This is the second year Thomas has won the award, which recognises the highest quality science to improve the understanding, prevention and treatment of Type 1 or Type 2 diabetes by early career researchers.
Thomas was recognised for his research proposal and presentation on understanding why the hormone somatostatin is released at elevated levels when individuals with type 1 diabetes have low glucose. This function is important to understand because too much somatostatin can impact on the ability to release the hormone glucagon – the body's natural process for normalising blood glucose levels and preventing low blood glucose (hypoglycaemia).
The dangers of hypoglycaemia in type 1 diabetes
Individuals with type 1 diabetes who are dependent on insulin therapy often experience hypoglycaemia that can cause unpleasant and sometimes dangerous symptoms. Approximately 30-40% of individuals with type 1 diabetes suffer, on average, 1-2 episodes of dangerously low (severe hypoglycaemia) blood glucose per year, which can lead to seizures and / or coma. Severe hypoglycaemia is fatal in around 10% of individuals with type 1 diabetes.
This increased risk of hypoglycaemia and severe hypoglycaemia is attributed to the body's physiological defence mechanisms for preventing hypoglycaemia being compromised. This includes the loss of an important hormone, glucagon, from the hormone-producing pancreatic cells within the islets of Langerhans. In healthy individuals, a drop in blood glucose normally leads to the release of glucagon from the islet alpha-cells, which acts on the liver to elevate / normalise blood glucose. Within the islets, the alpha-cells sit in close proximity to the delta-cells which release somatostatin, a hormone which inhibits glucagon secretion.
In the Rorsman Group, researchers have found that too much somatostatin release at low glucose contributes to the impaired glucagon response to hypoglycaemia in a type 1 diabetic mouse model and human type 1 diabetic pancreatic islets. What causes this abnormal hyper-secretion of somatostatin at low glucose however, is not known.
Blocking hormone signals to improve glucagon release
Thomas' research demonstrated that some of these islet alpha-cells may begin to preferentially produce and secrete another hormone, glucagon-like peptide-1 (GLP-1), that can stimulate delta-cell somatostatin at low glucose, causing elevated glucagon suppression from the alpha-cells which still secrete glucagon. Thomas also demonstrated that by blocking intra-islet GLP-1 signalling, that this could improve glucagon release from both mouse and human type 1 diabetic islets which would prevent dangerous hypoglycaemia from occurring. This suggests a novel strategy for therapeutic intervention in the management and prevention of hypoglycaemia in diabetes.
'We know that excessive somatostatin release from the delta cells plays a major role in restricting glucagon secretion from the alpha cells in type 1 diabetic pancreatic islets at low glucose,' said Thomas. 'However, the mechanism(s) contributing to this hypersecretion of somatostatin are largely unknown.
'I was ecstatic to be recognised for this prestigious award from Diabetes UK on this independent research. This research brings us one step closer to understanding the underlying mechanisms contributing to defective glucagon secretion at low glucose in individuals with type 1 diabetes. I am highly grateful to the MSIF pump-priming fund for helping me get this idea off the ground and to my mentors, Dr Anne Clark and Professor Patrik Rorsman for their continuous guidance and support.'