While the symptoms and treatment of type 1 and 2 diabetes may overlap, the origins of each significantly diverge. Type 1 diabetes pathogenesis is an autoimmune-driven story, and in this podcast, Todd Brusko offers listeners a clear and precise description of the latest understanding of the disease and how scientists are working for a type 1 diabetes cure.
Listen and learn
Todd M. Brusko is an associate professor within the Diabetes Institute at the University of Florida. He and Richard have an enriching and lively conversation in this podcast about Dr. Brusko’s field of study: the genes and biomarkers involved in type 1 diabetes and how the immune system responds in people with higher risk.
He says that the most apparent biomarkers are antibodies, but they’re not the end of the story. As a T-cell–driven autoimmune disease, it’s vital to assess how T-cells develop and understand the part they play. So, like most diseases that have stayed with us, researchers must grapple with these complex and different paths to disease diagnosis.
The variability of when one can develop these autoimmune type 1 diabetes symptoms is immense—from early childhood to old age. Typically, doctors see a peak in diagnosis right before puberty. But it’s complicated: the biomarkers are usually present well before the disease exhibits symptoms and there’s usually a triggering event that causes the disease to fully present itself.
He says researchers have followed a long-standing interest in viral infections as a triggering factor, acting to break the autoimmune tolerance. Something occurs, he adds, whether an underlying genetic susceptibility or an environmental event that triggers this autoimmune attack. Studies show that at inception, the insulin-producing beta cells have their “flags up,” and the immune system reacts. He also describes promising research into type 1 diabetes treatments, from delaying the disease to prevention and cures.
For more, see his lab’s website: bruskolab.diabetes.ufl.edu.
Available on Apple Podcasts: apple.co/2Os0myK
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