We take a look at some of the exciting diabetes research developments announced in March, and what the findings could mean for people living with or affected by diabetes.
In this month's article:
- ‘Molecular glue’ could protect insulin-making cells in type 2 diabetes
- More to insulin than just controlling blood sugar levels
- New understanding of the architecture of the pancreas could improve type 1 treatments
‘Molecular glue’ could protect insulin-making cells in type 2 diabetes
Researchers at the Icahn School of Medicine in the US have made a breakthrough in the quest to protect insulin-producing beta cells in people with type 2 diabetes.
They discovered a ‘molecular glue’ which could help beta cells stay healthy and continue producing insulin. Findings have been published in Nature Communications.
In type 2 diabetes, high blood sugar levels damage beta cells over time, leading to problems with insulin production. A protein, called ChREBP, normally helps beta cells respond to sugar in the blood. But in type 2 diabetes, it becomes overactive, triggering beta cell failure and death.
In this new study, researchers discovered small molecules, called molecular glues, that stop ChREBP from causing this harm.
Normally, a protein called 14-3-3 sticks to ChREBP, and keeps it locked outside the cell’s control centre, known as the nucleus. But in type 2 diabetes, ChREBP breaks free, enters the nucleus and damages beta cells.
For the first time, scientists have found a way to prevent this with a ‘molecular glue’ that works by strengthening the bond between ChREBP and 14-3-3. When they tested it in human beta cells in the lab, it protected the cells from damage, helping them survive and function properly.
This is an exciting but early-stage discovery. The team is now working to improve their glues and test them more in the lab. With further development, this new type of treatment could help slow or prevent beta cell loss in type 2 diabetes, allowing people to make more of their own insulin, improving blood sugar levels and protecting future health.
Donald Scott, Professor of Medicine at the Icahn School of Medicine, said:
“Our findings suggest a completely new strategy for preserving beta cell function in type 2 diabetes. This approach could complement existing diabetes treatments and help prevent disease progression.”
More to insulin than just controlling blood sugar levels
We know that type 2 diabetes is high blood sugar levels due to our bodies not making enough insulin, or the insulin it makes not working properly. But new research shows that insulin does much more than we thought.
Researchers in Germany revealed – for the first time – how insulin affects proteins in human muscle cells. Their findings are published in Nature Communications.
The team tracked changes in more than 13,000 proteins within the cell in response to insulin. They found that once insulin enters muscle cells, it immediately activates 159 different enzymes, which in turn influence hundreds of other proteins. These enzymes, known as protein kinases, act like tiny switches inside the cell, turning processes on and off to keep cells functioning properly.
The study showed that insulin does not just send a single, straightforward signal. Instead, it triggers a complex network of signals that spread through the cell in waves, much like knocking over a line of dominoes.
Specifically, they identified 30 key enzymes in charge of this network. This means that future treatments for type 2 diabetes could potentially target these specific enzymes to help insulin work more effectively in people with the condition.
The team also found that insulin may influence how genetic messages are translated into cell functions. This suggests that insulin could play a bigger role in the body than previously thought—beyond just controlling blood sugar.
By uncovering these new mechanisms, the study not only deepens our understanding of how type 2 diabetes develops but also highlights potential new targets for future treatments.
New understanding of the architecture of the pancreas could improve type 1 treatments
Research led by our fellow, Dr Pia Leete at the University of Exeter, has revealed new details about how clusters of cells in the pancreas are arranged.
This discovery could help researchers figure out why insulin-making beta cells are attacked in type 1 diabetes, and how to develop treatments that could protect them. The results were published in Diabetologia.
In rodents, scientists have found out that beta cells are mostly located in the centre of islets, surrounded by other hormone-producing cells. This is called a mantle-core (M-C) structure. But because human pancreas samples are so rare, few studies have explored whether human islets follow a similar pattern.
Dr Leete and her team used advanced imaging, mathematical analysis, and artificial intelligence to examine over 250,000 pancreas cells from 3,500 islets from people with and without type 1 diabetes.
They found evidence that human islets also follow a M-C structure, with beta cells in the centre and other cells forming a protective layer around them. This pattern was the same in both people with and without type 1 diabetes. This suggests that the M-C structure typically remains intact despite the immune system attack on beta cells.
But they also showed that beta cells were destroyed more quickly in the smallest islets from people with type 1 diabetes, and that this affected the M-C structure. This indicates that, in smaller islets, beta cell loss does impact M-C structure.
Why is this important? Understanding the architecture of human islets helps scientists better understand how the way cells are arranged affects their function and contributes to the development of type 1 diabetes. It also supports the idea that research using rodents can be useful for studying human islets.
These findings could lead to better treatments, such as transplants of donor islets or lab-grown beta cells.
Most excitingly, the researchers made their methods easy to use for other scientists, which could help drive even more progress in type 1 diabetes research.
