| Notes
|
The protein encoded by this gene is a microsomal enzyme that catalyzes the conversion of the stress hormone cortisol to the inactive metabolite cortisone. In addition, the encoded protein can catalyze the reverse reaction, the conversion of cortisone to cortisol. Too much cortisol can lead to central obesity, and a particular variation in this gene has been associated with obesity and insulin resistance in children. Two transcript variants encoding the same protein have been found for this gene. 11beta-HSD1 activity may predict individual susceptibility to glucocorticoid-induced osteoporosis. 11beta-Hydroxysteroid dehydrogenase types 1 and 2 are up- and downregulated in cortisol-secreting adrenal adenomas. Acts as dehydrogenase inactivating cortisol to cortisone. 11beta-HSD1 dehydrogenase activity in ""uncommitted"" omental preadipocytes may provide autocrine mechanism to protect preadipocytes from differentiation, facilitating proliferation. Data report on the in vitro oxysterol-metabolizing properties of human and rodent 11beta-hydroxysteroid dehydrogenase. Decrease of 11betaHSD1 mRNA abundance and enzyme activity is associated with colorectal cancer. Decreased 11betaHSD1 activity and expression in obesity may act as a compensatory mechanism to enhance insulin sensitivity through a reduction in tissue-specific cortisol concentrations. Effect of cellular differentiation on 11beta-hydroxysteroid dehydrogenase activity in the intestine. HIV patients treated with HAART showewd an increase in mRNA of this enzyme in adipose tissue, correlated with insulin resistance. Hexose-6-phosphate dehydrogenase directly determines the reaction direction of 11beta-Hydroxysteroid dehydrogenase1 in intact cells as an oxoreductase. Higher adipose 11-HSD1 activity is associated with features of metabolic syndrome. Human adrenal cortex and aldosterone secreting adenomas express both 11beta-hydroxysteroid dehydrogenase type 1 and type 2 genes. May regulate levels of glucocorticoids. Plasma cortisol levels could be predicted by a model incorporating adrenal HSD11B2 and tumor size. Mutations in the genes encoding 11beta-hydroxysteroid dehydrogenase type 1 and hexose-6-phosphate dehydrogenase interact to cause cortisone reductase deficiency. P.1088: ""...genetic variations in the HSD11B1 gene were associated with Type 2 diabetes mellitus, plasma insulin concentrations and insulin action, independent of obesity. REVIEW: role in cortisol metabolism and visceral obesity. The current study provides additional evidence that variability at the 11[beta]HSD1 gene begets the development of hypertension and that over the years changes in the environment have modified the effect of 11[beta]HSD1 on blood pressure in Pima Indians. The portal vein delivers cortisol to the liver, and inhibition of 11HSD1 in visceral adipose tissue may be valuable in ameliorating insulin resistance in obesity. There is colocalization of 11beta-HSD1 and GR in the chorionic trophoblast. By binding to GR, glucocorticoids induce the expression of 11beta-HSD1 by a possible intracrine mechanism. A molecular switch during osteoblast differentiation controls 11beta-Hydroxysteroid dehydrogenase expression and glucocorticoid synthesis. Crystal structure of human 11beta-hydroxysteroid dehydrogenase type I. Cultured human ovarian surface epithelium (HOSE) cells express IL-1-responsive 11betaHSD1 mRNA. Data suggest increased expression of the 11beta-HSD1 gene is associated with metabolic abnormalities in obese women and that increased expression may contribute to increased local conversion of cortisone to cortisol in adipose tissue of obese individuals. Glucocorticoids can positively induce 11beta-HSD1 expression in amnion fibroblasts, an effect further strengthened by proinflammatory cytokines. Idiopathic obesity is associated with transcriptional up-regulation of 11HSD1 in adipose tissue. Increases in 11beta-HSD 1 expression/activity by intrauterine membranes during late gestation may result in increased potential for a local increase in fetal membranes should be considered as an extraadrenal source of cortisol during late gestation. Role of the N-terminal region on enzymatic activity and the relevance of 11beta-HSD1 orientation into the endoplasmic reticulum lumen.
|