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Anti-appetite molecule released by fiber may be key to weight loss

The discovery of an "anti-appetite" molecule, which tells the brain to stop eating, makes a medication to "switch off" hunger a possibility in the future.
By Alex Cukan   |   April 30, 2014 at 10:36 PM   |   Comments

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LONDON, April 30 (UPI) -- The discovery of an "anti-appetite" molecule, which tells the brain to stop eating, makes a medication to "switch off" hunger a possibility in the future.

Researchers at Imperial College London and the Medical Research Council led an international team that identified acetate as the anti-appetite molecule which is naturally released to the brain when fiber is digested.

The study, published in Nature Communications, found acetate reduced appetite when directly applied into the bloodstream, the colon or the brain.

Lead author Gary Frost of the Department of Medicine at Imperial College London said when fiber is digested by bacteria in the colon, it ferments and releases large amounts of acetate as a waste product.

Using positron emission tomography scans, the researchers traced the acetate throughout the body and showed that it ended up in the hypothalamus region of the brain, which controls hunger.

A form of dietary fiber -- inulin -- contained in chicory and sugar beets was given to mice fed on a high-fat diet.

The study found mice fed on a high-fat diet with added inulin ate less and gained less weight than mice fed on a high-fat diet with no inulin. The mice fed on a diet containing inulin had a high level of acetate in their guts.

In stone-age times we ate about 100 grams per day (of fiber) but now we favor low-fiber ready-made meals over vegetables, pulses (beans) and other sources of fiber. Unfortunately our digestive system has not yet evolved to deal with this modern diet and this mismatch contributes to the current obesity epidemic," Frost said. "Our research has shown that the release of acetate is central to how fiber suppresses our appetite and this could help scientists to tackle overeating.”
© 2014 United Press International, Inc. All Rights Reserved. Any reproduction, republication, redistribution and/or modification of any UPI content is expressly prohibited without UPI's prior written consent.
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