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Scientists show both types of diabetes are caused by same underlying mechanism

20 Aug 2014

Work by scientists at the Universities of Manchester and Auckland suggest that both major forms of diabetes, type-1 and type-2, are the result of the same mechanism.

The findings, published today in the FASEB Journal (20 August), provide compelling evidence that juvenile-onset or type-1 diabetes and type-2 diabetes are both caused by the formation of toxic clumps of a hormone called amylin.  


The results, based on 20 years’ work in New Zealand, suggest that type-1 and type-2 diabetes could both be slowed down and potentially reversed by medicines that stop amylin forming these toxic clumps.  

Professor Garth Cooper, from The University of Manchester with his University of Auckland-based research team, led the study. 

As well as producing insulin, cells in the pancreas also produce another hormone called amylin. Insulin and amylin normally work together to regulate the body’s response to food intake. If they are no longer produced, then levels of sugar in the blood rise resulting in diabetes and causing damage to organs such as the heart, kidneys, eyes and nerves if blood sugar levels aren’t properly controlled.  

However, some of the amylin that is produced can get deposited around cells in the pancreas as toxic clumps, which then, in turn, destroy those cells that produce insulin and amylin. The consequence of this cell death is diabetes. 

Research published previously by Professor Cooper suggested that this is the causative mechanism in type-2 diabetes. This new research provides strong evidence that type-1 diabetes results from the same mechanism.  

The difference is that the disease starts at an earlier age and progresses more rapidly in type-1 compared to type-2 diabetes because there is more rapid deposition of toxic amylin clumps in the pancreas.  

Professor Cooper’s group expects to have potential medicines ready to go into clinical trials in the next two years and it is anticipated that these will be tested in both type-1 and type-2 diabetic patients. These clinical trials are being planned with research groups in England and Scotland. 
 

Notes for editors

For further information, please contact Alison Barbuti, Media Relations Officer, Faculty of Medical and Human Sciences, The University of Manchester, 0161 275 8383 or email alison.barbuti@manchester.ac.uk. 
 
Paper title “The pathogenic mechanism of diabetes varies with the degree of overexpression and oligomerization of human amylin in the pancreatic islet beta cells” is published in FASEB J - Journal of the Federation of American Societies for Experimental Biology, Bethesda, MD, USA  (http://www.fasebj.org/), the world's most cited biology journal on Wednesday 20 August 2014.


1. According to the American Heart Association [1], the prevalence of diabetes for all age groups worldwide was estimated to be 2.8% in 2000 and is projected to be 4.4% in 2030. The total number of people with diabetes is projected to rise from 171 million in 2000 to 366 million in 2030. Similar figures have been produced by other groups such as the International Diabetes Federation [2]. 

2. The cost to the NHS of treating diabetes is £10 billion, approximately 10% of the NHS budget [3]
3. The two common forms of diabetes are type-1 diabetes (also known as juvenile-onset diabetes, where there is an absolute requirement for insulin in order to ensure survival) and type-2 diabetes: these represent about ~5% and ~95% of all cases, respectively. 
4. In type-1 diabetes, immune cells are thought to destroy the pancreatic islet beta-cells which normally make insulin, thereby causing the disease. 
5. In type-2 diabetes, the pancreatic hormone amylin is thought to adopt an unusual shape that renders it toxic to beta-cells which it probably destroys over a longer period. 
6. Our work is supported by the Endocore Research Associates University of Auckland, New Zealand; the New Zealand Ministry of Business, Innovation and Employment; the Health Research Council of New Zealand; the Maurice Wilkins Centre; and The University of Manchester, Central Manchester University Hospitals NHS Foundation Trust and the Medical Research Council; and was facilitated by the Manchester Biomedical Research Centre and the UK National Institute for Health Research Greater Manchester Comprehensive Local Research Network.