Researchers have uncovered a possible new way of exercising glycaemic control in treating type 2 diabetes. The biological mechanism found to regulate the pancreatic islet beta cells that produce and release insulin had been previously unknown.
Its discovery means there is potential for new therapy in treating the dysfunctional beta cells in the pancreas that are symptomatic of type 2 diabetes. The condition is a fast-rising epidemic, particularly in the developed world, affecting around 285 million people worldwide.
The research, published in the journal Cell, was carried out at the University of California, San Diego School of Medicine. The study revealed the existence of a transmembrane binding protein called fractalkine. Its role is to mediate cell-to-cell adhesion but its receptor, known as CX3CR1, can stimulate insulin secretion when released from the cells.
Fractalkine also plays a crucial part in healthy beta cell function, improving glucose tolerance as well as stimulating insulin secretion. Diabetes is a disorder where insulin in the blood is too high because the pancreas does not produce enough or any insulin to convert the glucose so it can enter the body’s cells.
The San Diego research did not reveal if decreased fractalkine or impaired fractalkine signalling causes the dysfunctional cell function in diabetes. However, it did conclusively demonstrate that fractalkine improves or restores insulin secretion. This has potentially huge consequences for treating diabetes with fractalkine or a substitute could be used to improve insulin secretion in patients with type 2 diabetes.
Beta cell function or health could also be improved in the same way and thus provide more effective glycaemic control for patients.
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