An estimated 415 million people globally are living with diabetes.
Around 90% of diabetes cases are type 2 diabetes (T2D), which is characterized by the failure of pancreatic beta-cells to produce insulin, resulting in chronically elevated blood glucose.
A recent study from the University of Oxford found glucose metabolites (chemicals produced when glucose is broken down by cells), rather than glucose itself, is the key to the progression of type 2 diabetes.
In diabetes, the pancreatic beta-cells do not release enough of the hormone insulin, which lowers blood glucose levels. This is because a glucose metabolite damages pancreatic beta-cell function.
While researchers have known for some time that chronically elevated blood sugar (hyperglycemia) leads to a progressive decline in beta-cell function, what exactly causes beta-cell failure in T2D has remained unclear.
In the study, researchers found how chronic hyperglycemia causes beta-cell failure.
They showed, for the first time, that glucose metabolism, rather than glucose itself, is what drives the failure of beta-cells to release insulin in T2D.
Importantly, they also found that beta-cell failure caused by chronic hyperglycemia can be prevented by slowing the rate of glucose metabolism.
This suggests a potential way in which the decline in beta-cell function in T2D might be slowed or prevented.
The blood glucose concentration is controlled within narrow limits. When blood glucose is too low for more than a few minutes, consciousness is rapidly lost because the brain is starved of fuel.
Chronic elevation of the blood glucose concentration is also dangerous, as it gives rise to the serious complications found in poorly controlled diabetes such as retinopathy, nephropathy, peripheral neuropathy, and cardiac disease.
Insulin, released from pancreatic beta-cells when blood glucose levels rise, is the only hormone that can lower the blood glucose concentration and diabetes (high blood glucose) results if insulin secretion is insufficient.
In T2D, the beta-cells are still present (unlike T1D), but they have a reduced insulin content and the coupling between glucose and insulin release is impaired.
The team’s new study is important because it shows that a breakdown product of glucose metabolism, rather than glucose itself, is what causes the failure of beta-cells to release insulin in diabetes.
High blood glucose levels cause an increased rate of glucose metabolism in the beta-cell which leads to a metabolic bottleneck and the pooling of upstream metabolites.
The study was conducted by Dr. Elizabeth Haythorne et al and published in Nature Communications.
If you care about diabetes, please read studies that flaxseed oil is more beneficial than fish oil to people with diabetes, and Stanford study finds drug that prevents kidney failure in diabetes.
For more information about diabetes, please see recent studies that blueberries strongly benefit people with metabolic syndrome, and results showing new bandage for foot ulcers in people with diabetes.
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