ea0028p174 | Obesity, diabetes, metabolism and cardiovascular | SFEBES2012
Macfarlane David
, Raubenheimer Peter
, Bastin Mark
, Marshall Ian
, Andrew Ruth
, Walker Brian
Background & Aims: Observational studies implicate glucocorticoid excess, principally due to altered steroid metabolism in target tissues, in both the insulin resistance and liver fat accumulation that accompanies type 2 diabetes. To test the contribution of glucocorticoid signalling to metabolic dysfunction we blocked cortisol secretion (with metyrapone) and action (with the GR antagonist mifepristone) simultaneously in men with type 2 diabetes ± fatty liver.<p c...