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analysis
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high-throughput screening for potent and selective inhibitors of 11beta-hydroxysteroid dehydrogenase type I
analysis
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high-throughput screening for potent and selective inhibitors of 11beta-hydroxysteroid dehydrogenase type I
analysis
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use of microdialysis sampling coupled with liquid chromatography/electrospray ionization mass spectrometry to study 11beta-hydroxysteroid dehydrogenase type 1 catalyzed conversion of stable-isotope-labeled cortisone to cortisol in liver microsome. Results show species-specific reaction profiles, with a five times higher coversion rate in dog than in human and monkey liver microsome
analysis
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use of microdialysis sampling coupled with liquid chromatography/electrospray ionization mass spectrometry to study 11beta-hydroxysteroid dehydrogenase type 1 catalyzed conversion of stable-isotope-labeled cortisone to cortisol in liver microsome. Results show species-specific reaction profiles, with a five times higher coversion rate in dog than in human and monkey liver microsome
drug development
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isozyme 11beta-HSD1 is a target in treatment of metabolic diseases such as diabetes mellitus type 2 or obesity
drug development
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11beta-HSD1 will significantly contribute to the biotransformation of oracin in humans. The microsomal carbonyl reductase has a great potential to significantly impair the chemotherapy with the anticancer drug oracin
medicine
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exposure of fetus to high levels of synthetic glucocorticoid may have long-lasting effects on the hippocampal expression of hypothalamic-pituitary-adrenal-related genes into adulthood
medicine
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high-fat diet-induced obesity is accompanied by increased visceral fat preadipocyte differentiation in wild-type but not 11beta-HSD1 -/- mice
medicine
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methionine restriction disrupts the lipogenic/lipolytic balance, contributing importantly to adiposity resistance in Fischer 344 rats
medicine
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treatment of rats with dehydroepiandrosterone induces a shift from isoform 11beta-HSD1 to 11beta-HSD2 expression, increasing conversion from active to inactive glucocorticoids
medicine
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activation of cortisol by 11beta-hydroxysteroid dehydrogenase in granulosa cells increases with follicle development but is significantly decreased in ovarion cysts
medicine
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changes in ovarian cortisol metabolism are accompanied by corresponding changes in the levels of paracrine inhibitors of 11beta-hydroxysteroid dehydrogenase within growing ovarian follicles and cysts
medicine
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differentiation of cells causes a strong increase in 11beta-hydroxysteroid dehydrogenase protein levels, occuring late in the differentiation protocol. Reduction of 11beta-hydroxysteroid dehydrogenase activity in 3T3-L1 fibroblasts, achieved by pharmacological inhibition or adenovirally mediated delivery of short hairpin RNA constructs, specifically blocks the ability of inactive glucocorticoids to drive 3T3-L1 differentiation. Even modest increases in exogenous 11beta-hydroxysteroid dehydrogenase expression in 3T3-L1 fibroblasts, to levels comparable with endogenous 1 11beta-hydroxysteroid dehydrogenase in differentiated 3T3-L1 adipocytes, are sufficient to block adipogenesis
medicine
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in morbidly obese patients, 11beta-hydroxysteroid dehydrogenase 1 mRNA levlels are higher in subcutaneous adipose tissue than in visceral adipose tissue. Subcutaneous adipose tissue 11beta-hydroxysteroid dehydrogenase 1 levels increase parallel according to body mass index category. No correlation between subcutaneous adipose tissue or visceral adipose tissue with fasting glucose, total cholesterol, triglycerides, and high-density lipoprotein
medicine
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inhibition of 11beta-hydroxysteroid dehydrogenase type 1 activity reduces the availability of cortisol to activate the glucocorticoid receptor, down regulates gluconeogenesis and thus reduces plasma glucose levels in cortisone-induced diabetic KK mice. In mice treated with 11beta-hydroxysteroid dehydrogenase type 1-antisense oligonucleotide, plasma blood glucose levels are significantly reduced by up to 54% upon induction of diabetes. Cortisol and other diabetes end products are also reduced, and hepatic 11beta-hydroxysteroid dehydrogenase type 1 mRNA is suppressed by up to 84%
