Koopmans S J, Radder J K, Krans H M, Barge R M
Department of Endocrinology and Metabolic Diseases, University Hospital Leiden, Netherlands.
Neth J Med. 1992 Aug;41(1-2):82-90.
Amylin, also called islet amyloid polypeptide (IAPP), or diabetes-associated peptide (DAP) is a recently discovered 37 amino acid polypeptide which has been shown to be co-secreted with insulin from the pancreatic beta-cell. The peptide turned out to be the major constituent of pancreatic amyloid deposits which are frequently found in the pancreas of type II diabetic patients. Therefore, a role for amylin in the aetiology of type II diabetes was hypothesized. To investigate this possibility, several studies have been performed to elucidate whether amylin is able to impair insulin secretion and action, two characteristic features of type II diabetes mellitus. These studies suggest that it is unlikely that amylin has a direct inhibitory effect on insulin secretion. Amyloid deposits, however, which are derived from the in situ polymerization and precipitation of amylin, may impair beta-cell function during type II diabetes by damaging and covering beta-cells. Furthermore, it has been shown that amylin has the potential to antagonize the action of insulin on glucose metabolism by increasing hepatic glucose production and by decreasing muscle, but not adipocyte glucose uptake. For these reasons, it has been suggested that amylin might be involved in the pathophysiology of type II diabetes and obesity, disease states which are characterized by abnormal beta-cell function and insulin resistance. In addition, amylin was shown to induce hypocalcaemia by inhibiting osteoclast-mediated bone resorption in a calcitonin-like manner. Therefore, amylin is likely to be involved in both the modulation of glucose and calcium metabolism.
胰淀素，也称为胰岛淀粉样多肽（IAPP）或糖尿病相关肽（DAP），是最近发现的一种由37个氨基酸组成的多肽，已被证明与胰岛素一起从胰腺β细胞共同分泌。结果发现，该肽是胰腺淀粉样沉积物的主要成分，在II型糖尿病患者的胰腺中经常发现。因此，有人推测胰淀素在II型糖尿病的病因学中起作用。为了研究这种可能性，已经进行了几项研究，以阐明胰淀素是否能够损害胰岛素分泌和作用，这是II型糖尿病的两个特征。这些研究表明，胰淀素不太可能对胰岛素分泌有直接抑制作用。然而，源自胰淀素原位聚合和沉淀的淀粉样沉积物，可能在II型糖尿病期间通过损害和覆盖β细胞来损害β细胞功能。此外，已经表明，胰淀素有可能通过增加肝脏葡萄糖生成和减少肌肉（而非脂肪细胞）对葡萄糖的摄取来拮抗胰岛素对葡萄糖代谢的作用。基于这些原因，有人提出胰淀素可能参与II型糖尿病和肥胖症的病理生理学，这两种疾病状态的特征是β细胞功能异常和胰岛素抵抗。此外，胰淀素被证明以降钙素样方式抑制破骨细胞介导的骨吸收，从而诱导低钙血症。因此，胰淀素可能参与葡萄糖和钙代谢的调节。
