POMC and adrenal gland hyperfunction: 1, 25). In studies in healthy subjects using limited assessments of metabolic flux, glucocorticoid receptor antagonism with RU38486 has been shown to achieve substantial drug levels in adipose tissue (17) and to lower serum triglycerides (31, 40) and reduce EGP (15). We show that glucocorticoid blockade was technically successful in elevating ACTH and preventing significant rebound hypercortisolemia (Fig. 2), resulting in lower fasting glucose and insulin levels and improved insulin sensitivity at multiple sites.