**2.7 Glucocorticoids (GCs)**

GCs sources from both exogenous and endogenous have been recognized to be implicated in NAFLD development. Individuals with Cushing's syndrome, who have elevated GCs levels are associated with characteristic metabolic phenotype, including IR, central obesity, and DM, and many of these patients will have hepatic steatosis. Inhibition of fatty acid β-oxidation and activation of hepatocyte DNL have been reported as the potential mechanisms through which GCs stimulate hepatic lipid accumulation. Still, several individuals will have normal cortisol levels, indicating that tissue-specific pathways are involved in this metabolic dysfunction [4].
