The Dialogue of Diabetes with Decio Eizirik, MD, PhD

Over the past 60 years, the incidence of type I diabetes in parts of the word has increased sixfold, and we don't know why. In the Eizirik Lab at the Indiana Biosciences Research Institute, Dr. Decio Eizirik and his team research type 1 diabetes in a way that not many others do. Press play to discover:

• How might the bacteria in our guts relate to type I diabetes?
• What role genetic predisposition versus environmental factors play in the manifestation of clinical type I diabetes, and how to identify high-risk patients
• What is indicated by the manifestation of type I diabetes later in life

Type I diabetes is an autoimmune disease wherein the immune system begins recognizing pancreatic beta cells as foreign, and attacks and destroys them as a result. As the disease progresses, the type 1 diabetes patient will lose most of their pancreatic beta cells, which are responsible for the production of insulin. Consequently, these patients become dependent upon insulin for the rest of their lives, often requiring continuous glucose monitoring and multiple insulin injections per day.

Most research on this disease has focused primarily on the immune system, but in the Eizirik Lab, the focus is more on the pancreatic beta cells, and the dialogue between these cells and the body's immune system. It is Dr. Eizirik's goal to qualify the words that comprise this dialogue, to understand why and when it goes wrong, and to determine whether there's a way to make this dialogue more 'polite.'

Dr. Eizirik discusses the details of his research and more, including the specific functions of beta cells, therapies that target the T cells of the immune system, attempts at combining therapies and reeducating the immune system, the role of extracellular vesicles, chemokines, and cytokines in the dialogue between beta cells and the immune system, and the possibility of natural beta cell regeneration.

https://www.indianabiosciences.org/eizirik/research Available on Apple Podcasts: apple.co/2Os0myK