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Oxford research reveals high blood glucose reprograms the metabolism of pancreatic beta-cells in diabetes.

Doctor checking blood sugar level with glucometer. Treatment of diabetes concept.

Glucose metabolites (chemicals produced when glucose is broken down by cells), rather than glucose itself, have been discovered to be 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.

An estimated 415 million people globally are living with diabetes. With nearly 5 million people diagnosed with the condition in the UK, it costs the NHS some £10 billion each year. Around 90% of cases are type 2 diabetes (T2D), which is characterised by the failure of pancreatic beta-cells to produce insulin, resulting in chronically elevated blood glucose. T2D normally presents in later adult life, and by the time of diagnosis, as much as 50% of beta cell function has been lost. While researchers have known for some time that chronically elevated blood sugar (hyperglycaemia) leads to a progressive decline in beta-cell function, what exactly causes beta-cell failure in T2D has remained unclear.

Now a new study led by Dr Elizabeth Haythorne and Professor Frances Ashcroft of the Department of Physiology, Anatomy and Genetics at the University of Oxford has revealed how chronic hyperglycaemia causes beta-cell failure. Using both an animal model of diabetes and beta-cells cultured at high glucose, 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 demonstrated that beta-cell failure caused by chronic hyperglycaemia can be prevented by slowing the rate of glucose metabolism.

Read the full story on the University of Oxford website

 

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