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Aaron Vinik Part 1, INGAP Research

In part 1 of this Exclusive Interview, Dr. Aaron Vinik talks with Diabetes in Control Publisher Steve Freed during the AACE 2017 convention in Austin, Texas about the current progress of INGAP and the challenges yet to be overcome.

Aaron Vinik, MD, PhD, FCP, MACP is the Director of Research and Professor of Medicine, Pathology and Neurobiology at Eastern Virginia Medical School in Norfolk, Virginia. His his research and recent discovery of a gene, INGAP, could prove to be a cure for diabetes.

Transcript of this video segment:

Steve Freed: Diabetes in Control and we’re here with a very special guest Doctor Aaron Vinik who’s very well known and I don’t think there’s a paper that doesn’t have his name on it. And we’ve interviewed Dr. Vinik in the past and you can go to our website and see some other interviews.  What really got me interested in meeting Dr. Vinik is I read a research paper called INGAP and when I read this paper, I thought this might be the cure for diabetes and I had to interview this guy. So, he’s my favorite interviewee he makes it interesting and you’ll see for yourself. So maybe that would be the first question even though you’re here presenting, we’ll talk about that. The first question is, where is that research on INGAP today?

Dr. Vinik: Thanks very much. Thanks for all the nice remarks you’ve made. I think you’ve just being making those remarks over and over to all the people you’ve interviewed so I don’t feel special even though you tried to make me feel special, it’s okay with me. (laughter) So INGAP is alive and well. The biggest problem, I think, with INGAP is a very simple problem but a difficult one to overcome. We’ve now have shown in different animal models, including the original work that was done on guinea pigs, and the work that we did in rabbits, and then in dogs, then in monkeys and finally in humans. So we went up the scale and none of the species were resistant to the ability of INGAP to stimulate growth of proliferation of pancreatic beta cells and complete islets, which is what we really wanted.You know, we’re in the era now that we’re beginning to realize that diabetes is not a disease of a single hormone. It’s not an absence of relative deficiency of insulin anymore. It’s complex and I think you probably interviewed Ralph DeFronzo, he’s one of the awardees at this meeting. He started off with a duo, then a trio, a quartet, and a pintet, and a sextet, and a septet and an octet and I just recently added two more to his and called it the dreadful dectet.

So there are 10 different biological abnormalities that occur in diabetes now, so we’re learning a whole lot about the condition that we didn’t know before. So, basically if you think of what is required, a lot of people are trying just to stimulate stem cells to grow into beta cells to make insulin. We realized that was very wrong. You have to stimulate a stem cell to grow and differentiate into a whole islet so it will make not only the insulin, but it can make the counter-regulatory hormones like glucagon. And that has advanced incredibly. Since the early days of when Roger Unger spoke about the work on glucagon and spoke about the rediscovery of the role of glucagon. It has now grown into glucagon and glucagon-like peptides and what are really important for the constituents of the management of diabetes. But in addition to that, how we’re beginning to understand the need to have the counter-regulation so that if I get you to grow new islets, I need you to grow not only insulin cells but glucagon cells so we can balance up every time your blood sugar falls, you have the hormone that will bring it back up again. And that’s really important. First, we can do that. We’ve done it in the animal models and we have beautiful pictures now as we have increased and enhanced our capabilities of capturing all these cells histochemically. But when I looked at programmed cell death, or apoptosis or Hara-kiri, as some people would call it, these new formed islets are still subject to the same destructive forces that are present in both type 1 and type 2 diabetes and it’s a very sad thing because otherwise it would’ve been a piece of cake and it would’ve been done along time ago. We’ve tried different molecules, some that looked promising but have yet failed to fulfill their promise.

The people who have licensed INGAP from Eastern Virginia Medical School are fighting furiously to come up with an appropriate molecule. Jerry Adler, who has come to us from the University of Virginia and joined Eastern Virginia Medical School, has used one of these anti-inflammatory agents in combination with INGAP and achieved a 75% remission rate in the NOD mouse, which is about as good as you can get. The trouble with the molecule that he’s got as an anti-inflammatory molecule is it’s toxic to humans. So, we are still wrestling with that and although I would like to say we’re close, it still alludes us, just that anti-inflammatory molecule. So, the one arm is fulfilled but the other arm we are waiting for and I’m not going to make you any promises because a lot of people are trying to make molecules that will actually neutralize the destructive forces that are present in our bodies.