Ludvik B, Kautzky-Willer A, Prager R, Thomaseth K, Pacini G
Klinik für Innere Medizin III, Abteilung für Endokrinologie und Stoffwechsel, University of Vienna, Austria.
Diabet Med. 1997 Jun;14 Suppl 2:S9-13. doi: 10.1002/(sici)1096-9136(199706)14:2+<s9::aid-dia397>3.3.co;2-4.
The presence of amyloid deposits in the pancreas was first described at the beginning of the 20th century. However, it was not until 1987 that the structure of the amylin molecule was identified. Amylin is a 37-amino-acid peptide hormone that is co-secreted with insulin by the pancreatic beta-cells in response to a nutrient stimulus. It is deficient in patients with Type 1 diabetes and elevated in patients in the early stages of Type 2 diabetes, a condition which is characterized by hyperinsulinaemia. Elevation of plasma amylin levels has also been described in patients with impaired glucose tolerance, obese subjects and in pregnant women with both normal glucose tolerance and gestational diabetes mellitus. However, it appears that deficiencies of amylin secretion appear before those of insulin in patients in the later stages of Type 2 diabetes. Early experimental studies suggested that amylin inhibits basal insulin secretion, and induces insulin resistance in skeletal muscle, leading to the hypothesis that it has a role in the aetiology of Type 2 diabetes. However, a number of more recent experimental studies have indicated that amylin is a third active pancreatic islet hormone that works with insulin and glucagon to maintain glucose homeostasis. Amylin appears to regulate glucose inflow to the circulation by influencing the rate of gastric emptying, and thus the rate at which meal-derived glucose enters the system, and also by inhibiting glucose release and hepatic glucose production in the postprandial period.
胰腺中淀粉样沉积物的存在最早于20世纪初被描述。然而，直到1987年胰岛淀粉样多肽分子的结构才被确定。胰岛淀粉样多肽是一种由37个氨基酸组成的肽类激素，在营养刺激下由胰腺β细胞与胰岛素共同分泌。1型糖尿病患者体内缺乏该激素，而在2型糖尿病早期患者体内其水平升高，2型糖尿病的特征是高胰岛素血症。糖耐量受损患者、肥胖受试者以及糖耐量正常和患有妊娠期糖尿病的孕妇体内血浆胰岛淀粉样多肽水平也有升高的描述。然而，在2型糖尿病后期患者中，胰岛淀粉样多肽分泌不足似乎比胰岛素分泌不足出现得更早。早期的实验研究表明，胰岛淀粉样多肽抑制基础胰岛素分泌，并在骨骼肌中诱导胰岛素抵抗，从而产生了它在2型糖尿病病因学中起作用的假说。然而，最近的一些实验研究表明，胰岛淀粉样多肽是胰腺胰岛的第三种活性激素，它与胰岛素和胰高血糖素共同作用以维持葡萄糖稳态。胰岛淀粉样多肽似乎通过影响胃排空速率，进而影响餐源葡萄糖进入系统的速率，以及通过在餐后抑制葡萄糖释放和肝脏葡萄糖生成来调节葡萄糖进入循环的流量。
