The research demonstrated that a protein called fractalkine, which usually helps ‘glue’ cells together, can also stimulate insulin secretion.
Researchers said it could offer a new treatment to improve glycaemic control, but stopped short of suggesting it could be a ‘cure’.
Experiments with mice and cultured human islets showed that administering fractalkine improved glucose tolerance.
Researchers also found that when a cell-surface receptor for fractalkine, called CX3CR1, was removed mice had impaired insulin secretion and glucose tolerance. The addition of fractalkine then had no effect in either the mice or isolated islets.
Fractalkine is expressed in the liver and blood vessels and helps cells bind together and communicate. Though it is a membrane-bound protein, it can also be released by cells.
Researchers do not know if lower fractalkine levels or impaired fractalkine signalling directly causes reduced beta cell function in diabetes.
However, fractalkine could offer a potential new therapy for improving insulin secretion and improve beta cell health, as it is known to promote beta cell differentiation and prevent beta cell death.
Lead author Dr Jerrold Olefsky of the University of California, San Diego said: ‘If successfully developed, this could be an important new complement to the therapeutic arsenal we use in type 2 diabetes.
‘It is not likely to "cure" diabetes, but it would certainly do a good job at providing glycaemic control.’