What is your presentation about?
This presentation is one side of a debate that considers whether hyperinsulinemia is a cause of type 2 diabetes. I will present data from pre-clinical animal models and human studies that illustrate a primary, causal role for hyperinsulinemia in obesity, insulin resistance, beta-cell stress, and therefore, ultimately, dysglycemia and type 2 diabetes. I will argue for a broad definition of beta-cell dysfunction that includes both excess and insufficient insulin secretion, and I will provide recommendations for research directions and clinical practices in the future.
What makes this topic important in 2022?
Insulin was discovered 101 years ago in Canada, but we still do not fully understand the extent of its causal role in diabetes. This topic is timely because multiple therapeutic interventions (dietary, pharmacological, surgical) that enable diabetes treatment, and even remission, may work at least in part by lowering excess insulin levels.
How did you become involved with this area of diabetes research or care?
I came to this area by accident, as an islet biologist studying the phenotype of mice that produce less insulin, and are therefore genetically incapable of sustained hyperinsulinemia. This loss-of-function approach has illuminated a key physiological mechanism of obesity, insulin resistance, fatty liver, beta-cell stress, premature aging, and cancer susceptibility.
What are you most looking forward to at the 82nd Scientific Sessions?
I’m looking forward to lively debate that will help move the field forward and I am looking forward to connecting with many cherished colleagues.