We take a look at some of the exciting diabetes research developments announced in November 2025, and what the findings could mean for people living with or affected by diabetes.
In this month's article:
- New clues to why type 1 diabetes is more aggressive in young children
- Replacing beta cells and resetting the immune system to treat type 1
- New drug could help prevent sight loss in people with diabetes
New clues to why type 1 diabetes is more aggressive in young children
With funding from the Type 1 Diabetes Grand Challenge, Professor Sarah Richardson and her team have made a major breakthrough in understanding why type 1 diabetes is more aggressive in young children. They discovered that nearly all their insulin-producing beta cells are destroyed before the cells can mature.
In young children, especially under age seven, the immune system’s destruction of beta cells typically happens very quickly. This raises the risk of needing emergency care at diagnosis and makes the condition harder to manage.
Until now, scientists have struggled to study how beta cells develop in early life. Young children have many tiny clusters of pancreas cells that are still forming.
In a new study in Science Advances, Professor Richardson and team used advanced techniques to study these small clusters in rare pancreas samples from over 250 people of different ages, with and without type 1 diabetes.
They found that in children without diabetes, these small clusters are plentiful and grow rapidly in the first years of life.
But in children with type 1 diabetes, these small clusters were almost completely missing – destroyed by the immune system before they had a chance to grow.
Some people diagnosed at older ages kept a few larger cell clusters and could still make small amounts of insulin, but this was not true for young children.
The findings suggest that these early, small clusters are especially vulnerable to the immune attack. Their rapid destruction prevents them from maturing, leaving very few beta cells later in life. This explains why children diagnosed young typically produce no insulin of their own.
This research highlights how important these early clusters are for healthy pancreas development and points toward new treatments to protect them. It also strengthens the case for early screening in children to identify type 1 diabetes before these crucial cells are destroyed.
Professor Sarah Richardson said:
“These tiny insulin-producing beta cell clusters – once overlooked – hold big clues to understanding type 1 diabetes. This new perspective has the potential to reshape how we screen, treat, and even prevent type 1 diabetes. Protecting small beta cell clusters early could be key to stopping type 1 diabetes before it starts.”
Replacing beta cells and resetting the immune system to treat type 1
An early new study in mice offers hope for a potential new way to prevent or even cure type 1 diabetes.
The treatment from researchers at Sanford Medicine uses a combination of blood stem cells and pancreas cells, called islets, from donors.
To cure type 1 diabetes, scientists – including those funded by Diabetes UK and the Type 1 Diabetes Grand Challenge – are working on ways to replace insulin-making beta cells destroyed by the immune system.
One option is islet transplants, where clusters of cells from a donor pancreas are given to someone with type 1 diabetes. But when someone receives donor cells from another person, the body naturally fights them off. And in people with type 1, the immune system is programmed to seek out and destroy beta cells. So, strong immunosuppressant drugs are needed to try to halt this, which can have serious side effects.
To get around the need for immunosuppressants, the Stanford team innovated a new approach.
Alongside giving a transplant of donor islet cells, they used donor blood stem cells – which can help build a new immune system.
They gave the two types of donor cells to mice that either already had type 1 diabetes or were at high risk of developing it, and added an immunotherapy drug to the treatment. This allowed the donor blood stem cells time to settle in and mix with the mice’s own cells, creating a ‘hybrid immune system’.
This seemed to ‘reset’ their immune system so that it didn’t attack the donated islet cells. As a result:
- 19 out of 19 mice were protected from developing type 1 diabetes
- All nine mice with existing type 1 diabetes were able to stop insulin therapy and produce their own insulin throughout the six-month study, without immunosuppressants.
Importantly, all the drugs and methods used in the mice are already used in human medicine.
Professor Seung K. Kim, who led the study, said:
“The possibility of translating these findings into humans is very exciting. The key steps in our study – which result in animals with a hybrid immune system containing cells from both the donor and the recipient – are already being used in the clinic for other conditions. We believe this approach will be transformative for people with type 1 diabetes.”
While more work is needed to understand the safety and effectiveness of this treatment, this study opens the door to a new way to safely reset the immune system and restore insulin production.
This study was published in the Journal of Clinical Investigation.
New drug could help prevent sight loss in people with diabetes
Our researchers at Queen’s University Belfast have uncovered a promising new drug to treat early eye damage, before it becomes irreversible.
Diabetic eye disease, or retinopathy, happens when high blood sugar levels damage the blood vessels and nerve cells in the retina. Early damage can happen long before people notice any problems with their vision, and current treatments tend to only work at the later stages of the disease.
The team led by Professor Tim Curtis tested a new drug designed to work at an earlier stage and stop eye damage in its tracks. The study was published in Diabetologia.
In rats with diabetes, the drug, called 2-HDP, protected the retina’s nerve cells and blood vessels, reduced inflammation, and helped preserve visual function. The drug works by neutralising harmful molecules that accumulate in the retina during diabetes and contribute to sight loss.
To check the importance of these findings for humans, the team also looked at retinal tissue from people with diabetes and found the presence of the same toxic molecules targeted by 2-HDP. This suggests that the drug may have the potential to target these damaging molecules in people as well.
Computer simulations also showed that the drug can easily enter cells within the body, raising the possibility of developing tablet-based treatments in the future.
Professor Tim Curtis said:
“This breakthrough highlights the importance of early intervention in diabetic retinal disease and the pressing need for new, targeted treatments that can protect vision before lasting damage occurs.”
