testis, it protects cells from the growth-inhibiting and/or pro-apoptotic effects of cortisol, particularly during embryonic development. Mutations in this gene cause the syndrome of apparent mineralocorticoid excess and hypertension. The since the main functions of this HSD-11βs are for the regulation of glucocorticoids, the two isozymes are linked to various overstimulation or depletion of glucocorticosteroids that result in chemical imbalances in the human body. The effects of the enzyme as it relates to specific body functions and its associated disorders are listed below. Effect of Hyperlipidemia on 11β-hydroxysteroid-dehydrogenase 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. Activity of HSD-11βs in organs HSD-11βs are active in organs and in the adrenal gland. The two isoenzymes take on various duties. During an active state, HSD-11β promotes the increase in glucocorticoids in the hepatocytes and also enhances gluconeogenesis. The type 2 isozyme converts active glucocorticoid hormones to inactive metabolites in target tissues such as kidney, salivary glands, intestines, etc. The activation of the two isozymes of HSD-11β in the kidneys and liver triggers the extra-adrenal formation in alloxan diabetes, which affiliates with the reduction in the synthesis of glucocorticoid hormones in the adrenal glands. The extra-adrenal formation leads to the increased local formation of corticosterone in the liver and has a high activity of reactions with gluconeogenesis. These gluconeogenesis reactions add to the continued metabolic disorders similar to that of diabetes. Thus HSD-11β Type 1 can serve as a potential treatment agents for diabetes,