Today the Telegraph, and other news outlets, covered a story about research from the universities of Manchester, UK and Auckland, New Zealand discussing the role amylin may play in beta cell death.
What is the story all about?
The news story focuses on new research surrounding the hormone amylin published in the Journal of the Federation of American Societies of Experimental Biology. Amylin is another hormone produced by pancreatic beta cells alongside insulin. But because beta cells produce approximately 100 times as much insulin as they produce amylin, this hormone was only discovered in 1986 (we’ve known about insulin since 1921). Amylin’s role in the body is associated with gastric emptying and satiety (feeling full after eating), but it has also been shown that amylin can build up in large deposits in the pancreases of people with type 2 diabetes, and these deposits are thought to trigger the death of beta cells. This story focuses on the role of amylin in beta cell death.
What did the scientists do in their study?
To investigate what happened when too much amylin built up in the pancreas, the scientists worked with mice that were genetically modified to have pancreatic beta cells that over-produce amylin. They had two groups of mice that overproduced amylin at different rates: ‘homozygotes’ that expressed very high levels of amylin, and ‘hemizygotes’ that produced about half as much amylin, but still far more than would usually be made by a beta cell.
They then did a number of tests to monitor what happened to the mice. The homozygotes quickly developed diabetes and the scientists could see that the beta cells quickly disappeared. The scientists likened the rapid progression to diabetes as being similar to type 1 diabetes. The hemizygotes, progressed to diabetes much more slowly, so the research team likened this to type 2 diabetes.
The team examined how the amylin produced by the cells behaved in the pancreas to find out which aspects of amylin overproduction might be involved in driving beta cell death. They found that there was a marked difference in the way the cells responded to extreme overproduction as compared to overproduction, but in both cases, amylin overproduction led to diabetes and beta cell loss. This shows that the build up of large deposits of amylin as previously observed in type 2 diabetes, is not the only mechanism by which amylin can influence beta cell death.
What does this mean for people with type 1 diabetes?
Although the headline of the Telegraph claims the cause of diabetes has been found, this claim is not made by the authors themselves. They suggest that it is possible that amylin overproduction might have a role in a subset of cases of type 1 diabetes, and that this would be an interesting avenue for further investigation.
This study is primarily interesting to people involved in type 1 research because it indicates that amylin may have a role in driving beta cell death – but this is still likely to be a result of disrupted beta cell function. So it may be that by targeting the pathways through which amylin drives beta cell death we could develop treatments that protect beta cells from destruction. But there is still a great deal of work to be done in understanding the role of amylin in beta cell death in type 1 diabetes before it is likely to lead to new ways of treating type 1 diabetes in the clinic.
Is any other research on amylin taking place?
Yes. When type 1 diabetes develops, beta cells are destroyed, so as well as losing the ability to produce insulin, people with type 1 also lose the ability to produce amylin. As part of our research treatment research strategy, JDRF has supported work to understand if giving people with type 1 a synthetic form of amylin, called pramlintide, alongside their insulin, might help in achieving good glucose control. These studies are ongoing and we await the results with interest.