Pancreatic Beta-cell Dysfunction in Type 2 Diabetes

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102

초록

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.

키워드

glucotoxicity; lipotoxicity; mechanisms; β-cell death; β-cell loss; STIMULATED INSULIN-SECRETION; UNFOLDED PROTEIN RESPONSE; FATTY-ACID PALMITATE; ELECTRICAL-ACTIVITY; EUROPEAN SUBJECTS; ER STRESS; AUTOPHAGY; GLUCOSE; MASS; APOPTOSIS
제목
Pancreatic Beta-cell Dysfunction in Type 2 Diabetes
저자
Khin, Phyu Phyu; Lee, Jong Han; Jun, Hee-Sook
DOI
10.1177/1721727X231154152
발행일
2023-01
유형
Review
저널명
European Journal of Inflammation
권
21