Islet Amyloid

It has been reported from postmortem studies in subjects with type 2 diabetes that most of the subjects' pancreas islets contain amyloid in considerable quantities.

Amyloid consists of islet amyloid polypeptide (IAPP), or amylin, deposits. IAPP is normally contained in the insulin granule, and therefore cosecreted together with insulin (in a 10-fold lower quantity). Although amyloid is also present in islets of monkeys and cats, which have developed diabetes, it is absent in diabetic rodents, although rodents do secrete IAPP (63). Small aggregates of IAPP are cytotoxic (in vitro), which has been suggested to be due to "channel formation" by aggregating IAPP molecules, which can lead to calcium influx into beta cells; another possibility is intracellular aggregation after interaction with liposomal membranes. While hyperglycemia itself may accelerate IAPP aggregation, FFA (or NEFA) may enhance cytotoxicity of the aggregates (64). Although it is tempting to speculate that increased insulin secretion automatically leading to more IAPP secretion in insulin-resistant subjects would lead to IAPP aggregation, the finding that first-degree relatives secrete less IAPP (and insulin) than controls contradicts this hypothesis (65). Since islet amyloid is absent in most insulin-resistant nondiabetic subjects, it seems more probable that amyloid formation is a relatively late occurrence during the pathophysiology of type 2 diabetes.

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