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The presence of amylin immunoreactivity in non-diabetic islets, and the biological activities demonstrated in the above studies, suggest that amylin is a newly recognised hormone, which is synthesised in the pancreatic islets and functions as a modulator of insulin action in the control of carbohydrate metabolism. The effects of amylin or CGRP treatment on skeletal muscle in vitro are consistent with the condition of muscles seen in type 2 diabetics. Furthermore, we believe that the deposition of amylin as amyloid is due to an over production of the peptide, which is present in sufficiently high levels in the blood to produce the pathophysiological events seen in type 2 diabetes. These observations, together with the result that CGRP, and perhaps amylin, decreases insulin secretion both in vivo and in vitro, and the demonstration that the amylin gene structure from a non-diabetic individual corresponds exactly to the amino acid sequence obtained from 5 diabetic pancreases, lead to the hypothesis that an abnormality of amylin and/or CGRP homeostasis underlies the pathogenesis of type 2 diabetes mellitus.


Journal article


Diabetes 1988: proceedings of the 13th Congress of the International Diabetes Federation. ICS800

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