Usually, insulin makes it possible to store blood sugar in the form of glucose in the liver or adipose tissue (fat). The stored glucose is needed for the satisfactory function of the heart, brain and so on according to the body's demands.
Many times, the mechanism gets disrupted either because insulin is no longer produced (type 1 diabetes), or because the receptors located on the surface of liver cells are desensitized (type II diabetes). Thus, the cell becomes incapable of assimilating glucose.
Such a dysfunction causes a rise in blood sugar levels leading to the onset of numerous complications.
In the new study, led by Philippe Valet, researchers have found that our cells are equipped with a second pathway for the assimilation of glucose, which involves "apelin".
The protein is not only a "key" that is different from insulin, but it also passes through a different receptor or "doorway".
The new discovery may prove to be effective mainly in case of type II diabetics where the receptor or doorway is impaired rather than the key.
The findings make it possible to short-circuit this mechanism and achieve sugar assimilation by a completely different pathway from that mediated by insulin.
Usually, the second pathway is only responsible for a small proportion of sugar integration.
But, the tests in mice have revealed that in case of type II diabetes, activation of apelin mediated route improves the regulation of blood sugar levels.
"We now have to check the action of this protein in man. In parallel, we are developing a synthetic molecule that may be used if the tests in man are positive," concluded Valet.