Smart Insulin and Stem Cell Transplantation: Research Highlights October 2024

This month's articles:

A step towards making insulin “smarter”

A new type of “smart” insulin is showing promise in early-stage research. In animals, insulin I found that it only turns on when my blood sugar levels are high and stays off when my blood sugar levels are low.

In the UK, millions of people with all types of diabetes use insulin to manage their blood sugar levels. This requires careful balancing and is difficult to get right. So scientists are trying to develop smarter insulins that sense blood sugar levels and respond in appropriate ways. This will dramatically simplify the lives of diabetics.

In new research Published in Nature magazinean international research team tested a new type of “smart” insulin they developed called NNC2215. Equipped with a special molecular switch.

When blood sugar levels are low, molecules called glucosides lock NNC2215 in the “off” position, preventing blood sugar levels from dropping further. When blood sugar levels rise, glucose (sugar) in the blood replaces glucosides, turning NNC2215 “on” and lowering blood sugar levels.

In studies using rats and pigs, researchers found that NNC2215's switch worked as expected. It could be turned on and off depending on changes in blood sugar levels. And it was as effective as regular insulin without lowering high blood sugar too much.

NNC2215 has not yet been tested in humans, and many more steps are needed before it can be tested. However, these findings are encouraging.

Dr Elizabeth Robertson, our research director, said:

“This research represents an important step forward in the global effort to develop the next generation of ‘smart’ insulin. These are expected to alleviate the constant challenge of managing high and low blood sugar levels and improve the physical and mental health of millions of diabetics around the world who rely on insulin therapy. I am.

“We are excited to be a part of this effort through this initiative. Type 1 Diabetes Grand Challenge Program”

World's first stem cell transplant boosts insulin production in type 1 patients

A new type of stem cell therapy made from one's own cells is showing early promise in treating people with conditions such as: type 1 diabetes This is because they make their own insulin.

Stem cells are like shapeshifters and can transform into almost any type of cell your body needs. In the pursuit of new treatments and cures for type 1 diabetes, scientists have been working to convert stem cells into insulin-producing beta cells.

It is hoped that these stem cells, which have become beta cells, will replace stem cells destroyed by the immune system of patients with type 1 diabetes.

To date, most clinical trials of stem cell therapy for patients with type 1 diabetes have used donor stem cells. Because these stem cells are foreign, trial participants must take immunosuppressants to prevent the immune system from recognizing and destroying the stem cells. These drugs come with serious side effects.

In a new study, Published in cella 25-year-old woman with type 1 diabetes has become the first person in the world to receive a stem cell transplant made from her own cells. Scientists hope this approach could reduce or eliminate the need for immunosuppressants.

Peking University researchers extracted cells from the participants and used chemicals in the lab to create chemically induced cells known as pluripotent stem cells. They then reprogrammed the stem cells to become beta cells and injected about 1.5 million of them into the woman's stomach.

Two and a half months after the procedure, the woman's new beta cells were producing enough insulin to be able to stop taking insulin injections. A year later, she was still producing her own insulin and her blood sugar levels were within range 98% of the time. The researchers also found no significant safety concerns.

This is an important and exciting development in stem cell therapy for type 1 diabetes. However, the participants in this trial had previously undergone liver transplants and were already taking immunosuppressants. That means we can't be sure if the new type of stem cell treatment was the only reason she didn't reject the transplanted cells, or if the immunosuppressants played a role.

So far, two other participants have also received stem cell treatments, and researchers expect to report their results soon. If that's the case, more studies with more people will be needed to see if and how well the treatment works.

We invest in cutting-edge research to accelerate progress and bring effective beta cell therapies to market faster. Type 1 Diabetes Grand Challenge.

Cell regeneration with electrical impulses in type 2 diabetic patients

some people have type 2 diabetes I was able to stop taking insulin after undergoing a new procedure that uses electrical impulses to improve my body's response to insulin alongside blood sugar-lowering drugs. Semaglutide.

Researchers at the University Medical Center Amsterdam have conducted the first trials of a new treatment called recellularization by electroporation therapy (ReCET). It aims to improve the body's sensitivity to its own insulin using pulsed electric fields that target cells in the intestine involved in blood sugar control.

The idea is to regenerate these cells to improve insulin use and lower blood sugar levels.

In this study, 14 people with type 2 diabetes underwent ReCET surgery, which was performed under sedation. They then started taking semaglutide, an existing type 2 diabetes drug. GLP-1 agonist. This drug helps the body produce more insulin.

Participants were followed up at 6, 12, and 24 months. This study was set up to examine the safety of the ReCET procedure and it is expected that no significant safety concerns will be reported.

Over two years, 12 out of 14 people (86%) no longer needed to take insulin to keep their blood sugar levels within their target range.

This is exciting. However, it should be noted that this is an early safety study and the study was not designed to examine the effectiveness of the treatment. It is also not clear whether the ReCET procedure provided any additional benefit, as the participants were taking GLP-1 drugs.

Next, it will be important to compare ReCET with other existing type 2 treatments in head-to-head trials, including comparisons with GLP1-s alone.

We also need to see if any benefits are long-lasting and which Type 2 people it might help. The team is already working on further research, and the answer may be clear.

Dr Celine Bush, lead author of the study, said:

“These findings are very encouraging and suggest that ReCET is a safe and viable procedure that, when combined with semaglutide, can effectively eliminate the need for insulin therapy.”

These results were presented at the 2024 European Gastroenterology Week (UEGW) in Vienna.

Discovery of new cause of diabetic retinopathy

With our funding, researchers at Queen's University Belfast will discovered a new factor that may help explain why diabetic retinopathy It progresses and causes visual impairment. This study shows that a protein called pentraxin 3 (PTX3) may be causing harmful inflammation in the eyes of people with diabetes.

Diabetic retinopathy is a common complication of diabetes caused by damage to blood vessels in the eye due to high blood sugar levels. Inflammation can worsen this eye damage, but scientists aren't sure what causes it.

Researchers led by Professor Reinhold Medina have for the first time taken a closer look at the role of PTX3 in retinopathy, as recent evidence has shown that PTX3 is produced within the eye. They compared two groups of mice with diabetes. One group has PTX3 in the retina, and the other group does not make the protein. The researchers observed the mice for nine months.

The researchers found that mice lacking PTX3 had less eye damage. These mice had fewer signs of retinal inflammation and better visual acuity compared to PTX3 mice. In PTX3 mice, this protein was found to activate specific cells that cause swelling.

The research team then looked at samples from people with diabetic retinopathy and found that those with more severe eye problems had higher levels of PTX3. These results suggest that PTX3 is involved in the progression of retinopathy by promoting ocular inflammation.

This knowledge opens the door to the development of new treatments that target and block PTX3.

Dr Lucy Chambers, our Head of Research Communications, said:

“Eye problems are a very frequent and frightening complication of diabetes. By advancing our understanding of the biological factors that contribute to eye damage, this research will help more diabetics suffer from the devastating effects on their vision.” We may be on the way to new and better treatments that can prevent harm.”