This review explores the interplay between obesity, immunosenescence, and insulin resistance. Obesity, characterized by excessive fat accumulation, leads to metabolic dysregulation and cellular senescence in adipocytes. Senescent adipocytes release pro-inflammatory factors through the senescence-associated secretory phenotype (SASP), which can be transmitted to other cells, including immune cells, leading to immunosenescence. Immunosenescence, the senescence of immune cells, disrupts the clearance of senescent T-cells, contributing to chronic inflammation and impaired insulin signaling. This chronic inflammation disrupts insulin's metabolic actions, leading to insulin resistance and various metabolic disorders. The review highlights the role of senescent adipocyte cells in obesity-associated immunosenescence and subsequent metabolic dysregulation. It also suggests novel therapeutic approaches, such as targeting senescent T-cells or using senotherapeutics, to improve metabolic syndrome. The complex relationship between obesity, insulin resistance, and immunosenescence underscores the need for further research to develop effective treatments.This review explores the interplay between obesity, immunosenescence, and insulin resistance. Obesity, characterized by excessive fat accumulation, leads to metabolic dysregulation and cellular senescence in adipocytes. Senescent adipocytes release pro-inflammatory factors through the senescence-associated secretory phenotype (SASP), which can be transmitted to other cells, including immune cells, leading to immunosenescence. Immunosenescence, the senescence of immune cells, disrupts the clearance of senescent T-cells, contributing to chronic inflammation and impaired insulin signaling. This chronic inflammation disrupts insulin's metabolic actions, leading to insulin resistance and various metabolic disorders. The review highlights the role of senescent adipocyte cells in obesity-associated immunosenescence and subsequent metabolic dysregulation. It also suggests novel therapeutic approaches, such as targeting senescent T-cells or using senotherapeutics, to improve metabolic syndrome. The complex relationship between obesity, insulin resistance, and immunosenescence underscores the need for further research to develop effective treatments.