It has been suggested that a vicious circle of maintaining a high volume of adipose tissue and skeletal muscle inflammation, triggers the development and acceleration of sarcopenic-obesity with a complex interplay between a number of mechanisms that are beyond the scope of this review (i.e. adipocyte-like phenotype of muscle progenitor cells, insulin resistance, impaired neuromodulation of contraction, leptin resistance, impaired endocrine function, reduced release of adiponectin, increased glycation products and oxidative stress etc.)(23, 63, 66). The gene discussed is LEP; the disease is Obesity.