Sarcopenic obesity, a chronic condition, is today a major public health problem with increasing prevalence worldwide, which is due to progressively aging populations, the increasing prevalence of obesity, and the changes in lifestyle during the last several decades. Patients usually present to healthcare facilities for obesity and related comorbidities (type 2 diabetes mellitus, non-alcoholic fatty liver disease, dyslipidemia, hypertension, and cardiovascular disease) or for non-specific symptoms related to sarcopenia per se (e.g., fatigue, weakness, and frailty). Because of the non-specificity of the symptoms, sarcopenic obesity remains largely unsuspected and undiagnosed. The pathogenesis of sarcopenic obesity is multifactorial. There is interplay between aging, sedentary lifestyle, and unhealthy dietary habits, and insulin resistance, inflammation, and oxidative stress, resulting in a quantitative and qualitative decline in muscle mass and an increase in fat mass. Myokines, including myostatin and irisin, and adipokines play a prominent role in the pathogenesis of sarcopenic obesity. It has been suggested that a number of disorders affecting metabolism, physical capacity, and quality of life may be attributed to sarcopenic obesity, although it is not as yet established whether sarcopenia and obesity act synergistically. There is to date no approved pharmacological treatment for sarcopenic obesity. The cornerstones of its management are weight loss and adequate protein intake combined with exercise, the latter in order to reduce the loss of muscle mass observed during weight loss following diet unpaired with exercise. A consensus on the definition of sarcopenic obesity is considered essential to facilitate the performance of mechanistic studies and clinical trials aimed at deepening our knowledge, thus enabling improved management of affected individuals in the near future.
