With increasing age, continuous exposure to stressors leads to pancreatic β-cells senescence. Pancreatic β-cells control glucose homeostasis by secreting insulin and dysfunction to such metabolic regulation emerges as a pivotal contributor to the development of type 2 diabetes (T2D). Irreversible cell cycle arrest, altered secretory patterns, and decreased proliferative capacity characterize aspects of pancreatic beta cell senescence. Consequently, β-cells lose their capacity to regenerate, leading to reduced β-cell mass and disrupting glucose homeostasis, thus influencing the pathophysiology of type 2 diabetes (T2D) due to these changes. The subsequent decline in beta cell function and mass, coupled with the deleterious effects of the senescence-associated secretory phenotype (SASP), contributes significantly to insulin resistance and the progression of T2D. A key mechanism involves SASP, a hypersecretory state linked to structural and metabolic changes, prolonged DNA damage responses, and the upregulation of several cell cycle inhibitors, all associated with pancreatic beta cell senescence. This chapter explores the complex interplay between these molecular factors and their implications for the pathogenesis of T2D. Further, it examines the therapeutic potential of targeting senescent cells through senotherapeutics that include senolytic and senomorphic therapies. While these strategies hold much promise, further research is imperative to elucidate the underlying mechanism to optimize clinical applications.