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Beta cell ‘hubs’ play role in Type 2 diabetes

27 July 2016

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Dr David Hodson, University of Birmingham

 

Research published in Cell Metabolism has shown that type 2 diabetes might be due to a handful of insulin-producing cells failing, rather than all of them. 

Type 2 diabetes occurs when the pancreas fails to produce enough insulin, meaning that glucose stays in the blood rather than being converted into energy.

The few in charge

When working properly, insulin-producing beta cells that sit within the pancreas, respond quickly to changes in blood glucose levels by releasing some of their stored insulin. It’s long been thought that a few privileged beta cells may be responsible for orchestrating how the pancreas responds to blood glucose levels. 

This research suggests that just 1-10% of the beta cells are actually in charge, and the research team have termed these the ‘beta cell hubs’. They found that wiping out the activity of these ‘hubs’ stops them from communicating with the other beta cells, disrupting the ability of the whole pancreas to respond to glucose and release insulin. When the ‘hubs’ are turned back on, the network of communication is brought back into play. 

New therapies for type 2 diabetes

Dr David Hodson and Professor Guy Rutter, both funded by Diabetes UK, believe that the findings could pave the way for therapies that target the ‘hubs’ and keep them functioning properly. 

It’s a significant step forwards in understanding the biology behind type 2 diabetes, although future research is needed to establish whether the findings can be translated into a human setting. 

Dr Hodson, a Diabetes UK RD Lawrence Fellow from the University of Birmingham who co-led the study, explained, “It has long been suspected that ‘not all cells are equal’ when it comes to insulin secretion. 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.”

“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.”

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