Cushing's syndrome (CS), including visceral obesity, dyslipidemia, hypertension and diabetes among its many manifestations, is “a model” of metabolic syndrome. Glucocorticoid (GC) excess, through a combination of effects on liver, muscle, adipose tissue and pancreas, increases gluconeogenesis and impairs insulin sensitivity, leading to carbohydrate abnormalities. Dyslipidemia is a common finding in CS as a consequence of GC-related increased lipolysis, lipogenesis and adipogenesis. CS patients experience typical changes in body composition, with fat redistribution resulting in accumulation of visceral adipose tissue. Hypertension, myocardial and vascular abnormalities along with the metabolic changes and the characteristic coagulopathy increase cardiovascular morbidity and mortality. Metabolic syndrome features can persist long after normalisation of cortisol levels.