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Sulfonylurea Receptor Polymorphism Increases Risk of Type 2 Diabetes 
WESTPORT, CT (Reuters Health) Jun 06 - 
In the French population, a common genetic variation in sulfonylurea receptor 
1 (SUR1), a protein of the ATP-sensitive potassium channel that plays a 
central role in glucose-induced insulin secretion, is associated with an 
increased risk of non-insulin dependent diabetes mellitus (NIDDM). Dr. 
Philippe Amouyel, of Institut Pasteur in Lille, France, and a multicenter 
team report the finding in the June 1st issue of the American Journal of 
Medical Genetics. Their study included 122 subjects with NIDDM, 70 of whom 
were treated with sulfonylureas, and 1250 nondiabetic controls. The subjects 
were genotyped for the SUR1 intron 16-3t/c polymorphism. Only 21% of controls 
were homozygous for the c allele (ie, cc genotype), compared with 30% of 
NIDDM patients. Subjects with the cc genotype had a 70% increased risk NIDDM 
compared with tt genotypes, Dr. Amouyel told Reuters Health. A link between 
SUR1 polymorphism and response to sulfonylurea therapy also emerged in the 
study. "NIDDM patients bearing at least one c allele and treated with 
sulfonylurea agents had fasting plasma triglyceride concentrations 35% lower 
than non-c-allele bearers," according to the researcher. These findings may 
allow physicians to treat NIDDM according to a patient's genetic makeup. Such 
pharmacogenetic approaches "offer the best short-term applications of 
genetics to human health management," Dr. Amouyel said. "Indeed, in such 
situations, genotyping will have a clear interest for the patient: to 
increase the chances to receive the most efficient drug and to avoid 
deleterious side effects." 
Am J Med Genet 2001;101:4-8. 
Except from MedLine
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