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Variation in bitter-taste receptor gene increases risk for alcoholism

A team of researchers, led by investigators at Washington University School of Medicine in St. Louis, has found that a gene variant for a bitter-taste receptor on the tongue is associated with an increased risk for alcohol dependence. The research team studied DNA samples from 262 families, all of which have at least three alcoholic individuals. The families are participating in a national study called the Collaborative Study of the Genetics of Alcoholism (COGA). COGA investigators report in the January issue of the American Journal of Human Genetics on the variation in a taste receptor gene on chromosome 7 called TAS2R16.

"In earlier work, we had identified chromosome 7 as a region where there was likely to be a gene influencing alcoholism risk," says principal investigator Alison M. Goate, D. Phil., the Samuel and Mae S. Ludwig Professor of Genetics in Psychiatry at Washington University. "There's a cluster of bitter-taste receptor genes on that chromosome, and there have been several papers suggesting drinking behaviors might be influenced by variations within taste receptors. So we decided to look closely at these taste receptor genes."

Because taste receptors tend to vary a lot in the general population, Goate and colleagues had the opportunity to look at a large number of differences in genetic sequences and determine whether certain sequences might influence risk. In this study, they concentrated on TAS2R16, which helps regulate the response to bitter tastes.

They found a single base variation in the TAS2R16 receptor gene that seemed to put people at an increased risk for alcoholism. In cell culture experiments, Goate found that the variant receptor produced by this gene was less responsive to bitter compounds.

"The more common variant is more sensitive to bitter tastes, and people with that variant had a lower risk of being alcohol dependent," Goate says.

Goate hopes to replicate these findings in human taste tests, to verify
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Contact: Jim Dryden
jdryden@wustl.edu
314-286-0110
Washington University School of Medicine
9-Jan-2006


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