Globally, approximately 415 million people live with diabetes, with about 90% of these cases being type 2 diabetes (T2D).
T2D is marked by pancreatic beta-cell failure to produce sufficient insulin, resulting in chronically elevated blood glucose levels.
Recently, a study from the University of Oxford revealed that glucose metabolites (chemicals produced when cells break down glucose) play a more critical role in the progression of T2D than glucose itself.
Role of Glucose Metabolites
In individuals with diabetes, pancreatic beta-cells fail to release enough insulin, a hormone that lowers blood glucose levels. This dysfunction is attributed to glucose metabolites damaging the pancreatic beta-cells.
Although it has been known that persistent high blood sugar (hyperglycemia) leads to a progressive decline in beta-cell function, the exact cause of beta-cell failure in T2D has been elusive.
The researchers demonstrated that glucose metabolism, not glucose itself, drives the failure of beta-cells to release insulin in T2D.
Furthermore, they found that slowing the rate of glucose metabolism could prevent beta-cell failure caused by chronic hyperglycemia.
These findings suggest a potential avenue for slowing down or preventing the decline in beta-cell function in T2D.
Importance of Insulin and Blood Glucose Concentration
Blood glucose concentration is tightly controlled. A consistent low blood glucose concentration can quickly lead to unconsciousness, as the brain is deprived of fuel.
On the other hand, chronic high blood glucose concentration can lead to serious complications commonly found in poorly controlled diabetes, such as retinopathy, nephropathy, peripheral neuropathy, and cardiac disease.
Insulin, which is released from pancreatic beta-cells when blood glucose levels rise, is the only hormone capable of lowering blood glucose concentration.
In T2D, while the beta-cells are still present (unlike in T1D), their insulin content is reduced, and the coupling between glucose and insulin release is impaired.
The University of Oxford’s study is crucial as it demonstrates that a breakdown product of glucose metabolism, not glucose itself, causes the failure of beta-cells to release insulin in diabetes.
This finding provides a new understanding of the mechanisms underlying T2D and offers potential avenues for novel therapeutic strategies.
The study, conducted by Dr. Elizabeth Haythorne and colleagues, has been published in Nature Communications.
If you care about diabetes, please read studies that pomace olive oil could help lower blood cholesterol, and honey could help control blood sugar.
For more information about diabetes, please see recent studies about Vitamin D that may reduce dangerous complications in diabetes and results showing that plant-based protein foods may help reverse type 2 diabetes.
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