Diabetes Research Center, School of Medicine, Ningbo University, Ningbo, China.
Department of nephrology, Ningbo Medical Center Li Huili Eastern Hospital Affiliated to Ningbo University.
Arch Physiol Biochem. 2020 Jul;126(3):235-241. doi: 10.1080/13813455.2018.1510967. Epub 2018 Oct 6.
Islet dysfunction is a hallmark of type 2 diabetes mellitus (T2DM). Compelling evidence suggests that accumulation of islet amyloid in the islets of Langerhans significantly contribute to β-cell dysfunction and diabetes. Emerging evidence implicates a role for cystic fibrosis transmembrane-conductance regulator in the regulation of insulin secretion from pancreatic islets. Impaired first-phase insulin responses and glucose homeostasis have also been reported in cystic fibrosis patients. The transforming growth factor-β protein superfamily is central regulators of pancreatic cell function, and has a key role in pancreas development and pancreatic disease, including diabetes and islet dysfunction. It is also becoming clear that islet inflammation plays a key role in the development of islet dysfunction. Inflammatory changes, including accumulation of macrophages, have been documented in type 2 diabetic islets. Islet dysfunction leads to hyperglycemia and ultimately the development of diabetes. In this review, we describe these risk factors and their associations with islet dysfunction.
胰岛功能障碍是 2 型糖尿病（T2DM）的一个标志。大量证据表明，胰岛中胰岛淀粉样蛋白的积累显著导致β细胞功能障碍和糖尿病。新出现的证据表明囊性纤维化跨膜电导调节剂在调节胰腺胰岛胰岛素分泌中的作用。囊性纤维化患者也报告了第一相胰岛素反应和葡萄糖稳态受损。转化生长因子-β蛋白超家族是胰腺细胞功能的中央调节剂，在胰腺发育和胰腺疾病（包括糖尿病和胰岛功能障碍）中起关键作用。目前也越来越清楚，胰岛炎症在胰岛功能障碍的发展中起着关键作用。在 2 型糖尿病的胰岛中已经记录到炎症变化，包括巨噬细胞的积累。胰岛功能障碍导致高血糖，最终导致糖尿病的发展。在这篇综述中，我们描述了这些危险因素及其与胰岛功能障碍的关系。
