Obesity, characterized by excessive fat accumulation, is linked to metabolic dysregulation and immune system dysfunction. Senescence, a cellular aging process, occurs in adipose tissue of obese individuals, leading to the release of pro-inflammatory factors known as SASP. This process contributes to immunosenescence, the aging of immune cells, which impairs the clearance of senescent T-cells and exacerbates chronic inflammation. This inflammation disrupts insulin signaling, leading to insulin resistance and metabolic disorders. The interplay between obesity, immunosenescence, and insulin resistance is complex, involving cellular senescence, chronic inflammation, and immune system dysfunction. Senescent T-cells and adipocytes contribute to the production of SASP, which promotes inflammation and impairs immune function. Targeting senescent T-cells or using senotherapeutics may offer new therapeutic strategies for metabolic syndrome and obesity-related diseases. Obesity also affects immune cell function, leading to reduced vaccine effectiveness and increased susceptibility to infections. The accumulation of senescent T-cells in visceral adipose tissue is associated with chronic inflammation and insulin resistance. Obesity-induced inflammation can lead to the polarization of macrophages, contributing to insulin resistance and metabolic disorders. The connection between obesity and immunosenescence is further supported by the role of inflammatory cytokines, such as TNF-α and IL-6, in promoting insulin resistance. Targeting senescent T-cells and reducing inflammation may be promising approaches for treating obesity-related metabolic disorders. The review highlights the importance of understanding the mechanisms underlying the interplay between obesity, immunosenescence, and insulin resistance, and suggests potential therapeutic strategies for improving metabolic health.Obesity, characterized by excessive fat accumulation, is linked to metabolic dysregulation and immune system dysfunction. Senescence, a cellular aging process, occurs in adipose tissue of obese individuals, leading to the release of pro-inflammatory factors known as SASP. This process contributes to immunosenescence, the aging of immune cells, which impairs the clearance of senescent T-cells and exacerbates chronic inflammation. This inflammation disrupts insulin signaling, leading to insulin resistance and metabolic disorders. The interplay between obesity, immunosenescence, and insulin resistance is complex, involving cellular senescence, chronic inflammation, and immune system dysfunction. Senescent T-cells and adipocytes contribute to the production of SASP, which promotes inflammation and impairs immune function. Targeting senescent T-cells or using senotherapeutics may offer new therapeutic strategies for metabolic syndrome and obesity-related diseases. Obesity also affects immune cell function, leading to reduced vaccine effectiveness and increased susceptibility to infections. The accumulation of senescent T-cells in visceral adipose tissue is associated with chronic inflammation and insulin resistance. Obesity-induced inflammation can lead to the polarization of macrophages, contributing to insulin resistance and metabolic disorders. The connection between obesity and immunosenescence is further supported by the role of inflammatory cytokines, such as TNF-α and IL-6, in promoting insulin resistance. Targeting senescent T-cells and reducing inflammation may be promising approaches for treating obesity-related metabolic disorders. The review highlights the importance of understanding the mechanisms underlying the interplay between obesity, immunosenescence, and insulin resistance, and suggests potential therapeutic strategies for improving metabolic health.