The main cause of type 2 diabetes discovered – Digital Journal


Medical laboratory scientist at bench with micropipettes. — Courtesy of the US National Institutes of Health (Public Domain)

Oxford Research has revealed how high blood glucose reprograms pancreatic beta cell metabolism in diabetes, acting as an important causative factor of type 2 diabetes. This is significant because glucose metabolites (chemicals produced when cells break down glucose), rather than glucose itself, have been found to be key to the progression of type 2 diabetes.

With diabetes, the pancreas beta cells do not release enough hormone insulin, which lowers blood glucose levels. This is because a glucose metabolite impairs the function of the beta cells of the pancreas. Elevated blood glucose levels cause an increased rate of glucose metabolism in beta cells, leading to a metabolic bottleneck and accumulation of upstream metabolites.

About 90 percent of global diabetes cases are type 2 diabetes (T2D). T2D typically presents in late adulthood, and by the time of diagnosis, up to 50 percent of beta cell function has been lost. In T2D, beta cells have reduced insulin content and the coupling between glucose and insulin release is impaired.

Scientists have previously established that chronically elevated blood sugar (hyperglycemia) leads to a progressive decline in beta cell function. Hyperglycemia triggers a vicious spiral in which a rise in blood glucose leads to beta cell damage and decreased insulin secretion, causing a further rise in blood glucose and a further decline in glucose function. beta cells. However, it is still not clear what exactly causes beta cell failure in T2D.

the new study reveals how chronic hyperglycemia causes beta cell failure. This was demonstrated using an animal model of diabetes and beta cells cultured with high glucose. Both experiments demonstrated that glucose metabolism, rather than glucose itself, is the factor driving the failure of beta cells to release insulin in T2D.

The importance of the research in terms of medical understanding is that by reducing the rate at which glucose is metabolized and the rate at which these glucose metabolites accumulate, the effects of hyperglycemia can be prevented. This suggests a potential way in which the decline in beta cell function in T2D could be slowed or prevented.

The researchers found that blocking an enzyme called glucokinase, which regulates the first step in glucose metabolism, has the potential to prevent genetic changes and maintain glucose-stimulated insulin secretion even in the presence of chronic hyperglycemia. This is a potentially useful way of trying to prevent beta cell decline in diabetes.

The investigation appears in the newspaper nature communicationsentitled “Altered Glycolysis Triggers Altered Mitochondrial Metabolism and mTORC1 Activation in Diabetic β-Cells”.


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