The discovery of a protein which triggers the release of insulin has made a team of researchers “super excited”.
It is thought the finding could help determine an earlier intervention to preventing type 2 diabetes.
The study, which was carried out at the Johns Hopkins’ Department of Biology in the US, focused on a protein which helps neurons grow, a process which is called nerve growth factor (NGF).
Through their work, they discovered that NGF receptors have other useful functions outside of the nervous system.
Graduate student Jessica Houtz, who led the study, said: “I was super excited. I thought it was really cool that this unique feature of neurotrophic signaling in neurons was conserved in beta cells and had this different function outside of the nervous system.”
The research was carried out on mice after the NNGF receptor was removed from their pancreatic beta cells. Although the cells could produce insulin they were unable to release the hormone in the amounts required.
The same process was replicated in human beta cells, but the research team say they are unsure of how the system could affect people with diabetes.
Co-author Professor Rejji Kuruvilla has been focused on how the NGF process helps promote nerve cell survival for many years.
She said: “So it has been hypothesized or postulated that in type 2 diabetes that by the time a patient is diagnosed they have already lost 80 per cent of beta cell function.
“I think it’s absolutely critical to figure out the pathways that are important for beta cell function so that we can manipulate these pathways for early intervention of the disease, as opposed to managing a chronic disease after.”
More work is to be carried out on the NGF process in humans, and the team are hopeful that further findings might help find drugs which could treat people who are on the verge of developing diabetes.
Houtz added: “We’ve started to get our hands on some human islets and see how this pathway functions in human islets.
“But we know that the architecture and cell composition in human islets is slightly different than mouse islets so how exactly these islet micro-environment factors are functioning in human islets is still to be determined.”

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