Washington [US]Jul 10 (ANI): University of Cambridge scientists say 1 in 3,000 rare genetic effects have a greater impact on risk of developing type 2 diabetes than previously identified genetic effects identified the mutation.
This study was published in Nature Communications. Type 2 diabetes is thought to be caused in part by genetic factors, but many of these genes are still unknown. Previous large-scale studies have relied on efficient “array genotyping” methods to measure genetic variation across the genome.
This approach is usually good at capturing common genetic differences between people, but each of them results in only a small increase in the risk of diabetes.
Recent advances in technology have enabled more comprehensive gene measurements by reading the full DNA sequences of more than 20,000 genes that encode human proteins. Proteins are essential molecules that enable our body to function.
In particular, this new approach enables, for the first time, a large-scale approach to study the effects of rare genetic variations on various diseases, including type 2 diabetes.
By examining data from more than 200,000 adults in a UK biobank study, researchers from the Epidemiology Unit of the Medical Research Council (MRC) at the University of Cambridge used this approach to correlate loss of the Y chromosome. We identified a genetic variation.
It is a well-known biomarker of biological aging that occurs in a small portion of the man’s circulating white blood cells, indicating a weakening of the body’s cell repair system. This biomarker has previously been linked to age-related diseases such as type 2 diabetes and cancer.
Researchers have identified a rare variant of the GIGYF1 gene that significantly increases the susceptibility to loss of the Y chromosome and increases the risk of developing type 2 diabetes by a factor of six. In contrast, common type 2 diabetes-related mutations result in a much smaller increase in risk, usually much less than double.
About 1 in 3,000 have such a GIGYF1 gene mutation. The risk of developing type 2 diabetes is around 30% compared to around 5% of the larger population. In addition, those who had these variants had other signs of wider aging, including weaker muscle strength and more body fat.
GIGYF1 is said to regulate the signal transmission of insulin and cell growth factors. Researchers say their results identify this as a potential target for future research, understand the general link between metabolism and cell aging, and inform future treatments. I’m going.
Dr. John Perry of the MRC Epidemiology Unit, senior author of this paper, said, “Reading an individual’s DNA is an effective way to identify genetic mutations that increase the risk of developing a particular disease, although there are many variants in complex diseases play a role such as type 2 diabetes. In many cases, it only marginally increases the risk. This particular variant, although rare, has a significant impact on individual risk. “Professor Nickwareham, Director of the MRC Epidemiology Unit, said: I added it this way. It highlights the exciting scientific potential of sequencing the genomes of so many people. We are confident that this approach will usher in a new era of useful genetic discoveries that will help us better understand common diseases such as type 2 diabetes. It may be able to provide better ways to treat or prevent the condition. An ongoing study shows how the loss of functional mutations in GIGYF1 increases the risk of developing such significant type 2 diabetes. Your future studies will also explore other associations between adult biological aging biomarkers and metabolic disorders. (ANI)