From Our 2008 Archives
Scientists ID Gene Regulating Blood Glucose Levels
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FRIDAY, June 6 (HealthDay News) — Researchers who've identified a gene that regulates glucose levels but does not increase the risk of type 2 diabetes say their finding may help improve understanding of the underlying causes of diabetes.
"Elevations of blood glucose are diagnostic of diabetes. This finding demonstrates there are gene variants that are important in day-to-day regulation of glucose, but they do not appear to play a significant role in disease risk," co-senior author Richard M. Watanabe, an associate professor of preventive medicine and physiology & biophysics at the Keck School of Medicine at the University of Southern California, said in a prepared statement.
"The identification of these variants increases our basic knowledge about regulation of glucose and may also be useful in future genetic studies to help discriminate between genetic variants that do or do not contribute to disease susceptibility," Watanabe said.
The researchers analyzed genetic information from thousands of people and concluded a gene on chromosome 2 that encodes for the enzyme glucose-6-phosphatase catalytic 2 (G6PC2) is associated with fasting glucose levels.
"G6PC2 is primarily expressed in the beta cells of the pancreas and is responsible for converting glucose-6-phosphate back to glucose. Genetic variation of G6PC2 may be responsible for reducing insulin secretion and causing the glucose concentration to increase," Watanabe said.
With each additional copy of the higher frequency variant of the gene, glucose concentrations increased. Chronically elevated glucose levels may be a precursor to type 2 diabetes, Watanabe noted.
The study is published in the July issue of The Journal of Clinical Investigation.
"Genetics is identifying a whole new set of genes, proteins and pathways that are related to diabetes and blood sugar control. Our next challenge is to figure out how these genes work," study co-author Dr. Thomas A. Buchanan, professor of endocrinology at Keck, said in a prepared statement.
— Robert Preidt
SOURCE: University of Southern California Health Sciences, news release, June 3, 2008
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