Enzymes of the oxidoreductase class that catalyze the dehydrogenation of hydroxysteroids. (From Enzyme Nomenclature, 1992) EC 1.1.-.
A low-affinity 11 beta-hydroxysteroid dehydrogenase found in a variety of tissues, most notably in LIVER; LUNG; ADIPOSE TISSUE; vascular tissue; OVARY; and the CENTRAL NERVOUS SYSTEM. The enzyme acts reversibly and can use either NAD or NADP as cofactors.
An high-affinity, NAD-dependent 11-beta-hydroxysteroid dehydrogenase that acts unidirectionally to catalyze the dehydrogenation of CORTISOL to CORTISONE. It is found predominantly in mineralocorticoid target tissues such as the KIDNEY; COLON; SWEAT GLANDS; and the PLACENTA. Absence of the enzyme leads to a fatal form of childhood hypertension termed, APPARENT MINERALOCORTICOID EXCESS SYNDROME.
A class of enzymes that catalyzes the oxidation of 17-hydroxysteroids to 17-ketosteroids. EC 1.1.-.
Catalyze the oxidation of 3-hydroxysteroids to 3-ketosteroids.
Hydroxysteroid dehydrogenases that catalyzes the reversible conversion of CORTISOL to the inactive metabolite CORTISONE. Enzymes in this class can utilize either NAD or NADP as cofactors.
A group of enzymes that catalyze the reversible reduction-oxidation reaction of 20-hydroxysteroids, such as from a 20-ketosteroid to a 20-alpha-hydroxysteroid (EC 1.1.1.149) or to a 20-beta-hydroxysteroid (EC 1.1.1.53).
A microsomal cytochrome P450 enzyme that catalyzes the 17-alpha-hydroxylation of progesterone or pregnenolone and subsequent cleavage of the residual two carbons at C17 in the presence of molecular oxygen and NADPH-FERRIHEMOPROTEIN REDUCTASE. This enzyme, encoded by CYP17 gene, generates precursors for glucocorticoid, androgen, and estrogen synthesis. Defects in CYP17 gene cause congenital adrenal hyperplasia (ADRENAL HYPERPLASIA, CONGENITAL) and abnormal sexual differentiation.
A 3-hydroxysteroid dehydrogenase which catalyzes the reversible reduction of the active androgen, DIHYDROTESTOSTERONE to 5 ALPHA-ANDROSTANE-3 ALPHA,17 BETA-DIOL. It also has activity towards other 3-alpha-hydroxysteroids and on 9-, 11- and 15- hydroxyprostaglandins. The enzyme is B-specific in reference to the orientation of reduced NAD or NADPH.
The main glucocorticoid secreted by the ADRENAL CORTEX. Its synthetic counterpart is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions.
Enzymes that catalyze the oxidation of estradiol at the 17-hydroxyl group in the presence of NAD+ or NADP+ to yield estrone and NADH or NADPH. The 17-hydroxyl group can be in the alpha- or beta-configuration. EC 1.1.1.62
A naturally occurring glucocorticoid. It has been used in replacement therapy for adrenal insufficiency and as an anti-inflammatory agent. Cortisone itself is inactive. It is converted in the liver to the active metabolite HYDROCORTISONE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p726)
Enzymes which transfer sulfate groups to various acceptor molecules. They are involved in posttranslational sulfation of proteins and sulfate conjugation of exogenous chemicals and bile acids. EC 2.8.2.
A subclass of enzymes which includes all dehydrogenases acting on primary and secondary alcohols as well as hemiacetals. They are further classified according to the acceptor which can be NAD+ or NADP+ (subclass 1.1.1), cytochrome (1.1.2), oxygen (1.1.3), quinone (1.1.5), or another acceptor (1.1.99).
A group of polycyclic compounds closely related biochemically to TERPENES. They include cholesterol, numerous hormones, precursors of certain vitamins, bile acids, alcohols (STEROLS), and certain natural drugs and poisons. Steroids have a common nucleus, a fused, reduced 17-carbon atom ring system, cyclopentanoperhydrophenanthrene. Most steroids also have two methyl groups and an aliphatic side-chain attached to the nucleus. (From Hawley's Condensed Chemical Dictionary, 11th ed)
A coenzyme composed of ribosylnicotinamide 5'-diphosphate coupled to adenosine 5'-phosphate by pyrophosphate linkage. It is found widely in nature and is involved in numerous enzymatic reactions in which it serves as an electron carrier by being alternately oxidized (NAD+) and reduced (NADH). (Dorland, 27th ed)
Reversibly catalyze the oxidation of a hydroxyl group of carbohydrates to form a keto sugar, aldehyde or lactone. Any acceptor except molecular oxygen is permitted. Includes EC 1.1.1.; EC 1.1.2.; and 1.1.99.
The rate dynamics in chemical or physical systems.
A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.
A potent androgenic steroid and major product secreted by the LEYDIG CELLS of the TESTIS. Its production is stimulated by LUTEINIZING HORMONE from the PITUITARY GLAND. In turn, testosterone exerts feedback control of the pituitary LH and FSH secretion. Depending on the tissues, testosterone can be further converted to DIHYDROTESTOSTERONE or ESTRADIOL.
A tetrameric enzyme that, along with the coenzyme NAD+, catalyzes the interconversion of LACTATE and PYRUVATE. In vertebrates, genes for three different subunits (LDH-A, LDH-B and LDH-C) exist.
A metabolite of TESTOSTERONE or ANDROSTENEDIONE with a 3-alpha-hydroxyl group and without the double bond. The 3-beta hydroxyl isomer is epiandrosterone.
A zinc-containing enzyme which oxidizes primary and secondary alcohols or hemiacetals in the presence of NAD. In alcoholic fermentation, it catalyzes the final step of reducing an aldehyde to an alcohol in the presence of NADH and hydrogen.
Tetrahydrocortisol is a metabolite of cortisol, a glucocorticoid hormone produced by the adrenal gland, which is used as a clinical marker to help diagnose conditions such as Cushing's syndrome and congenital adrenal hyperplasia.
An enzyme that oxidizes an aldehyde in the presence of NAD+ and water to an acid and NADH. This enzyme was formerly classified as EC 1.1.1.70.
Tetrahydrocortisone is a weak, endogenous glucocorticoid hormone, specifically a 3α,17,21-trihydroxy-5β-pregnane, that is synthesized in the adrenal gland from tetrahydrocortisol and further metabolized in the liver.
Enzymes that catalyze the dehydrogenation of GLYCERALDEHYDE 3-PHOSPHATE. Several types of glyceraldehyde-3-phosphate-dehydrogenase exist including phosphorylating and non-phosphorylating varieties and ones that transfer hydrogen to NADP and ones that transfer hydrogen to NAD.
An agent derived from licorice root. It is used for the treatment of digestive tract ulcers, especially in the stomach. Antidiuretic side effects are frequent, but otherwise the drug is low in toxicity.
Cytoplasmic proteins that specifically bind MINERALOCORTICOIDS and mediate their cellular effects. The receptor with its bound ligand acts in the nucleus to induce transcription of specific segments of DNA.
An enzymes that catalyzes the reversible reduction-oxidation reaction of 20-alpha-hydroxysteroids, such as from PROGESTERONE to 20-ALPHA-DIHYDROPROGESTERONE.
An enzyme that catalyzes the dehydrogenation of inosine 5'-phosphate to xanthosine 5'-phosphate in the presence of NAD. EC 1.1.1.205.

