Islet pathology of non-insulin-dependent diabetes mellitus (NIDDM)

Abstract

Islet amyloid polypeptide (IAPP) gives rise to islet amyloid fibrils in NIDDM. Islet amyloid tends to replace islet cells, especially beta-cells and may act as a diffusion barrier. It has also been proposed that IAPP amyloid fibrils are beta-cell cytotoxic. The pathogenesis of islet amyloid is not clear and several factors are probably necessary for amyloid formation. One factor is an amyloidogenic amino acid sequence of IAPP and a second is probably a high local concentration of IAPP. Islet amyloid is not seen in the normal human pancreas and has not been described in the pancreata of transgenic mice over-expressing human IAPP. However, islet amyloid is rapidly deposited in in vitro cultivated islets from these transgenic animals and in isolated normal human islets transplanted into nude mice. Consequently, besides an amyloidogenic structure and high production of IAPP, further factors are necessary for islet amyloid formation in NIDDM.