What is the underlying trigger for type two diabetes?

type two diabetic
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Researcher, Dr Elizabeth Haythorne, from the University of Oxford, has conducted a study with the intention of figuring out the reasons why specialised pancreatic cells fail to fulfil their functions of maintaining healthy blood sugar.

What happens to the body when it has type two diabetes?

Type two diabetes is becoming increasingly common. Affecting over 450 million people worldwide, type two diabetes arises when pancreatic beta cells fail to secrete adequate insulin.

A rise in circulating glucose triggers the pancreatic specialist beta cells to produce insulin.

Insulin allows sugars to be absorbed by the body’s tissue where it is metabolised to create energy. The sugar must be absorbed by the tissue in order to avoid hyperglycemia which is caused by high blood sugar levels.

Type two diabetes takes a great toll on the individual, as well as the state. Type two diabetes causes great financial strain due to the regular need for medication and hospital visits. Unfortunately, there is not yet a cure for type two diabetes. However, researchers at the University of Oxford might have just indicated the reason why specialist cells mutate and fail to perform their function.

The vicious cycle of hyperglycemia and diabetes

Research has recently been published from the Ashcroft Group, at the University of Oxford, was led by post doctorate researcher, Dr Elizabeth Haythorne.

Dr Haythorne used a combination of techniques examining the protein and gene changes that could be deemed responsible for cell mutations in diabetics.

Through her research, Dr Haythorne discovered that prolonged hyperglycemia impairs mitochondrial metabolism and therefore, energy production.

The data also indicated that multiple genes and proteins involved in the metabolic pathways glycolysis and gluconeogenesis were up regulated in an abnormal fashion.

The evidence shows that the data collected indicates that hyperglycemia causes a significant dis-regulation of major metabolic pathways in pancreatic beta cells.

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