medicine
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significant decrease in 11beta-hydroxysteroid dehydrogenase reductase activity in mice with glycogen storage disease type 1b, whereas mice with glycogen storage disease type 1a show a marked increase in enzyme activity
medicine
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significant decrease in 11beta-hydroxysteroid dehydrogenase reductase activity in patients with glycogen storage disease type 1b, whereas patients with glycogen storage disease type 1a show a marked increase in enzyme activity
medicine
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significant induction of 11beta-hydroxysteroid dehydrogenase type 1 gene expression and activity in patients with alcoholic liver disease during long-term and short-term abstinence from alcohol
medicine
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sucrose can promote increased 11beta-hydroxysteroid dehydrogenase type 1 and hexose-6-phosphate dehydrogenase message in mesenteric fat while concomitantly decreasing 11beta-dehydroxysteroid dehydrogenase message and increasing hexose-6-phosphate dehydrogenase message in liver
medicine
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11beta-HSD1 inhibition may be a valid target for the treatment of diabetes
medicine
11beta-HSD1 inhibition may be a valid target for the treatment of diabetes
medicine
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11beta-HSD1 is a drug target for treatment of insulin resistance, diabetes and cardiovascular disease
medicine
inhibiting 11beta-HSD1 activity signifies a promising therapeutic strategy in the treatment of type 2 diabetes and related diseases
medicine
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measures of 11beta-HSD1 enzyme activity can predict the response of bone formation markers to therapeutic glucocorticoids
medicine
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at baseline, mRNA levels are similar in skeletal muscle of diabetic and control sugjects for 11beta-HSD1, 11beta-HSD2, and hexose-6-phosphate dehydrogenase. 11beta-HSD1 activity is reduced in diabetic subjects, while 11beta-HSD2 activity is increased. After application of dexamethasone, 11beta-HSD1 mRNA increases in both groups, whereas 11beta-HSD2 mRNA decreases. 11beta-HSD1 activity increases in diabetic subjects, but not in controls, whereas 11beta-HSD2 activity does not change in either group; mRNA levels are similar in diabetic and control subjects for 11beta-hydroxysteroid dehydrogenase 1 and 11beta-hydroxysteroid dehydrogenase 2. 11beta-Hydroxysteroid dehydrogenase 2-activity is higher in diabetic patients. After treatment with dexamethasone, 11beta-hydroxysteroid dehydrogenase 1-mRNA increases in both groups, whereas 11beta-hydroxysteroid dehydrogenase 2-mRNA decreases. 11beta-Hydroxysteroid dehydrogenase 1-activity increases in diabetic patients, but not in control, whereas 11beta-hydroxysteroid dehydrogenase 2-activity does not change in either group
medicine
curcumin is inhibitory to isoform 11beta-HSD1 in intact cells with IC50 value of 5.79 microM, competitive. Treatment with curcumin reduces serum glucose, cholesterol, triglyceride, low density lipoprotein levels in high-fat-diet-induced obese rats
medicine
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the enzyme activity is inversely associated with urinary cortisol/cortisone levels and it is not associated with the subclinical hypercortisolism complications
medicine
in breast cancer tissue, cholesterol epoxide hydrolase ChEH metabolizes cholesterol-5,6-epoxide into cholestane-3beta,5alpha,6beta-triol, which is transformed into the oncometabolite 6-oxo-cholestan-3beta,5alpha-diol by 11beta-hydroxysteroid-dehydrogenase 11betaHSD2. ChEH inhibition and 11betaHSD2 silencing inhibit 6-oxo-cholestan-3beta,5alpha-diol production and tumor growth. Patient breast cancer samples show significantly increased 6-oxocholestan-3beta,5alpha-diol levels and greater ChEH and 11betaHSD2 protein expression compared with normal tissues, and 11betaHSD2 and ChEH overexpression correlate with a higher risk of patient death
pharmacology
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isozyme 11beta-HSD1 is a target in treatment of metabolic diseases such as diabetes mellitus type 2 or obesity
pharmacology
the enzyme is an important therapeutic target for diabetes in humans