Perinatal development and adult blood pressure. (1/205)

A growing body of evidence supports the concept of fetal programming in cardiovascular disease in man, which asserts that an insult experienced in utero exerts a long-term influence on cardiovascular function, leading to disease in adulthood. However, this hypothesis is not universally accepted, hence animal models may be of value in determining potential physiological mechanisms which could explain how fetal undernutrition results in cardiovascular disease in later life. This review describes two major animal models of cardiovascular programming, the in utero protein-restricted rat and the cross-fostered spontaneously hypertensive rat. In the former model, moderate maternal protein restriction during pregnancy induces an increase in offspring blood pressure of 20-30 mmHg. This hypertensive effect is mediated, in part, by fetal exposure to excess maternal glucocorticoids as a result of a deficiency in placental 11-ss hydroxysteroid dehydrogenase type 2. Furthermore, nephrogenesis is impaired in this model which, coupled with increased activity of the renin-angiotensin system, could also contribute to the greater blood pressure displayed by these animals. The second model discussed is the cross-fostered spontaneously hypertensive rat. Spontaneously hypertensive rats develop severe hypertension without external intervention; however, their adult blood pressure may be lowered by 20-30 mmHg by cross-fostering pups to a normotensive dam within the first two weeks of lactation. The mechanisms responsible for this antihypertensive effect are less clear, but may also involve altered renal function and down-regulation of the renin-angiotensin system. These two models clearly show that adult blood pressure is influenced by exposure to one of a number of stimuli during critical stages of perinatal development.  (+info)

Structural analysis of the 11beta-hydroxysteroid dehydrogenase type 2 gene in end-stage renal disease. (2/205)

