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Pancreatic islet dysfunction in type 2 diabetes mellitus.

Authors
  • Hu, Fei1
  • Qiu, Xiaohui2
  • Bu, Shizhong1
  • 1 Diabetes Research Center, School of Medicine, Ningbo University, Ningbo, China. , (China)
  • 2 Department of nephrology, Ningbo Medical Center Li Huili Eastern Hospital Affiliated to Ningbo University.
Type
Published Article
Journal
Archives of physiology and biochemistry
Publication Date
Jul 01, 2020
Volume
126
Issue
3
Pages
235–241
Identifiers
DOI: 10.1080/13813455.2018.1510967
PMID: 30293453
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

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.

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