Scientists from University College London and Imperial College London in the United Kingdom have identified new genetic locations that might make some people more prone to developing type 2 diabetes. Share on Pinterest Scientists identify 111 new genetic locations that indicate susceptibility to type 2 diabetes. Type 2 diabetes affects hundreds of millions of people worldwide, and the numbers have skyrocketed in recent years. According to the World Health Organization (WHO), the number of people with diabetes has almost quadrupled in the past few decades, from 108 million in 1980 to 422 million in 2014. In the United States, 29 million people currently have diabetes, and 86 million are thought to have prediabetes. Until now, researchers were aware of 76 chromosomal locations, or “loci,” that underlie this metabolic disease. However, new research analyzed the human genome further and found an additional 111. The new study – published in the American Journal of Human Genetics – was co-led by Dr. Nikolas Maniatis of University College London’s (UCL) Genetics, Evolution, and Environment department, together with Dr. Toby Andrew of Imperial College London’s Department of Genomics of Common Disease.

Identifying the type 2 diabetes genetic loci Using a UCL-developed method of genetic mapping, Maniatis and team examined large samples of European and African American people, summarizing 5,800 cases of type 2 diabetes and almost 9,700 healthy controls. They found that the new loci – together with the ones previously identified – control the expression of more than 266 genes surrounding the genetic location of the disease. Most of the newly discovered loci were found outside of the coding regions of these genes, but within so-called hotspots that change the expression of these genes in body fat. Of the newly identified 111 loci, 93 (or 84 percent) were found in both European and African American population samples. After identifying genetic loci, the next step was to use deep sequence analysis to try to determine the genetic mutations responsible for the disease.