The prevalence of obesity, diabetes and heart failure increases with aging, and there is evidence that these age-related disorders share common pathologic features such as chronic low-grade inflammation and systemic metabolic dysfunction. Cellular senescence was initially discovered by in vitro studies, but it is now widely accepted that this process also occurs in vivo with aging. The p53 signaling pathway has a central role in the regulation of cellular senescence, and several lines of evidence indicate that cellular senescence has a causative role in the progression of age-related disorders. In obesity, chronic low-grade inflammation of visceral fat is characterized by production of pro-inflammatory cytokines and infiltration of immune cells, which induces systemic insulin resistance (hyperinsulinemia) that leads to the development of diabetes. Recently, p53-induced cellular senescence was reported to have a critical role in this process. In murine heart failure models, cellular senescence due to activation of p53 not only contributes to adipose tissue inflammation and systemic insulin resistance, but also to the progression of heart failure. This review outlines the pathological role of cellular senescence occurring in white adipose tissue in the development of obesity, diabetes, and heart failure.