Chronic glucocorticoid (GC) exposure in humans is well known to result in whole-body insulin resistance and obesity. Cushing syndrome, an endocrine disorder characterized by chronic endogenous or exogenous GC overexposure, increases visceral and trunk subcutaneous adipose tissue and causes insulin resistance.1,2 Likewise, abdominal obesity associated with the metabolic syndrome is linked with insulin resistance, cardiovascular risk, and decreased survival. Although endogenous Cushing syndrome is rare, the current prevalence of oral GC use in as high as 2.5% of the population makes insulin resistance and obesity resulting from exogenous GC exposure an important public health problem.3 Moreover, subtle forms of endogenous GC excess are seen in the setting of chronic stress owing to activation of the hypothalamic-pituitary-adrenal (HPA) axis, leading to increased production of adrenal cortisol. Furthermore, so-called common obesity is believed to be associated with abnormalities in the HPA axis including the presence of increased local production of GCs in the adipose tissue, alterations in cortisol circadian rhythm, and enhanced susceptibility of the HPA axis to be activated, all of which result in greater GC exposure over time. Thus, the study of GC-induced obesity and its adverse metabolic profile has become increasingly important.