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For the first time, the existence of a protein that helps in the regulation of pancreatic islet beta cells has been discovered. Researchers at the University of California, San Diego School of Medicine identified fractalkine whose function is to produce and release insulin. Their study could be instrumental in the development of a new drug for type 2 diabetes.
Fractalkine is a transmembrane binding protein which mediates cell-to-cell adhesion though its receptor, CX3CR1, and can also be released from cells to circulate in the blood and stimulate insulin secretion, said Jerrold M. Olefsky, MD, associate dean for scientific affairs and distinguished professor of medicine, and colleagues in the latest issue of Cell.
“Our discovery of fractalkine’s role in beta cells is novel and has never been talked about in prior literature,” said Dr Olefsky. More importantly, the research highlights fractalkine’s apparently vital role in normal, healthy beta cell function. In mouse models and in cultured human islets, the researchers found administering the protein stimulated insulin secretion and improved glucose tolerance, both key factors in diabetes. In contrast, fractalkine had no effect in mice or islets when the fractalkine receptor was deleted.
“Whether or not decreased fractalkine or impaired fractalkine signaling are causes of decreased beta cell function in diabetes is unknown,” he said. “What we do know, without doubt, is that administration of fractalkine improves or restores insulin secretion in all of the mouse models we have examined, as well as in human islet cells.”
The report also mentions that fractalkine or a protein analogue may be “a potential treatment to improve insulin secretion in type 2 diabetic patients. It might also improve beta cell function or beta cell health, beyond simply increasing insulin secretion, since fractalkine prevents beta cell apoptosis (cell death) and promotes the beta cell differentiation programme.
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