Omid Veiseh, PhD, Bioengineer at Rice University talks about a new implant that could be replacing monitors and insulin pumps for patients with type 1 diabetes.
Interview conducted by Ivanhoe Broadcast News in 2022.
You’re helping the immune system fight some of the deadliest diseases?
VEISEH: Yeah. So, we’re interested in harnessing the power of the immune system to repair tissue, to fight cancer, to manage infections, and we want to tap into that and focus its efforts towards mediating the diseases.
It seems like we’ve come a long way because now I’m hearing a lot about this. It’s not about let’s pump more drugs into your system to see how we can fight it. It’s more like let’s let everybody fight their own battle inside them.
VEISEH: Yes, certainly. I think medicine has become a lot more personalized and in particular with these debilitating immuno diseases like type one diabetes where the immune system has gone haywire and has started attacking its own insulin producing cells, we’re working on innovative ways to prevent that and to replace the damaged tissues.
It’s funny because type one diabetes, I mean, it’s only been 100 years since insulin was developed. You just celebrated that, right?
VEISEH: That’s correct, by some Canadian researchers banning. So, it was a very pivotal discovery that really revolutionized treatment for these patients.
It seems like in the past 100 years, you’ve done a lot. Scientists have done a lot to help the problem, but not fix it because you’ve got all these monitors now, these glucose devices that you put on the outside of your skin and you watch it through your watch, and you do all this, but nothing to battle the disease inside.
VEISEH: Yeah, and that’s exactly true. For a patient, of course, they’re well, better off now, now they’re living longer and there is a remedy. It’s not a cure and when you talk to patients, we learn that all of these devices, while helpful, it’s also a constant reminder of the disease, the burden that they have to carry. So long term, we hope that we can have the body regulate its own blood glucose. That’s only possible by replacing those cells that have been lost. We need to think about tissue engineering strategies like the ones my lab has been working on to help protect these cells from the host immune system and create the environment around them that enable these cells to live, to sense the blood glucose and secrete insulin in a manner that matches the physiological needs.
So, when you’re talking about T1D I’m going to just back up for one second and talk about how it is all boils down to beta cells in the pancreas not working like they should.
VEISEH: Yeah. So, diabetes is a big disease. There are different types of diabetes. I think most people are familiar with type two, which is a lifestyle disorder, which the body has too much insulin, but in type one patients, it’s the exact opposite where the immune system has destroyed their insulin producing cells and they have no insulin. Instead, they have to self-monitor their blood glucose and replace the function of the pancreas manually through insulin injections.
So, what you’re trying to do is?
VEISEH: What we’re trying to do is leverage beta cells that are now possible today. In the last five years, there’s been remarkable progress in innovative ways where you can take stem cells from a universal donor and in a lab grow these into beta cells. These are the cells that have specialized function in their abilities to sense blood glucose and secrete insulin. We want to now use these cells, combine them with innovative tissue engineering strategies that protect them from the host immune system because if we just administered the cells back in, they would be killed just like the patient’s own original cells. If we can provide a scaffold that protects them from the host immune system, but also includes blood vessels that are engineered to surround these beta cells, now they can be connected to the host vasculature system. We can get good measurements, the cells can get good measurements of the blood glucose and secrete insulin, replacing the need to have handheld monitors or insulin injections. We think that this is the closest that’s possible to a cure.
How would you get the scaffolding and the cells to the right place? How does that all work?
VEISEH: So, what we’re imagining as our first-generation product is an implant that would be placed in the intraperitoneal space.
You’ll have to break that one down for me.
VEISEH: So, it’s an implant that would be placed in the stomach area. There’s quite a lot of space within the organs. That site is nicely vascularized itself, and it connects nicely with various organs, including the liver. So, we think that because of the conditions of that site, an implant that is specifically engineered to house these beta cells using our scaffolding strategy to keep these cells protected from the host immune system and provide them with the nutrients that they need to survive could be a feasible strategy. So, we hope that these implants could last for many, many years. After every maybe 5 to 10 years, patients could come in and have the old implant taken out and a new one put in. Instead of having to do daily treatments, it would be perhaps a once every five-year option.
That’s amazing. So, the beta cells would live for 5 to 10 years. They don’t die?
