We take a look at some of the exciting diabetes research developments announced in October, and what the findings could mean for people living with or affected by diabetes.
In this month's article:
- A step forward in making insulin 'smarter'
- World-first stem cell transplant helps person with type 1 diabetes produce insulin
- Regenerating cells with electrical impulses in people with type 2 diabetes
- New driver of diabetic retinopathy discovered
A step forward in making insulin ‘smarter’
A new type of ‘smart’ insulin has shown promise in early-stage research. In animals, the insulin was found to only turn on when blood sugar levels are high and stay off when levels are low.
Millions of people with all types of diabetes in the UK use insulin to manage their blood sugar levels. This requires a careful balancing act and it’s difficult to get right. So, scientists are trying to develop cleverer insulins that can sense blood sugar levels and respond in the right way. This would make life for people with diabetes dramatically simpler.
In new research published in Nature, an international research team tested a new type of ‘smart’ insulin they’ve developed, called NNC2215. It has a special molecular switch.
When blood sugars are low, a molecule called glucoside locks NNC2215 in the ‘off’ position so it won’t lower blood sugars further. When blood sugar levels rise, glucose (sugar) in the blood replaces the glucoside, switching NNC2215 ‘on’ so it will bring blood sugars down.
In studies with rats and pigs, researchers found NNC2215’s switch worked as they’d hoped. It was able to turn on and off in response to changing blood sugar levels. And it was as effective as regular insulin at lowering high blood sugar, without causing it to drop too low.
NNC2215 hasn’t been tested in humans yet, and there will be many more steps before it could be. But these findings are encouraging.
Dr Elizabeth Robertson, our Director of Research, said:
“This research represents a significant step forward in the global effort to develop the next generation of ‘smart’ insulins. The hope is that these will ease the constant challenge of managing blood sugar highs and lows, and improve the physical and mental health of millions of people worldwide with diabetes who rely on insulin therapy.
"We’re excited to part of this endeavour through our Type 1 Diabetes Grand Challenge programme.”
World-first stem cell transplant helps person with type 1 produce insulin
A new type of stem cell treatment, created from a person’s own cells, is showing early promise in allowing people with type 1 diabetes to make their own insulin.
Stem cells are like shape-shifters - they can turn into almost any type of cell the body needs. In the quest for new treatments and a cure for type 1 diabetes, scientists have been working to turn stem cells into insulin-making beta cells.
The hope is these stem cells-turned-beta cells could replace those that have been destroyed by the immune system in people with type 1 diabetes.
Until now, most clinical trials of stem cell therapies in people with type 1 diabetes have used donor stem cells. Because these stem cells are foreign, trial participants need to take immunosuppressant drugs to prevent their immune system from recognising and destroying them. These drugs come with significant side effects.
In a new study, published in Cell, a 25-year-old woman with type 1 diabetes became the first person in the world to receive a stem cell transplant created from her own cells. Scientists hope that this approach could reduce or eliminate the need for immunosuppressants.
Researchers at Peking University, Beijing, extracted cells from the participant and used chemicals in the lab to make what are known as chemically induced pluripotent stem cells. They then reprogrammed the stem cells to become beta cells, and injected around 1.5 million into the woman’s stomach.
Two-and-a-half months after this procedure, the woman’s new beta cells were producing enough insulin for her to stop insulin injections. A year later, she was still producing her own insulin, and her blood sugars were in range for 98% of the time. The researchers also didn’t see any major safety concerns.
This is an important and exciting development in stem cell therapies for type 1 diabetes. But the participant in this trial was already taking immunosuppressants because of a prior liver transplant. This means we can’t be sure if the new type of stem cell procedure alone was the reason she didn’t reject the transplanted cells, or if the immunosuppressants played a role.
So far, two other participants have also had the stem cell procedure, and the researchers are set to report their results soon. There will then need to be more studies, with more people to check if and how well the treatment works.
To speed up progress and get us to effective beta cell therapies quicker, we’re investing in cutting-edge research through the Type 1 Diabetes Grand Challenge.
Regenerating cells with electrical impulses in people with type 2 diabetes
Some people with type 2 diabetes were able to stop taking insulin after receiving a new procedure, which uses electrical impulses to improve the body’s response to insulin, alongside the blood sugar lowering medication semaglutide.
Researchers at the Amsterdam University Medical Centre ran the first trial of a new treatment, called Recellularisation via Electroporation Therapy (ReCET). It aims to improve the body’s sensitivity to its own insulin using pulsed electrical fields that target cells in the gut involved in blood sugar control.
The idea is to regenerate these cells, making them better at using insulin and bringing down blood sugar levels.
In the trial, 14 people living with type 2 diabetes had the ReCET procedure, which is done under sedation. They then began taking an existing type 2 diabetes medication: semaglutide, a GLP-1 agonist. This medication helps the body to produce more insulin.
Participants were followed up at six, 12 and 24 months. The study was set up to look at the safety of the ReCET procedure and promisingly there weren’t any serious safety concerns reported.
Over the two years, 12 of the 14 people (86%) no longer needed to take insulin to keep their blood sugars stayed in a target range.
This is exciting. But we need to keep in mind this was an early safety study, and the research wasn’t designed to look at the treatment’s effectiveness. As participants were taking a GLP-1 medication it also isn’t clear if the ReCET procedure gave any additional benefit.
Next, it will be important to compare ReCET with other existing type 2 treatments in head-to-head trials, including against GLP1-s alone.
We’ll also need to see if any benefits last longer term and which groups of people with type 2 it could hold potential to help. The team are already working on more studies, so answers will be coming.
Dr Celine Busch, lead author of the study, said:
“These findings are very encouraging, suggesting that ReCET is a safe and feasible procedure that, when combined with semaglutide, can effectively eliminate the need for insulin therapy.”
These results were presented at United European Gastroenterology Week (UEGW) 2024 in Vienna.
New driver of diabetic retinopathy discovered
With our funding, researchers at Queen’s University Belfast have uncovered a new factor that could help explain why diabetic retinopathy progresses and causes vision problems. The research shows a protein, called Pentraxin 3 (PTX3), might be driving harmful inflammation in the eyes of people with diabetes.
Diabetic retinopathy is a common complication of diabetes caused by high blood sugar levels damaging blood vessels in the eye. Inflammation can make this eye damage worse, but scientists haven’t been sure what causes it.
Recent evidence has shown that PTX3 is made in the eye, so our researchers led by Professor Reinhold Medina delved into its role in retinopathy for the first time. They compared two groups of mice with diabetes: one group who had PTX3 in the retina and a second group who didn’t make the protein. The researchers monitored the mice over nine months.
The researchers found that the mice without PTX3 showed less eye damage. These mice had fewer signs of inflammation in the retina and better vision, compared to the PTX3 mice. In the PTX3 mice, they saw that the protein activated certain cells that cause swelling.
The team then looked at samples from people with diabetic retinopathy and found that PTX3 levels were higher in people with more severe eye problems. These results suggest that PTX3 is involved in retinopathy progression by fuelling inflammation in the eye.
This knowledge opens the door to developing new treatments that target and block PTX3.
Dr Lucy Chambers, our Head of Research Communications, said:
“Eye problems are a frightening and too frequent complication of diabetes. By advancing our understanding of the biological factors contributing to eye damage, this research could take us closer to new and better treatments that help more people with diabetes avoid devastating harm to their sight.”
