In an effort to understand how genes work, a collaborative study which includes the University of Southern California (USC) has identified a gene that regulates glucose levels. The results, which will be published in the July issue of the Journal of Clinical Investigation and is currently available online, may provide further 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 for day-to-day regulation of glucose, but they do not appear to play a significant role in disease risk," says Richard M. Watanabe, Ph.D., associate professor of preventive medicine and physiology & biophysics at the Keck School of Medicine of USC and co-senior author of the paper.
The study determined that this variant is not associated with an increased risk for type 2 diabetes.
"The identification of these variants increases our basic biologic 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," continues Watanabe.
The study examined genetic information from more than 24,000 people. Researchers scanned the genomes of more than 5,000 participants by combining the genome-wide association (GWA) findings from the Finland-United States Investigation of Non-insulin-dependent Diabetes Mellitus (FUSION) study and the SardiNIA study of aging.
The results determined that 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," says Watanabe. "Genetic variation of G6PC2 may be responsible for reducing insulin secretion and causing the glucose concentration to increase."