Diabetes may result from the failure of a privileged few cells, rather than the behaviour of all cells, researchers say, a finding that may pave the way for therapies for the disease.
Researchers used optogenetic and photopharmacological targeting to precisely map the role of the cells required for the secretion of insulin.
The significant role of beta cell ‘hubs’ in the pancreas has been demonstrated for the first time, suggesting that diabetes may due to the failure of a privileged few cells, rather than the behaviour of all cells, they said.
Researchers believe that the findings could pave the way for therapies that target the ‘hubs’.
“It has long been suspected that ‘not all cells are equal’ when it comes to insulin secretion,” said David Hodson, from University of Birmingham in the UK.
“These findings provide a revised blueprint for how our pancreatic islets function, whereby these hubs dictate the behaviour of other cells in response to glucose,” said Hodson.
Type 2 diabetes occurs when the pancreas fails to produce enough insulin to function properly, meaning that glucose stays in the blood rather than being converted into energy.
Beta cells make up around 65-80 per cent of the cells in the islets of the pancreas.
Their primary function is to store and release insulin and, when functioning correctly, can respond quickly to fluctuations in blood glucose concentrations by secreting some of their stored insulin, researchers said.
The findings show that just 1-10 per cent of beta cells control islet responses to glucose, they said.
“These specialised beta cells appear to serve as pacemakers for insulin secretion. We found that when their activity was silenced, islets were no longer able to properly respond to glucose,” said Hodson.
“This study is interesting as it suggests that failure of a handful of cells may lead to diabetes,” said Guy Rutter from Imperial College London in the UK.
The findings were published in the journal Cell Metabolism.