Visceral Responses

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A full belly is a simple but sure sign that the body has recently taken in energy as food, and stomach distension has long been known to reduce appetite. One way that this physical state is communicated to the brain is via distension-sensitive nerve fibers that carry signals from the stomach and intestine, ultimately reaching appetite-control centers. Neural signals reflecting the energy-processing state of the liver may also be transmitted to the brain via the vagus nerve.

Insulin is also believed to act directly on neurons in the hypothalamus to suppress appetite, and several other hormones manufactured in the intestine and released into the bloodstream after meals are known to travel to the brain and produce the same effect. Among these, cholecystokinin is an important factor in causing short-term satiety, but its actions are limited to signaling termination of individual meals. Another peptide called PYY, released from the small intestine, does the same. So far only one gut-generated peptide that acts to spur appetite has been identified: ghrelin is made and released in the stomach before feeding and may signal anticipation of a meal.

In people who are already obese, it is possible that dysfunctional generation of such short-term signals indicating whether food has recently been consumed, or is about to be, could skew the brain's energy-regulation mechanisms. Losing as little as 10 pounds, for example, can cause ghrelin output to rise, provoking increased hunger.

Over the long term, signals emanating from body fat itself might also contribute to abnormal energy management. For many years, fat was viewed primarily or exclusively as a passive site for energy storage and release in the form of fatty acids, but with the discovery of leptin, adipose tissue was recognized as an endocrine gland whose activity has widespread effects on health.

Leptin is still the only fat-derived hormone conclusively shown to participate directly in regulation of fat stores, but a group of others, often collectively referred to as adipokines, are under investigation as well. Adiponectin, for example, is a molecule produced and secreted exclusively by fat cells that normally circulates in the bloodstream in high concentrations. Adiponectin levels are lower than average in obese subjects for unknown reasons, and experimental mice lacking adiponectin are extremely heavy, although the mechanism underlying this effect is also mysterious. Some intriguing research suggests that under certain circumstances adiponectin might have a direct appetite-stimulating effect in the brain. Although such findings are very preliminary, they point to the possibility that adiponectin, too, could serve as a direct signal from fat cells to the brain indicating a need to take in energy. As such, it might offset leptin's appetite-suppressing role in energy regulation.