Insulin research builds on Nobel Laureate’s work

The breakthrough, which builds on earlier Nobel-Prize winning research, could have implications for the treatment of diabetes which is caused when not enough insulin is released by the pancreas to meet the body’s demands.

The team of scientists from the University of Manchester, Charite University in Berlin, and the University of Heidelberg say the findings could also be important in understanding other diseases, as hormone and protein secretion is an important function of all types of cell.

“Large numbers of proteins, including hormones such as insulin, are constantly being produced by our cells and carry out essential functions in the body,” explained Dr Martin Pool, based in Manchester’s Faculty of Life Sciences.

“In order for them to work, these proteins have to be transported to the right place and it is this process – of fundamental importance to all living organisms – that we are interested in.”

Dr Pool’s work – to be published in the highly respected journal Science – is based on a 30-year-old hypothesis of how proteins are transported across cell membranes and directed to their correct location.

That hypothesis was devised and proven by Dr Gunter Blobel and led to him receiving the Nobel Prize in Physiology or Medicine in 1999.

But the Anglo-German team has taken Dr Blobel’s investigations a step further as they have been able to physically see the processes at work using sophisticated electron microscopes.

“Previous work had provided a framework of how the system worked but we were limited to models and cartoons of how it might look and actually function,” said Dr Pool.

“Visualising the structure using a technique called cryo-electron microscopy has confirmed that many of the earlier proposals of the model were in fact correct.

“This process occurs in all cells, although our work has concentrated on mammalian pancreatic cells.

“Understanding how these specialised secretary cells release insulin is of great significance and might be important in understanding why this process goes wrong in type-2 diabetes.”