Oosterwijk C, Höppener J W, van Hulst K L, Lips C J
Department of Internal Medicine, Utrecht University Hospital, The Netherlands.
Int J Pancreatol. 1995 Aug;18(1):7-14. doi: 10.1007/BF02825416.
Islet amyloid polypeptide (IAPP or amylin) is the main component of pancreatic islet amyloid found in the vast majority of patients with noninsulin-dependent (Type-2) diabetes mellitus (NIDDM). IAPP may also act as a hormone that antagonizes the effects of insulin on peripheral tissues, but the results with IAPP overproducing transgenic mice and other recent findings indicate that IAPP overproduction is unlikely to induce peripheral insulin resistance in NIDDM. However, IAPP may contribute to the progression of NIDDM by impairing beta-cell function via islet amyloid formation. This may be initiated by locally elevated IAPP concentrations, induced by insulin-resistance-associated beta-cell hyperactivity. In order to improve therapeutic results, we propose strategies to inhibit IAPP production and islet amyloid formation during the pathogenesis of NIDDM.
胰岛淀粉样多肽(IAPP或胰淀素)是绝大多数非胰岛素依赖型(2型)糖尿病(NIDDM)患者胰岛淀粉样变的主要成分。IAPP也可能作为一种激素,拮抗胰岛素对周围组织的作用,但IAPP过度表达的转基因小鼠实验结果及其他近期研究结果表明,IAPP过度表达不太可能在NIDDM中诱导外周胰岛素抵抗。然而,IAPP可能通过胰岛淀粉样变损害β细胞功能,从而促进NIDDM的进展。这可能由胰岛素抵抗相关的β细胞功能亢进诱导的局部IAPP浓度升高引发。为了提高治疗效果,我们提出在NIDDM发病机制中抑制IAPP产生和胰岛淀粉样变形成的策略。