Pancreatic Beta-cell Dysfunction in Type 2 Diabetes

• Published in: European journal of inflammation Vol. 21
• Main Authors: Khin, Phyu Phyu, Lee, Jong Han, Jun, Hee-Sook
• Format: Journal Article
• Language: English
• Published: London, England SAGE Publications 01.01.2023; SAGE PUBLICATIONS, INC; SAGE Publishing
• Subjects: Cell growth; Cytokines; Diabetes; Fatty acids; Insulin; glucotoxicity; β-cell loss; β-cell death; mechanisms; lipotoxicity
• ISSN: 1721-727X; 2058-7392
• DOI: 10.1177/1721727X231154152

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.