Findings could produce treatments to reduce cravings, expand calorie burn
FRIDAY, Oct. 31 (HealthDay News) -- An antibody that breaks down and suppresses an appetite stimulant produced by the human body has been discovered.
Scientists with The Scripps Research Institute say the antibody catalyst, GHR-11E11, increased the metabolic rate in fasting mice and curbed their eating even after the rodents went 24 hours without food.
The antibody counteracts ghrelin, a gastric hormone that promotes weight gain and fat storage through metabolic actions that decrease the breakdown of stored fat for energy as well as energy expenditure itself. The body releases the substance to encourage eating during periods of calorie restriction. The findings were published in this week's online issue of the Proceedings of the National Academy of Sciences.
"Our study showed that this novel catalytic ghrelin antibody could specifically seek out and degrade ghrelin," co-lead investigator Kim Janda, a professor of chemistry, said in a news release from the institute. "While this antibody lacks a high level of catalytic efficiency, our study clearly demonstrates that even a basal level of catalysis can effectively modulate feeding behavior. These findings not only validate antibody-based therapeutics, but strongly suggest that catalytic anti-ghrelin antibodies might help patients reach and maintain their weight-loss goals."
Because obesity has a complex nature, any antibody-based treatment would likely be combined with other weight-loss strategies, including medicinal, nutritional, exercise, educational and psychosocial components, Janda said. However, he added, more research is needed to better understand the effect of the antibodies over the long-term and other issues.
According to recent reports from the World Health Organization, about 1 billion people worldwide are overweight or obese, with most of these in the developed world.
The U.S. government has more about weight management.
-- Kevin McKeever
SOURCE: The Scripps Research Institute, news release, Oct. 27, 2008
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