Research toward understanding the developmental risk of type 1 diabetes is a step closer after a major funding grant to The University of Queensland’s Diamantina Institute.
The Juvenile Diabetes Research Foundation, the world’s largest charitable funder of type 1 diabetes research, has awarded UQ’s Dr Emma Hamilton-Williams a $750,000 five-year JDRF Career Development Award for her research into identifying immune pathways responsible for causing the debilitating disease.
Dr Hamilton-Williams said Type 1 diabetes occurred when the pancreas ceased to make insulin, a hormone produced by beta cells in the pancreas.
“This happens because the immune system destroys the cells that make insulin,” she said.
“Insulin allows the body’s cells to take up glucose from the blood, and is needed to regulate carbohydrate and fat metabolism.”
Australia has one of the highest rates of type 1 diabetes in the world, with about 1825 Australians diagnosed each year.
It is also one of the most common chronic diseases in children, and can potentially lead to temporary or permanent blindness, chronic kidney disease and amputation.
Dr Hamilton-Williams said significant advances had been made in treatments, but there was still no cure.
She and her group are researching the link between genetic and non-genetic factors which influence the development of type 1 diabetes in the hope of developing novel therapies to target those at risk.
“I’m really thrilled at this award,” Dr Hamilton-Williams said.
“This is an amazing opportunity to further my goals in this critical area of type 1 diabetes research.
“Children and families with type 1 diabetes still have their hopes pinned on researchers to find a true cure for their disease. We need to do all the research we can.
“It has already been discovered that there is an association between gut bacteria and several autoimmune and inflammatory diseases.”
Dr Hamilton-Williams said increasing evidence also suggested a role for gut bacteria in type 1 diabetes.
“The composition of bacteria in the gut is influenced by both environmental and genetic factors, and my research will test whether genes that have a predisposition to an increased risk of developing type 1 diabetes alter the intestinal environment, therefore affecting the intestinal immune response, causing type 1 diabetes,” she said.
Volunteers will be recruited to observe the difference between patients with type 1 diabetes and their healthy siblings and unrelated healthy individuals.
The siblings have some subclinical autoimmunity and about 6 per cent will later develop diabetes.
“They will monitor changes in the intestine, measured by faeces samples, and the subsequent link of developing type 1 diabetes,” Dr Hamilton-Williams said.
“They will work together with the proteomics team at the Diamantina Institute to screen samples to pinpoint these biomarkers.”
The team will also use DNA sequencing to assess which populations of bacteria are in the gut of the study participant.
This will allow Dr Hamilton-Williams to test in pre-clinical models whether the transfer of gut bacteria from a protected individual to a genetically susceptible individual can prevent disease.
Healthy siblings have been shown to demonstrate inflammation in the blood cells, which is likely to represent exaggerated responses to environmental triggers such as food, infections and stress.
“While most siblings of type 1 diabetes patients don’t go on to get diabetes, I am examining which markers could predict the few that do progress to disease,” Dr Hamilton-Williams said.
“This work may also uncover novel targets that could be used to design drugs to prevent or treat type 1 diabetes.”
Media contact: Caroline Davy, Marketing and Communications Manager, The University of Queensland Diamantina Institute, (07) 3443 7027 or email@example.com