In type 2 diabetes, muscle and fat cells become unable to take in glucose from the blood – causing blood sugar levels to rise. Professor Bryant believes that a molecule called ‘cellugyrin’ is involved in helping glucose to enter fat and muscle cells, but that it may not work properly in people with type 2 diabetes. This research will help us find out more about the underlying processes of how type 2 develops, so we can find new ways to treat it.
Background to research
Insulin is needed to keep blood glucose levels constant. It does so by telling fat and muscle cells to take glucose in from the bloodstream. For this to happen, channels (called ‘GLUT4’) are sent from storage units at the centre of fat and muscle cells to the cell surface. These channels let glucose enter the cells, travelling in from the blood.
In type 2 diabetes, this doesn’t happen: the fat and muscle cells don’t respond to insulin (known as insulin resistance), and so they don’t send GLUT4 to the surface. This means that glucose builds up in the bloodstream.
Professor Bryant has discovered a molecule, called cellugyrin, which she believes plays an important role in directing GLUT4 from the storage units to the surface of fat and muscle cells. But we don’t yet know precisely how cellugyrin does this.
Professor Bryant and her team will study fat and muscle cells grown in the lab and see how they react to insulin. She will study exactly how insulin triggers the movement of GLUT4 channels from storage units to the surface of the cell.
In particular, she will look at the role that cellugyrin plays in regulating these processes in much more detail. Her team will also investigate what happens when you interrupt these processes, to give them some idea of how vital cellugyrin is in helping glucose to enter cells.
Potential benefit to people with diabetes
This research will give us a more detailed understanding of why insulin stops working in type 2 diabetes, and could lead to the development of new ways of diagnosing and treating people with type 2 diabetes in the future.