Abstract:
One of the pathological features of type-2 diabetes mellitus (T2DM) is the presence of islet amyloid deposits comprising mainly human amylin (hA)/hIAPP. Recent studies suggested that soluble oligomers of human amylin may be the primary cause of β-cell damage and thus contribute to the onset/development of T2DM. However, the molecular basis of this process remains to be fully elucidated. We aimed to investigate the connection between soluble oligomers and hA cytotoxicity, and their correlation with diabetes development using a rodent model of diabetes.
