
Type 2 diabetes is one of the most common chronic conditions worldwide.
Since the 1950s, a group of medications called sulfonylureas has been widely used to help manage this disease. These drugs are known to lower blood sugar by forcing the pancreas to release more insulin.
However, their effectiveness tends to decrease over time, and they often come with more side effects compared to newer diabetes medications.
A recent study from researchers in Spain has found a potential reason why sulfonylureas become less effective and might even speed up the progression of type 2 diabetes.
The study was led by scientists from IDIBELL, the University of Barcelona, the Bellvitge University Hospital, and CIBERDEM, and was published in the journal Diabetes, Obesity and Metabolism.
Diabetes happens when the body can’t properly manage sugar in the blood. One key hormone involved is insulin, which helps sugar enter the cells for energy. This hormone is made by beta cells in the pancreas.
In type 2 diabetes, the body becomes resistant to insulin, and the pancreas tries to keep up by making more. Over time, this wears out the beta cells. Once they stop working, blood sugar levels rise, and the condition gets worse.
For a long time, scientists believed that the main problem was that these beta cells simply died. But newer research shows that they may also “forget” their role.
In other words, they lose their identity and stop producing insulin properly, even though they are still alive. This loss of identity was seen in mice before, but this new study confirms it happens in humans too.
The researchers looked at how a common sulfonylurea drug, glibenclamide, affects healthy beta cells in lab conditions. They found that after being exposed to this drug, the cells lost the ability to produce insulin and responded poorly to glucose. They also showed higher levels of stress inside the cells and an increased risk of cell death.
This discovery is important because it helps explain why sulfonylureas lose their power over time. When beta cells lose their identity, they no longer function as insulin producers, which could make diabetes worse in the long run.
Interestingly, the study also found that this damage is linked to stress in a part of the cell called the endoplasmic reticulum, which helps make proteins. This stress seems to be one way that sulfonylureas harm the beta cells.
There is some good news, though. While dead cells cannot be brought back, beta cells that have lost their identity might be reactivated in the future.
That means scientists could one day find ways to reverse this process and help the pancreas produce insulin again. More studies are needed, but this research opens the door to new therapies that could offer longer-term solutions for people with type 2 diabetes.
Understanding the hidden risks of common medications like sulfonylureas is key to improving treatment. This study highlights the importance of developing safer, more effective options for managing this growing global health issue.
The study is published in Diabetes, Obesity and Metabolism.
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