The investigators who included M. Alan Permutt, M.D., professor of medicine and of cell biology and physiology; Rosalind J. Neuman, Ph.D., professor of mathematics in psychiatry; and Samuel Klein, M.D., the Danforth Professor of Medicine and Nutritional Science and director of the Center for Human Nutrition focused on 36 small genetic variations, called single nucleotide polymorphisms (SNPs), in the CD36 gene. A SNP involves a single base-pair change in the DNA.
The team evaluated DNA taken from more than 2,000 African-Americans because variations in the gene are more common in individuals of African and Asian descent than in other racial groups. The researchers expect, however, that these findings also will be applicable in other populations.
"The idea was to look at the different variations in the gene and see whether they were more prevalent in people who also had elevated cholesterol, abnormal blood glucose or the other components of the metabolic syndrome," says first author Latisha Love-Gregory, Ph.D., research instructor in the Division of Geriatrics and Nutritional Science.
Love-Gregory says the research team demonstrated an association between SNPs in the gene and metabolic syndrome.
"There is additional work to do to determine if the function of these genetic variants actually contributes to the development of type 2 diabetes or heart disease," she explains. "We do expect that a number of different changes, in both CD36 and other genes, will be related to these diseases. What we'd like to learn, however, is whether the changes identified in the gene alter the CD36 protein in ways that change its function to make a person more vulnerable."
The team determined that five of the SNPs they examined are more common in people who have symptoms of metabolic syndrome, but a sixth seemed to have a more favorable metabolic effect. The "protective" SNP makes people produce lower amounts of CD36 protein.
|Contact: Jim Dryden|
Washington University School of Medicine