Principal Investigators

Professor Neil Hanley, University of Manchester

Professor Benjamin Glaser, Hadassah – Hebrew University Medical Centre


387 million people are living with diabetes worldwide. This is expected to rise to 592 million by 2035.

Our bodies need insulin to turn glucose into energy. When the body doesn’t produce insulin this is type-1 diabetes. It means that beta-cells, which produce insulin have been attacked by the body’s own immune system.  Increasing the number of working beta-cells is a huge focus of diabetes research. It has been proven difficult to promote beta-cells division in people.

There are in fact times when these beta cells do divide naturally (during embryo development and in a rare genetic disease). In this project, Professor Hanley and Professor Glaser studied the mechanisms which prevent beta cells from replicating in adults and children, and those that causes these cells to replicate in foetuses. 

By studying how the very early tissues are put together during development, the researchers discovered growth signatures, i.e. which genes are involved in driving how tissues grow and how cells divide. Their work had shown that these signatures tended to be shut down in adult beta cells, which led them to identify the genetic code responsible for this shut-down. If these cells can be reawaken, and stimulated to start dividing, it would allow the body to produce more beta cells capable of making insulin which would help in conquering diabetes.  In further work studying which genes are switched on or off in individual cells, the researchers have discovered the very different sets of genes active in insulin-producing beta cells compared to alpha cells, which make the hormone glucagon (the hormone that tends to have the opposite effect to insulin). Exciting work in recent years has shown, surprisingly, that it is possible to switch between being a beta cell or an alpha cell. The more we understand about the genetic code in charge of this decision, the better the chance we have of harnessing the switch for therapeutic benefit, meaning that we might be able to turn alpha cells into beta cells for people with diabetes.