“If we can target the inflammation that compromises insulin production, then maybe we can ‘turn down the dial’ on type 2 diabetes and prevent long-term damage,” says Clara Westwell-Roper, a UBC MD/PhD candidate at CFRI and 2013 Featured Trainee at CFRI. She recently published a paper that details her discovery that the cells that produce insulin can be damaged over time by inflammation in the pancreas. The paper was published in the journal Diabetes, and was co-authored by Dr. Bruce Verchere (supervisor) and Dr. Jan Ehses.
“More and more, we’re coming to understand that the immune system plays an important role in type 2 diabetes,” Westwell-Roper says.
What did you discover as a result of your research?
There are several metabolic and neurodegenerative diseases in which proteins interact with each other to form clusters of proteins called amyloids that can activate the immune system. We discovered that an amyloid-forming protein produced by beta cells in the pancreas of patients with type 2 diabetes interacts with white blood cells involved in the inflammatory response. The unfortunate result of the interaction is the release of pro-inflammatory proteins that directly damage beta cells, and this limits their ability to produce insulin.
How will your discovery improve care for those who have or who are at risk of type 2 diabetes?
This discovery may mean a potential drug target for treatment of type 2 diabetes. Our data show – for the first time –the possibility of targeting inflammation to alleviate the decrease in insulin production that results from amyloid formation. This means potentially better long-term treatment for patients with type 2 diabetes.
How will this research help children in British Columbia?
The number of Canadians with type 2 diabetes is on the rise; the Canadian Diabetes Association estimates that in the next 15 years, the global incidence of type 2 diabetes in children will increase by up to 50 per cent. Type 2 diabetes can be treated, but it doesn’t go away; people who are diagnosed with type 2 diabetes as children are at greater risk of complications – including blindness – from the disease later in life, simply because they have it for longer. If we can target the inflammation that impairs insulin production in the cells, then maybe we can “turn down the dial” and provide therapeutic interventions to prevent long-term cellular damage.
What are your next steps?
We need to understand more about the types of immune cells found within the pancreatic islets in type 2 diabetes. Our work raises the possibility of therapeutically targeting white blood cells called macrophages to turn off their production of inflammation-producing proteins. This won’t be easy, and certainly has its own challenges. However, because of what we know about the benefits of anti-inflammatories in other tissues in obesity and type 2 diabetes, we’re hopeful that we’re headed in the right direction.