We are a bit behind on this news, but better late than never, and it is definitely worth sharing. To all those out there who want something in the public eye, a little reminder: you need to send us timely press releases/info/links, please.
Anyway, the good news is that ethical diabetes research carried out by Exeter University and charity Animal Free Research UK has discovered important insights into the changes that can occur in insulin-producing cells – known as beta cells – in people with diabetes.
This could help protect them and find new ways to treat the condition.
Both type 1 and type 2 diabetes occur in part because of a loss of beta cells, where the body does not produce enough insulin to regulate blood sugar. However, scientists know that the body retains some beta cells that still function long after diagnosis.
The new findings by the University of Exeter’s Animal Free Research UK Centre of Excellence (ARC 2.0) are a step towards protecting these cells.
Over 4.9 million people are currently living with diabetes in the UK, with 90% of those with type 2, according to a report by Diabetes UK published last May.
The number of people living with diabetes has hit an all-time high to reach over 4.9 million, with 13.6m people now at increased risk of type 2 diabetes in the UK. It is a massive problem. Cases of diabetes diagnoses have doubled in the last 15 years. Solution are needed.
Dr Nicola Jeffery, who led the research at the University of Exeter, said: “Intervening early enough could be a route towards treating or preventing diabetes.”
Although in its early stage, the research uses human cells instead of animal models, to ensure the findings are more likely to lead to finding new treatments.
Dr Jeffery conducted laboratory tests using entirely human cells and reagents, rather than researching on animals which would not have given the same results.
By identifying which genes were differently activated in the cells which had changed, and inactivating these in turn, she found that a gene called HNRNPD was responsible for turning beta cells into delta cells, similarly to what the team had previously observed in humans.
Added Dr Jeffery: “Finding the gene responsible for transforming beta cells into delta cells is really exciting. Diabetes is a major global health challenge, and we urgently need to find new treatments and prevention strategies. If we can intervene early enough, we may be able to protect surviving beta cells and find new routes to helping people continue to produce enough insulin to manage diabetes.”
Professor Lorna Harries, who leads the University of Exeter’s Animal Free Research UK Centre of Excellence (ARC 2.0), said: “These are of course early days, and we now need to understand exactly how HNRNPD brings about the changes in pancreatic cell identity we have seen. Once we are armed with that information, we may be able to step in and intervene to prevent these changes in cell identity.”
Jarrod Bailey, Science Director at Animal Free Research UK, said: “This is an exciting and potentially very important discovery, which illustrates the power of focusing on human biology from the off. This could not have been done using animals, due to genetic differences that complicate rather than facilitate our understanding of human diseases like diabetes.”
The research is reported in the paper ‘Changes to the identity of EndoCβH1 beta cells may be mediated by stressinduced depletion of HNRNPD’, published in Cell & Bioscience.
Community Ambassador Steph Jones-Giles says “We are so proud to support the charity and the work of Professor Lorna Harries and Dr Nicola Jeffery. We are fortunate to work closely with the scientists and, in recent years, have been given a tour of the lab in Exeter alongside a visit from Dr Jeffery to give a talk to Bude U3A. This new discovery could not have been achieved using animals and this is the reason we do what we do, help fund better and kinder science. As ever a heartfelt thank you to the Bude community for their continued support. Because of you, we are on target to hit a fabulous £40,000 by the end of the year!”