Pancreatic Beta-cell Dysfunction in Type 2 Diabetesopen access
- Authors
- Khin, Phyu Phyu; Lee, Jong Han; Jun, Hee-Sook
- Issue Date
- Jan-2023
- Publisher
- SAGE Publications Inc.
- Keywords
- glucotoxicity; lipotoxicity; mechanisms; β-cell death; β-cell loss
- Citation
- European Journal of Inflammation, v.21
- Journal Title
- European Journal of Inflammation
- Volume
- 21
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/89112
- DOI
- 10.1177/1721727X231154152
- ISSN
- 1721-727X
- Abstract
- Pancreatic β-cells produce and secrete insulin to maintain blood glucose levels within a narrow range. Defects in the function and mass of β-cells play a significant role in the development and progression of diabetes. Increased β-cell deficiency and β-cell apoptosis are observed in the pancreatic islets of patients with type 2 diabetes. At an early stage, β-cells adapt to insulin resistance, and their insulin secretion increases, but they eventually become exhausted, and the β-cell mass decreases. Various causal factors, such as high glucose, free fatty acids, inflammatory cytokines, and islet amyloid polypeptides, contribute to the impairment of β-cell function. Therefore, the maintenance of β-cell function is a logical approach for the treatment and prevention of diabetes. In this review, we provide an overview of the role of these risk factors in pancreatic β-cell loss and the associated mechanisms. A better understanding of the molecular mechanisms underlying pancreatic β-cell loss will provide an opportunity to identify novel therapeutic targets for type 2 diabetes. © The Author(s) 2023.
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