In part 3 of this Exclusive Interview, Raghu Mirmira talks with Diabetes in Control Publisher Steve Freed about the two approaches from which a cure from type 1 might come.
Raghu G. Mirmira, PhD, MD is the director of pediatric research at Indiana University.
Transcript of this video segment:
Freed: So, if they asked you to look into the future from your knowledge — a cure for type 1 is around the corner, my personal feeling. We’re doing so much research and we’re learning so much. And it’s kind of simple, you replace the beta cell with a bunch of beta cells and you’ve cured it. Type 2 is another type of disease. It has to do with obesity. And education — and there’s just so many things involved that it’s a whole nother disease. Technically, they shouldn’t even be called diabetes, the same, because they’re completely different. So, where do you think the type 1 cure may come from?
Mirmira: So, that’s a great question. I think one of the things that we have to sort of temper in some respect on our enthusiasm is that as you pointed out that type 2 is kind of complex because there’s so many variables in type 2 diabetes. One of the points of my talk tomorrow is really sort of emphasizing that type 1 diabetes is probably as just as diverse and complex in many ways, because all of the things that we thought about the disease, being an autoimmune disease, an attack on beta cells, is really not entirely true across the board. And so, different individuals exhibit different what we call phenotypes. So, the reality is that it turns out that one size will probably not fit all in type 1 diabetes. And so, this big push internationally for personalized medicine, I think applies as much to type 1 as it does to type 2. And so, where will the cure come from? I think that one thing is sure and that is that we do need more beta cells, at least more functional beta cells in type 1 diabetes. And if we’re talking about a real cure, I think it will come from two angles. Angle one would be how do we increase the numbers or functions of beta cells that remain, and then the other angle is how do we keep the immune systems at bay. Once it gets activated, it’s going to — every time there’s new beta cells it’s going to see them. So, really the question will be the two approaches. We’re going to have to think about beta cells and how we can hide them from the immune system. And we’re going to have to think about the immune system and how to keep it at bay. And that’s really the point of my talk tomorrow is that it’s more than just the amount of autoimmune disease. We’ve got to think about the beta cells.
Freed: It’s interesting. I appreciate you sharing that information.
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