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These data suggest 11beta-HSD1 deficiency attenuates the hippocampal pro-inflammatory response to LPS, associated with increased capacity for aerobic glycolysis and mitochondrial ATP generation.
short review gives an overview on the main contradicting findings on the role of 11beta-HSD1 in the development of visceral obesity and diabetes type 2.
Ultraviolet- and infrared-induced 11 beta-hydroxysteroid dehydrogenase type 1 activating skin photoaging is inhibited by red ginseng extract containing high concentration of ginsenoside Rg3.
The authors show that lipoproteins including brain (apoE) and circulating (high-density lipoprotein, HDL) synergize to facilitate beta-amyloid transport across bioengineered human cerebral vessels.
results indicated that the HSD11B1 rs12086634 is associated with both type 2 diabetes (T2D) and metabolic syndrome (metS) but HSD11B1 rs846910 is associated with only T2D in South Indian population
The present study shows the temporal localisation of 11beta-HSD1 in uterus, highlighting its importance in the timing of gestation and suggesting its contribution in the myometrium contraction.
Neuroticism was associated with the rs12565406 polymorphism and had a mediatory role in the association between the polymorphism and postpartum depression. This finding elucidates the genetic background of neuroticism and postpartum depression.
This mini-review will focus on 11beta-HSD1 in skeletal muscle and its postulated link to obesity and insulin-resistance.
This study investigated the contribution of first trimester decidua to glucocorticoid availability at the fetal-maternal interface by assessing the expression and regulation of 11beta-HSD in human first trimester decidual tissues.
Moderate downregulation of 11beta-HSD1 can attenuate insulin insensitivity and the impairment of glucose-stimulated insulin secretion.
distributed extensively on the maternal side including decidual stromal cells and epithelial cells but scarcely on the fetal side except for localization in the fetal blood vessels of the chorionic villi
The reduction of DHT obese homozygotic twins could be linked to its increased degradation by AKR1C2 and HSD11B1, and increased estrogen levels could be linked to increased adiposity-related expression of aromatase in adipose tissue.
this study shows that the phenotypic switch of adipose tissue macrophages from M2 to mixed M1/M2 phenotype occurred through differentiation of adipocytes in obese individuals, and upregulation of intracellular 11beta-HSD1 might play a role in the process
11beta-HSD-2 plays an important role in the development of bone or osteoblast cell apoptosis, and the decreased expression of 11beta-HSD-2 may aggravate steroid induced bone/osteoblast cell apoptosis.
11beta-HSD1 may be an important enzyme in the pathogenesis of fatty liver and visceral obesity.
In HSD11B1 gene of rs3753519-stratified analysis, carriers of the minor allele presented significantly increased BMI, fasting plasma glucose and HOMA-IR. The study provides support for plausible implication of the HSD11B1 polymorphisms in susceptibility to develop undesirable effects of glucocorticoid replacement in Addison's disease.
Increased 11beta-HSD1 expression and its reductase activity in granulosa cells are the major causes of increased cortisol concentration in the follicular fluid of PCOS with insulin resistance.
Reciprocal regulation of the glucocorticoid metabolizing enzymes, 11beta-hydroxysteroid dehydrogenase types 1 and 2, is associated with steroid-responsiveness and disease remission in childhood nephrotic syndrome.
increased cortisol and 11beta-HSD1 abundance and decreased LOX abundance were observed in human amnion tissue after the labor-initiated spontaneous rupture of membranes
These findings indicated that 11beta-HSD1 inhibition can give a potential benefit in reducing obesity and lowering insulin resistance by modulating the insulin-signaling pathway and adipocytokine production.
Results describe the cloning, sequence and expression of 11beta-hydroxysteroid dehydrogenase type 1 from pig testis.
concluded that the 11beta-hydroxysteroid dehydrogenase (11beta-HSD1 and 2) system is involved in the regulation of cortisol activity in the testis and thus in the regulation of spermatogenesis
Effects of age, weaning and/or social isolation on the expression of genes regulating HSD11B1.
Data show that in the testis, caput epididymidis and bulbourethral gland of the immature pig, 11betaHSD1 and 2 catalyse inactivation of cortisol, supporting a role in limiting local actions of glucocorticoids within these tissues prior to puberty.
