Improving diagnosis and further understanding the role of genes in diabetes risk can pave the way for more personalised treatments, say researchers.
Dr Ines Cebola, postdoctoral researcher at Imperial College London, and Dr Shivani Misra, consultant in metabolic medicine at Imperial College Healthcare NHS Trust, presented their research on type 2 and rare diabetes, as well as personalised treatments at the recent Imperial College Academic Health Science Centre (AHSC) seminar series.
In a packed lecture theatre at St Mary’s Hospital, Dr Cebola explained how variations in non-coding sections of the genome might contribute to type 2-diabetes risk in the video above.
Type 2 diabetes is a common condition that causes the level of glucose in the blood to become too high. It can cause symptoms like excessive thirst and tiredness. It can also increase the risk of developing more serious conditions connected to the heart, eyes and nerves. It affects over 400 million people worldwide and genetic factors have long been known to have an important role in determining a person’s risk of type 2 diabetes, alongside other factors such as body weight, diet and age.
Dr Cebola explained how scientists at the College have mapped the regions in the genome that orchestrate gene activity in the cells of the pancreas that produce insulin, a hormone that regulates blood sugar.
In type 2 diabetes, the tissues become less responsive to insulin, resulting in blood sugar levels being too high. Most people can compensate when this happens by producing more insulin, but in people with type 2 diabetes, the pancreas cannot cope with this increased demand.
The team also identified genome sequences that drive gene activity in insulin-producing cells specifically. They found that these sequences are located in clusters, and that genetic variants known to be linked to diabetes risk are also found in these clusters.
Dr Cebola explained that these findings could lead to more personalised medicine as they may help stratifying the population according to their genetic risk of dysfunction of the insulin-producing cells specifically. This stratification of patients at higher risk of developing type 2 diabetes by dysfunction of the insulin-producing cells will allow clinicians in the future to administer more targeted treatments.