
Around 415 million people across the world are living with diabetes, and about 90% of them have type 2 diabetes (T2D).
This common form of diabetes is usually linked to the body’s inability to produce enough insulin due to problems with pancreatic beta-cells.
These cells are responsible for making insulin, which helps control blood sugar levels.
For a long time, scientists believed that high blood sugar itself was the main reason why type 2 diabetes gets worse over time. But a new study from the University of Oxford is challenging that idea and offering a new explanation.
This new research shows that it’s not the sugar itself that harms the insulin-producing cells—it’s the byproducts created when our bodies break down glucose. These byproducts are called glucose metabolites. They seem to interfere with how well the beta-cells work, stopping them from releasing insulin properly.
Previously, doctors and researchers knew that there was a connection between high blood sugar and damage to the beta-cells, but they didn’t understand how it worked.
This new study fills in that gap. It proves that the way our body processes glucose—not glucose itself—is to blame for the loss of beta-cell function in people with type 2 diabetes.
This is a big discovery because it could change how we treat type 2 diabetes. Most current treatments focus on lowering blood sugar levels.
But if the real problem is how glucose is metabolized inside cells, then a new type of treatment could be developed that slows down or changes this process. This might help protect the beta-cells and keep them working longer.
In people with type 2 diabetes, the pancreas still makes insulin, unlike in type 1 diabetes. But the insulin made isn’t enough, and the body’s cells don’t respond to it properly. Over time, this leads to high blood sugar, which can cause serious health issues like damage to the eyes, kidneys, nerves, and heart.
Keeping blood sugar levels in a healthy range is very important. If they drop too low, it can cause fainting or unconsciousness because the brain needs glucose to function. If blood sugar stays too high, it can lead to long-term complications.
The Oxford team’s research, led by Dr. Elizabeth Haythorne, shows that by focusing on how glucose is broken down, we may be able to stop or slow down the damage to beta-cells. This would be a major step forward in the fight against diabetes.
This study offers a new and exciting path for researchers and doctors. It gives hope to millions of people with type 2 diabetes that better treatments could be on the horizon—treatments that don’t just manage symptoms but actually protect the cells that produce insulin.
By shifting our focus from just lowering blood sugar to understanding and managing how the body processes glucose, we may finally find a way to change the course of type 2 diabetes for the better.
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