HSD11B1 was localized in mature adipocytes of early lactating cows, indicating that circulating glucocorticoids promote effects other than differentiation.
investigation of gene expression for 11HSD1, 11HSD2, and glucocorticoid receptor in granulosa cells and theca interna layers during follicular maturation and atresia: expression of 11HSD1 is developmentally regulated in maturing follicles
PGF2alpha but not PGE2 increases HSD11B1 bioactivity and protein expression by stimulating a posttranscriptional mechanism in stromal cells.
exercise training increases pulmonary expression of 11beta-HSD1, thus contributing to local glucocorticoid activation and suppression of pulmonary inflammation in obese mice
study demonstrates that glucocorticoid-induced insulin resistance was dependent on 11beta-HSD1, resulting in the critical activation of JNK signaling in adipocytes.
findings indicate that 11b-HSD1 regenerated glucocorticoids in the forebrain and decreased levels of Brain Derived Neurotrophic Factor in the hippocampus play a role in spatial memory deficits in aged wild-type mice.
11beta-HSD1 protein expression after caloric restriction was significantly up-regulated, while no difference was detected after re-feeding. Interestingly, upregulation of protein after CR (1.4-fold) was lower than the increase in enzymatic activity (2.6-fold).
11beta-HSD1 deficiency in myeloid phagocytes promotes angiogenesis.
These data identify suppression of CXCL2 and CXCL5 chemoattractant expression by 11beta-HSD1 as a novel mechanism with potential for regulation of neutrophil recruitment to the injured myocardium, and cardiac fibroblasts as a key site for intracellular glucocorticoid regeneration during acute inflammation following myocardial injury.
Brown adipose tissue (BAT) from aged 11beta-HSD1 KO mice showed elevated UCP1 protein and mitochondrial content, and a favorable profile of BAT function.
We envisage these data and models finding utility when investigating the muscle-specific functions of the 11beta-HSD1/G6PT/H6PDH triad.
11beta-HSD1-deficient mice are not protected from metabolic disease or hepatosteatosis in the face of a nonalcoholic fatty liver disease-inducing diet.
11beta-Hydroxysteroid dehydrogenase type 1 within muscle protects against the adverse effects of local inflammation.
these data suggest that corticosterone activation by 11beta-HSD1 in keratinocytes suppresses hapten-induced irritant dermatitis through suppression of expression of cytokines
Nr3c2 has a role in mouse skin development in a process that involves HSD11B1/HSD11B2
Loss of 11beta-HSD1 is associated with hepatocellular carcinoma.
These findings suggest that 11beta-HSD1 may contribute to the decline in Npas4 and Arc mRNA levels associated with memory impairment during ageing
Data (including data from knockout mice studies) suggest expression of 11bHSD1 (in cardiomyocytes, vascular smooth muscle, other cells) promotes infarct expansion/ventricular remodeling after myocardial infarction & limits angiogenesis/infarct repair.
Our results demonstrate an inhibitory effect of IGF-I on 11beta-HSD1 expression and activity within the pancreatic islets, which may mediate part of the IGF-I effects on cell proliferation, survival and insulin secretion
elevated in livers of offspring of restraint-stressed mothers
Data indicate that 11beta-HSD1 activity contributes substantially to diurnal and stress-induced increases in hippocampal CORT levels.
Dynamic increases in hippocampal 11b-HSD1 regenerated CORT levels during learning and retrieval play a key role in age- and stress-associated impairments of spatial memory.
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. Mutations in this gene and H6PD (hexose-6-phosphate dehydrogenase (glucose 1-dehydrogenase)) are the cause of cortisone reductase deficiency. Alternate splicing results in multiple transcript variants encoding the same protein.
11-beta-hydroxysteroid dehydrogenase 1
, hydroxysteroid 11-beta dehydrogenase 1
, hydroxysteroid (11-beta) dehydrogenase 1
, corticosteroid 11-beta-dehydrogenase isozyme 1
, short chain dehydrogenase/reductase family 26C, member 1
, 11-beta-hydroxysteroid dehydrogenase type 1
, 11-beta hydroxysteroid dehydrogenase
, 11 beta-hydroxysteroid dehydrogenase type 1
, 7-alpha-hydroxycholesterol dehydrogenase
, 11beta-hydroxysteroid dehydrogenase type 1
, Corticosteroid 11-beta-dehydrogenase, isozyme 1 (11-DH) (11-beta-hydroxysteroid dehydrogenase 1) (11-beta-HSD1) (11beta-HSD1A)
, cortocosteroid 11-beta dehydrogenase
, hydroxysteroid dehydrogenase, 11 beta type 1