Enhanced White Adipose Tissue Metabolism in Iatrogenic Cushing's Syndrome With FDG PET/CT

摘要

Glucocorticoids induce “catabolic” lipolysis, “ana- bolic” lipogenesis (adipocyte hypertrophy), and adipo- genesis (adipocyte hyperplasia) to remodel WAT into the characteristic Cushingoid distribution (1). Dexa- methasone-induced adipocyte differentiation (2) re- quired for ectopic WAT remodeling requires increased glycolytic mitochondrial metabolism (3), and thus ec- topic WAT FDG uptake. Increased lipogenesis utilizing glucose as a nonlipid substrate could also explain the widespread WAT FDG uptake in these cases (4). Dexa- methasone also induces a proinflammatory milieu within WAT (including raised serum amyloid A) (5), potentially increasing WAT FDG uptake associated with macrophage recruitment. The reduced fasting myocardial and skeletal muscle uptake presumably re- flects utilization of high circulating levels of free fatty acids and reduced insulin sensitivity.