S-acylation and the regulation of calcium-activated (BK) channels in pancreatic beta cells
Professor Michael Shipston aims to understand the mechanisms by which dietary fat regulates the activity of islet cell pores that help control the release of insulin. These mechanisms might provide a new target for Type 2 diabetes therapies.
Background to research
Pores in the surface of pancreatic beta cells help to control the cells’ electrical activity and, in turn, their ability to release insulin. Professor Michael Shipston and his team at the University of Edinburgh have recently shown that fat in the diet influences both the number and activity of beta cell pores via mechanisms that are linked to diabetes. However, at present this mechanism is poorly understood by scientists.
With support from Diabetes UK, Professor Shipston and his team will find out how dietary fats control the function of beta cell pores and, in turn, the release of insulin. They will study the effects of a key mechanism (called ‘palmitoylation’) on beta cell pores –from the function of a single pore in real time, to the role of the pore in controlling insulin release from cells and finally, to the modification of multiple pores by dietary fats in living mice. To do this they will use high-resolution electrical measurements of pores, imaging techniques to track their number and movement in living cells and a range of chemical tests to see how they are modified by fats.
Potential benefit to people with diabetes
These studies should reveal important new mechanisms that are vital to the release of insulin from beta cells in the pancreas. It should also help the researchers to find out if the modification of beta cell pores through ‘palmitoylation’ is a mechanism that can be targeted by new Type 2 diabetes therapies.