VEISEH: Yeah. In fact, there’s good proof of concept of this working in the clinic today. There’s something that’s available for patients. It’s called the Edmonton Protocol, another group of Canadians that have pioneered this area of research. So, the Edmonton Protocol consists of taking beta cells from cadaveric donors. So, these are islet cells that you extract from a deceased patient, and then we can re-administer these to a type one diabetic recipient that is already immunosuppressed. So, this happens when patients have had other transplants, perhaps a kidney transplant because of complications from type one diabetes. What’s remarkable here is that when these patients receive these transplants, they’re in some cases 15 years now insulin independent, meaning that these cells do work. They can kick in. They can restore the glycemic control that these patients need. The challenge, though, is immunosuppression is deleterious to the quality of life and not everybody qualifies for it and it has so many complications. Our solution is to get rid of the immunosuppression. By creating a biomaterial scaffold around ourselves, we can protect them from the immune system without the need to have widespread immunosuppression throughout their body.
Now you’ve already tried this in animals.
VEISEH: Yes.
How is that?
VEISEH: We’ve done several animal studies which are looking very encouraging. We’ve gone out now in rodents. They don’t live very long, but we’ve gone out for the foreseeable lifespan of a rodent, a type one diabetic rodent, which is about six months. They seem to be functioning just as well as a healthy pancreas would.
Now do you ever think about this as like we get this person on these implants and they stay on it for a while, will their beta cells ever start working normally? Will they need another implant someday?
VEISEH: Unfortunately, their own beta cells which have been killed off by the immune system, those aren’t going to come back. So, they need to be replaced.
You’re born with just your exact amount of beta cells? Is that how?
VEISEH: There’s a bit of cell division that can happen. In general, there’s a finite amount of beta cells in everybody and if those get killed off for reasons like type one diabetes, then unfortunately they do not repair themselves unlike other organs like the liver. Unfortunately, the pancreas does not have that ability.
Is there a number to those beta cells? Like 30 million or like?
VEISEH: We think that it would take about half a billion cells to treat a patient and that’s replacing what normally would have existed in their body.
Is that what goes into the implant, like how many cells?
VEISEH: Yeah. So that’s about the number of cells that goes into an implant and the hope is to create these implants that are of the size of perhaps a ping pong ball. That’s the size of an implant that we’re aiming to build.
That’s amazing. We keep hearing the fact that these vascular structures that you’re making, what are they made of? Why does that thing protect the beta cells?
VEISEH: So, we work with hydrogels and people might be familiar with Jell-O perhaps. So, structures like hydrogels contain a lot of water. That is good for keeping these cells alive. At the same time, they have a porous mesh around them. It’s almost like a filter and immune cells are relatively big. So, this mesh keeps the immune cells out and at the same time, nutrients, and oxygen as well as the insulin, can diffuse in and out of these biomaterial constructs. That’s what protects them from the host immune system.
I was talking to a researcher a while ago and they were talking about another type of diabetes that can be down the road, which would be type three or four, which is basically about your brain and how that could be part of Alzheimer’s. Does any of this ever go into that kind of study as well?
VEISEH: So, when we think about diabetes in particular, type one, what is the consequence of not having proper blood glucose correction? Even with the best tools that exist today for most patients, most of the day, the patients are not at the appropriate blood glucose levels. They’re either too high or too low. These implants, because of their self-regulating feature, allows you to maintain that consistency that the body needs. Of course, there’s going to be long term complications because of the mis-regulation that exists for patients today. There could be damage to heart or the brain or several different organs. Ultimately in the future, what we think is implants like ours that could really replace the need to do all of that.
Could save you from not just diabetes, but those people having heart problems or dementia so.
VEISEH: Yeah, exactly. I think we can dramatically not just alleviate the burden but also allow people to live longer, healthier lives because of improved blood glucose correction.
Do you have any specific numbers on your rodent studies at all? Like 90% of the rodents showed no insulin problems or?
VEISEH: I think in the rodents, when we get it to work, it works in every one of them. I think it’s just we’re in this situation where we’re focused on the duration. We could do a quick segment on like duration maybe, but I think what’s practical today is, we think these implants could last for perhaps many years. We have data that goes out to six months. Even at six months, I think when you talk to most patients, that’s probably the cutoff where if it lasted for six months, they would consider a procedure like this. If it was any shorter, maybe not, but any longer, even more likely.
I think something like this too, it doesn’t work, it’s not going to kill you. You’re just going to go have to take insulin.
VEISEH: Exactly. So, you know, and of course, we’ll have to do clinical trials to determine how this is going to work in patients. When we develop these systems, our number one priority is safety and making sure that these don’t cause any problems. So, the risk is it may not work and then the patients will, you know, still can, of course, to use the current treatments and we can always take the device out. That’s the beauty of that approach like this.
END OF INTERVIEW
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