This minireview discusses the very important biomedical problem of treating type 2 diabetes mellitus (T2D). T2D accounts for more than 90% of the total number of diagnosed cases of diabetes mellitus and can result from aging, inflammation, obesity and β-cell senescence. The main symptom of both T2D and type 1 diabetes (T1D) is an increase in blood glucose concentration. While T1D is insulin-dependent and is associated with the destruction of pancreatic β-cells, T2D does not require lifelong insulin administration. In this case, pancreatic β-cells are not destroyed, but their functional activity is deregulated. In T2D, metabolic stress increases the number of senescent β-cells while impairing glucose tolerance. The potential paracrine effects of senescent β-cells highlight the importance of the β-cell senescenceassociated secretory phenotype (SASP) in driving metabolic dysfunction. We believe that the main reason for the deregulation of the functional activity of pancreatic β-cells in T2D is associated with their "aging" or senescence, which may be induced by various stressors. We propose the use of peroxiredoxin 6 as a new senolytic drug, and the role of β-cell senescence in the development of T2D is discussed in this review.
Keywords: Type 2 diabetes mellitus ; Senescent β-cells ; Aging ; Inflammation ; Obesity.
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