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A human hormone, combined with a full stomach, offers clues for understanding our food intake

Bethesda, MD With the holidays come the traditions of sharing meals, desserts and treats with family, friends and co-workers. But the need to reduce the amount of food we consume daily during the holiday season and throughout the year -- has acquired a greater sense of urgency in the wake of America's obesity epidemic. As scientists look for ways to help us battle the bulge, a new study suggests that our own hormonal makeup may offer promising clues. A team of researchers has tested the hypothesis that gastric distension in humans can enhance the effect of cholecystokin (CCK) on the reduction of food intake. The researchers conclude that CCK's suppression of food intake is enhanced when the stomach is distended.

Background

CCK is a hormone released when digested fats and proteins are present, and reduces food intake. CCK stimulates enzyme secretion in the pancreas. The process eventually leads to inhibiting gastric emptying of the stomach's foods, thereby causing gastric distension. It has been suggested that increased gastric distension, induced by slowing of gastric emptying, may be the method by which CCK reduces food intake.

A New Study

The research team of Harry R. Kissileff, Julie C. Carretta, Allan Geliebter, and F. Xavier Pi-Sunyer, College of Physicians and Surgeons, Columbia University, New York, NY and the New York Obesity Research Center, St. Luke's/Roosevelt Hospital Center, New York, NY are the authors of a new study. Their investigation, entitled "Cholecystokinin and Stomach Distension Combine to Reduce Food Intake in Humans," appears in the November 2003 edition of the American Journal of PhysiologyRegulatory, Integrative and Comparative Physiology. The journal is one of 14 scientific journals published each month by the American Physiological Society (APS).

Methodology

Researchers used the protocol outlined below:

Subjects: Eight nonobese males and eight nonob
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Contact: Donna Krupa
djkrupa1@aol.com
703-527-7357
American Physiological Society
3-Dec-2003


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