ADA 2016: Unlocking precision medicine to treat diabetes

June 14, 2016 | by City of Hope

Thurmond-Debbie Debbie C. Thurmond

The American Diabetes Association's 76th Scientific Sessions — the largest annual of gathering on diabetes research, treatment and care — got underway June 10 in New Orleans. The five-day convention is a massive affair with nearly 2,500 research presentations and 16,000 attendees.

Debbie C. Thurmond, Ph.D., a professor at Beckman Research Institute of City of Hope, will be among the presenters. Thurmond joined the faculty at City of Hope just under a year ago as founding chair of the Department of Molecular and Cellular Endocrinology. Her lab researches the biological mechanisms that lead to diabetes with an aim of finding therapies that can halt or prevent the disease’s progression.

We asked Thurmond about the research she will be presenting this weekend and what else she’ll be tuning into at the ADA conference.

The ADA conference attracts researchers and doctors from all over the world. What’s it like to be there?

It can be overwhelming, but invigorating. As a scientist and somebody who works at an institution that promotes the translation of basic science into treatments, it’s great to get to interface with so many clinicians and hear them talk. I’m getting feedback on what I can be doing to facilitate their conversations with patients about what’s coming down the pike. And I can ask them about the progress and complications they are seeing in patients.

You’re giving a talk as part of a session on Beta-Cell Stimulus-Secretion Coupling. What’s the thrust of this research, and your findings?

The cells that secrete insulin, beta cells, live in a tiny mini-organ called an islet in your pancreas. Islets are like a small sphere in the pancreas, a cluster of these beta cells.

In type 2 diabetes, years before a person is diagnosed — sometimes decades before — their beta cells show a defect in the functioning of how they secrete their insulin. The purpose of my talk is that we have found that these defective beta cells are lacking a particular protein that we call PAK1, which is required to keep beta cells functioning properly. About 80 percent of that protein is gone. We’re trying to understand why.

So, if you are an individual who has naturally lower levels of PAK1, does that make you more susceptible to becoming diabetic? The data I’m presenting says yes. We used mice genetically engineered to have little PAK1 in their pancreas. If we put them on a Western diet — one with a high fat content that mimics a lot of fast food meals — in a few months those animals became diabetic. The animals on a healthy diet may still have problems, but they don’t become diabetic.

What might that tell us about the rates of diabetes?

It could be that we’re seeing more people being diagnosed with diabetes and prediabetes because people might be carrying an underlying genetic defect related to these beta cells. Under ideal lifestyle and dietary conditions, the body can cope, but when we consume really bad food it can’t. Diet alone can bring out the worst in our genetics. And that could be an explanation for the huge surge in diabetes and prediabetes.

We also can screen people for PAK1 levels to see if they have a genetic predisposition. If so maybe you could protect them, or stop the progression from prediabetic to type 2 diabetes. Ultimately we need to prevent prediabetes, and here, we’ve found a potential point of intervention.

Are there other presentations you are looking forward to at ADA this year, and what about them interests you?

In my lab, we also study skeletal muscle function. So I’m actively engaged in those sessions too. Eighty percent of excess blood sugar in your bloodstream is absorbed by the skeletal muscle. It is a huge reservoir for the excess glucose. Another name for prediabetes is insulin resistance, which is when the skeletal muscle is no longer doing that job.

In the field of diabetes and prediabetes care, there’s a problem brewing: a number of the drugs used for the last 10 years are being withdrawn from markets because of some severe complications. These drugs are called insulin sensitizers. Depending on how you count, it is estimated that 44 percent of the U.S. population could be considered prediabetic. The conservative number is 30 percent. So we have a huge population of people left without treatment options.

What kind of progress can people with diabetes expect to see in the coming years in terms of new forms of treatment?

Precision medicine. Diabetes is actually a spectrum of disease, which is why we need so many treatment options. Looking at people’s individual genetic signature will give us insight into what’s happening with their physiology. I think what you’re going to be seeing are more treatment strategies that are aimed at dealing with precision-based diagnoses.
It is so easy for people to get themselves genotyped now — so that could be a change we see very soon. 

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