Type-1 and type-2 diabetes are caused by the same hormone
22 August 2014
New evidence from research at at the Universities of Manchester
and Auckland shows 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 working
with his University of Auckland-based research team, led the study.
The findings are published in the Journal of the Federation of
American Societies for Experimental Biology.
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
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.
The pathogenic mechanism of diabetes varies with the degree of
overexpression and oligomerization of human amylin in the pancreatic
islet beta cells. Journal of the Federation of American Societies
for Experimental Biology. August 2014.