Project summary
When we eat, our blood sugar rises, and insulin helps bring it back down by moving a protein called GLUT4 to the surface of our cells, where it acts like a tiny door that lets sugar into the cell.
In type 2 diabetes, less GLUT4 reaches the surface, so more sugar stays in the blood. Professor Nia Bryant’s team want to find out why by exploring GLUT4’s journey inside the cell. Understanding this could open up new ways to improve blood sugar control and make living with type 2 diabetes easier to manage.
Background to research
Insulin plays a key role when our blood sugar rises. It nudges our muscle and fat cells to take sugar out of the bloodstream, which helps bring our levels back down.
One way it does this is by moving a protein called GLUT4 to the surface of these cells. GLUT4 acts like a tiny door that lets sugar move from the blood into the cell. When enough of these ‘doors’ reach the surface, blood sugar levels return to normal. In people living with type 2 diabetes, the body doesn’t respond properly to insulin, so less GLUT4 reaches the cell surface and more sugar stays in the blood.
GLUT4 has a tiny sugar tag called a glycan attached to it, and this tag seems to help direct where GLUT4 goes inside the cell. There are proteins that can latch onto these sugar tags. Lectins are one example, and people with insulin resistance – a key feature of type 2 diabetes - often have different amounts of lectins in their blood. This hints that lectins might influence how GLUT4 behaves.
But we still don’t know how GLUT4’s glycan works, or how lectins might affect it. And without this understanding, we can’t fully explain where GLUT4 goes inside the cell, or why it fails to reach the surface in people at risk of or with type 2 diabetes.
Research aims
Professor Nia Bryant and her team aim to find out what GLUT4’s glycan is made of, and how it helps guide GLUT4 to the cell surface where it can remove sugar from the blood. They will also investigate whether lectins, which stick to sugar tags, help direct GLUT4’s movement inside the cell.
To do this, the team will determine the glycan’s structure using advanced tools and use simple cell‑based tests to see how the glycan, and its interactions with lectins, affect where GLUT4 goes in type 2 diabetes.
Potential benefit to people with diabetes
By uncovering how GLUT4’s glycan helps guide it to the cell surface, this research could highlight new ways to boost GLUT4 where it’s needed most.
Over time, these insights could shape new treatments that help the body respond to insulin more effectively. This could delay or prevent the condition for those at risk of type 2 or give people living with the condition better blood sugar control and reduce their risk of serious diabetes complications.
