WASHINGTON, Nov. 14 (Xinhua) -- Neuroscientists in the United States found that a stretched gut, instead of a full stomach, plays an even bigger role in making people feel sated and telling them to stop eating, which has provided new clues to the treatment of obesity.

The study published on Thursday in the journal Cell showed that a kind of nerve endings called "intraganglionic laminar endings" (IGLEs) lining the intestine played an important role to transmit messages to the brain that lower appetite.

Scientists had previously classified gut sensory neurons into three types: mucosal endings that detect hormones that reflect nutrient absorption; IGLEs in the layers of muscle that surround the stomach and intestine and sense physical stretching of the gut; and intramuscular arrays whose function is still not known.

Those sensory nerves, coming together in a giant bundle, is the major neural pathway that transmits information from gut to brain, but the identities and functions of the specific neurons were still poorly understood.

The researchers from University of California, San Francisco, stimulated hormone-sensing mucosal endings in the mice intestine that had been hypothesized to control appetite. But they found that none of these were able to impact animals' feeding at all.

When they stimulated the IGLEs that sense stretching, the mice stopped eating. Also, stimulating stretch receptors in the intestine proved much more powerful at eliminating the appetites of the hungry mice than even the stomach stretch receptors, according to the study.

The researchers suggested that rapidly incoming food from the stomach stretched the intestine, thereby activating the vagal stretch sensors and powerfully blocking feeding.

The findings also suggest a potential explanation for why surgery to treat extreme obesity by reducing the size of the gut is so effective at promoting long-term appetite and weight reduction. Enditem

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