to constrict the last part of the stomach and slow down stomach emptying, thus causing a sense of fullness. It is also possible that CCK may act directly in the brain. However, the effects of CCK are short lived.

Peptide YY (PYY) is released from the cells in the small bowel and colon rapidly after food ingestion. It has been shown to reduce appetite. It acts via neuropeptide Y receptors; it decreases stomach motility, decreases release of secretions from the stomach and pancreas and finally increases absorption of water and electrolytes in the gut. PYY also acts directly in the brain by inhibiting certain neurons in the hypothalamus (specific region in the brain) that stimulate appetite. Unlike CCK, the effect of PYY lasts for several hours after a meal.

Ghrelin is secreted primarily from oxyntic cells in the stomach and, to a lesser extent, from cells of the bowel. Ghrelin is a strong appetite stimulant and it acts via certain neurons in the hypothalamus and brain stem. Blood levels of ghrelin are regulated by endogenous diurnal rhythm and by food intake. Ghrelin levels are high in the morning and low at night. Ghrelin levels increase during fasting (thus increasing appetite) and fall after food intake (decreasing appetite).

However the fall in ghrelin levels after fat intake is transient and returns to normal after 45 minutes, whereas carbohydrate intake causes a longer-lasting fall in ghrelin levels. Interestingly, ghrelin levels do not fall after ingestion of water, suggesting stomach distension has no role in its release. On the other hand, ingestion of small amounts of alcohol increases release of ghrelin and stimulates appetite. Research has found that obese persons do not show the rapid fall in ghrelin levels after meals, which in turn may lead to continued food intake and obesity.

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