Morton et al. (2001) investigated liver-dependent changes in lipid and lipoprotein metabolism in Hsd11b1 knockout mice ( Kotelevtsev et al. (1997) ). By measuring circulating levels of lipids and lipoproteins, Morton et al. (2001) observed lower plasma triglyceride levels, increased HDL cholesterol and apolipoprotein AI levels in Hsd11b1-deficient mice. Using Northern blot analysis, they detected exaggerated induction of genes encoding lipogenic enzymes and a marked suppression of genes for fat catabolism in Hsd11b1-null mice after fasting and refeeding. By measuring plasma glucose levels after fasting and refeeding, the authors determined that Hsd11b1-null mice have improved glucose tolerance. Morton et al. (2001) concluded that HSD11B1 deficiency produces an improved metabolic profile characterized by increased lipid catabolism, increased hepatic insulin sensitivity, and reduced intracellular glucocorticoid concentrations.
Hypercortisolism can occur in several disorders other than Cushing's syndrome [ 1,2 ]. When such patients present with clinical features consistent with Cushing's syndrome, they may also be referred to as having physiologic hypercortisolism or pseudo-Cushing's syndrome. Clinically, patients with these physiologic forms of hypercortisolism seldom have the cutaneous (ie, easy bruising, thinning, and friability) or muscle (ie, proximal muscle atrophy and weakness) signs of Cushing's syndrome [ 3 ]. However, these conditions/disorders should be excluded when evaluating patients for Cushing's syndrome. (See "Establishing the diagnosis of Cushing's syndrome", section on 'Exclude physiologic hypercortisolism' .)