Hyperlipidemia has a great effect on 11β-hydroxysteroid-dehydrogenase. Glucocorticoid is dependent on Glucocorticoid plasma concentration, cellular glucocorticoid receptor expression and the pre-receptor hormone metabolism that is catalyzed by 11β-HSD. There are two types of 11β-Hydroxysteroid dehydrogenases that control cortisol concentration: HSD-11β Type 1 and HSD-11β Type 2. HSD-11β Type 1 is responsible for converting cortisone to cortisol by acting as an oxo-reductase because it is NADP(H) dependent, while HSD-11β Type 2 inactivates cortisol to cortisone via NAD. 10-d hyperlipidemia increases the HSD-11β Type 1 expression in visceral and subcutaneous adipose tissues. Hyperlipidemia decreases HSD-11β Type 2 expression in the liver and adipose tissue. Hyperlipidemia has a great influence on HSD-11β Type 1 and HSD-11β Type 2. This demonstrates that there is likely a relationship between hyperlipidemia and cortisol metabolism. Cushing's Disease, synonymous with hypercortisolism, involves overwhelming the cortisol-neutralizing ability of 11β-HSD2 with high concentrations of cortisol. This allows cortisol to outcompete aldosterone and bind to mineralocorticoid receptors, resulting in the activation of several pathways that increase blood pressure.