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代谢应激、IAPP 和胰岛淀粉样变。

Metabolic stress, IAPP and islet amyloid.

机构信息

Department of Pathology & Laboratory Medicine, University of British Columbia, Vancouver, BC, Canada.

出版信息

Diabetes Obes Metab. 2012 Oct;14 Suppl 3:68-77. doi: 10.1111/j.1463-1326.2012.01657.x.

DOI:10.1111/j.1463-1326.2012.01657.x
PMID:22928566
Abstract

Amyloid forms within pancreatic islets in type 2 diabetes from aggregates of the β-cell peptide islet amyloid polypeptide (IAPP). These aggregates are toxic to β-cells, inducing β-cell death and dysfunction, as well as inciting islet inflammation. The β-cell is subject to a number of other stressors, including insulin resistance and hyperglycaemia, that may contribute to amyloid formation by increasing IAPP production by the β-cell. β-Cell dysfunction, evident as impaired glucose-stimulated insulin secretion and defective prohormone processing and exacerbated by metabolic stress, is also a likely prerequisite for islet amyloid formation to occur in type 2 diabetes. Islet transplants in patients with type 1 diabetes face similar stressors, and are subject to rapid amyloid formation and impaired proinsulin processing associated with progressive loss of β-cell function and mass. Declining β-cell mass is predicted to increase metabolic demand on remaining β-cells, promoting a feed-forward cycle of β-cell decline.

摘要

在 2 型糖尿病中,胰岛内的淀粉样物由β细胞肽胰岛淀粉样多肽(IAPP)的聚集形成。这些聚集物对β细胞有毒,诱导β细胞死亡和功能障碍,并引发胰岛炎症。β细胞受到许多其他应激源的影响,包括胰岛素抵抗和高血糖,这些应激源可能通过增加β细胞的 IAPP 产生而促进淀粉样物的形成。β细胞功能障碍,表现为葡萄糖刺激的胰岛素分泌受损和前激素处理缺陷,并因代谢应激而加重,也是 2 型糖尿病中胰岛淀粉样物形成的可能前提。1 型糖尿病患者的胰岛移植也面临着类似的应激源,容易发生淀粉样物形成和胰岛素原处理受损,导致β细胞功能和质量逐渐丧失。β细胞数量的减少预计会增加剩余β细胞的代谢需求,促进β细胞衰退的正反馈循环。

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