Insulin helps glucose to leave the bloodstream and enter fat and muscle cells. It does this by telling the cells to put more glucose ‘entry points’ on their surface, but this goes wrong in people with Type 2 diabetes. Professor Gould wants to understand the molecular details behind how and why insulin stops being effective in Type 2 diabetes. In the future, this could lead to new treatments to trigger more glucose entry points on the surface of fat and muscle cells again.
Background to research
Our cells use glucose as their energy source, and we get it from the food that we eat. Insulin is a hormone that helps glucose to enter fat and muscle cells in the body, so they can use it as fuel. Insulin tells the cells to put more ‘glucose entry points’ on their surface. These entry points allow glucose to leave the bloodstream and enter the cell, keeping blood glucose levels safe and healthy, and making sure our cells have enough fuel to work properly.
Normally, these glucose entry points are held in a storage unit inside each cell. When they are needed, they travel from the storage unit to the surface of the cell. But this process doesn’t work as well if you have Type 2 diabetes.
Professor Gwyn Gould has found two proteins involved in moving the glucose entry points from the storage units to the surface of fat cells. One of these proteins is called Sx16. Sx16 helps to keep the entry points inside the storage unit until insulin says to release them.
Professor Gould’s team will grow fat cells in the lab to study Sx16 in more detail. For example, they want to know how the levels of Sx16 inside the cell are controlled, or how these levels relate to keeping the glucose entry points inside the storage units. They will also look at how Sx16 works with other proteins to help the glucose entry points reach the surface of the cell when the time is right.
If Sx16 prevents the glucose entry points from leaving their storage units, this could be contributing to high levels of glucose in the bloodstream in some people with Type 2 diabetes. By understanding exactly how Sx16 works, the team hopes to find new ways to help glucose entry points get to the cell surface.
Potential benefit to people with diabetes
Type 2 diabetes is complex, and the molecular processes that lead to the condition might not be the same in everyone. The process of moving glucose from the bloodstream into cells is one that we know goes wrong for some people, so understanding more about this could help us to find ways to rescue it. The more we know about Type 2 diabetes, the more easily we can treat it in a way that works for each person.