BACKGROUND: Mutations in the 11beta-hydroxysteroid dehydrogenase type 2 (11betaHSD2) gene cause a rare form of low-renin hypertension leading to end-stage renal disease (ESRD) in some affected subjects. To date, no search for mutations in the HSD11B2 gene was performed in a large population to obtain an estimate its prevalence. METHODS: The HSD11B2 gene was analyzed in 587 subjects, including 260 ESRD patients (either dialysis or transplanted) for mutations in the exons 2 through 5 and corresponding intronic regions by polymerase chain reaction (PCR) using appropriate overlapping primers, gel analysis by single strand conformational polymorphism (SSCP), and sequencing of identified migration variants. RESULTS: The prevalence of single-nucleotide polymorphisms (SNPs) in ESRD patients and controls was 26%. The following genetic variants were found among all subjects investigated: exon 2 T442G (Leu148/Val, N = 70) and C470A (Thr156/Thr, N = 67), exon 3 G534A (Glu178/Glu, N = 69), and exon 5 C1274T (Asp388/Asp, N = 2). Four SNPs were identified in intron 4 only. In the control population, the prevalence of the variants Leu148 and Thr156 was 14% each. Glu178 was 11%, while no variants were found in exon 5. In ESRD patients, the prevalence of the variant Leu148 was 9%, and Thr156 was 8%. Glu178 was 13%, while the Asp388 variant was 0.7%. In patients with a short duration between the time of diagnosis of the renal disease and the onset of ESRD, the prevalence of the Leu148 and Glu178 variants was higher than in subjects with slowly progressing renal disease. The 11betaHSD2 activity of all of these SNPs is predictably unaltered. CONCLUSIONS: There is a high prevalence of SNPs of the HSD11B2 gene, without causing exonic mutations generating a 11betaHSD2 enzyme with altered activity. Based on statistical analyses, the frequency of homozygosity for mutated alleles of the HSD11B2 gene can be derived as <1/250,000 when a Caucasian population is considered.  (+info)

Multiple aspects of mineralocorticoid selectivity. (3/205)

Aldosterone regulates renal sodium reabsorption through binding to the mineralocorticoid receptor (MR). Because the glucocorticoid receptor (GR) is expressed together with the MR in aldosterone target cells, glucocorticoid hormones bound to GR may also intervene to modulate physiological functions in these cells. In addition, each steroid can bind both receptors, and the MR has equal affinity for aldosterone and glucocorticoid hormones. Several cellular and molecular mechanisms intervene to allow specific aldosterone regulatory effects, despite the large prevalence of glucocorticoid hormones in the plasma. They include the local metabolism of the glucocorticoid hormones into inactive derivatives by the enzyme 11beta-hydroxysteroid dehydrogenase; the intrinsic properties of the MR that discriminate between ligands through differential contacts; the possibility of forming homo- or heterodimers between MR and GR, leading to differential transactivation properties; and the interactions of MR and GR with other regulatory transcription factors. The relative contribution of each of these successive mechanisms may vary among aldosterone target cells (epithelial vs. nonepithelial) and according to the hormonal context. All these phenomena allow fine tuning of cellular functions depending on the degree of cooperation between corticosteroid hormones and other factors (hormonal or tissue specific). Such interactions may be altered in pathophysiological situations.  (+info)

Aldosterone receptor antagonism normalizes vascular function in liquorice-induced hypertension. (4/205)

The enzyme 11beta-hydroxysteroid dehydrogenase (11beta-HSD2) provides mineralocorticoid receptor specificity for aldosterone by metabolizing glucocorticoids to their receptor-inactive 11-dehydro derivatives. The present study investigated the effects of the aldosterone receptor antagonists spironolactone and eplerenone on endothelial function in liquorice-induced hypertension. Glycyrrhizic acid (GA), a recognized inhibitor of 11beta-HSD2, was supplemented to the drinking water (3 g/L) of Wistar-Kyoto rats over a period of 21 days. From days 8 to 21, spironolactone (5.8+/-0.6 mg. kg(-1). d(-1)), eplerenone (182+/-13 mg. kg(-1). d(-1)), or placebo was added to the chow (n=7 animals per group). Endothelium-dependent or -independent vascular function was assessed as the relaxation of preconstricted aortic rings to acetylcholine or sodium nitroprusside, respectively. In addition, aortic endothelial nitric oxide synthase (eNOS) protein content, nitrate tissue levels, and endothelin-1 (ET-1) protein levels were determined. GA increased systolic blood pressure from 142+/-8 to 185+/-9 mm Hg (P<0.01). In the GA group, endothelium-dependent relaxation was impaired compared with that in controls (73+/-6% versus 99+/-5%), whereas endothelium-independent relaxation remained unchanged. In the aortas of 11beta-HSD2-deficient rats, eNOS protein content and nitrate tissue levels decreased (1114+/-128 versus 518+/-77 microgram/g protein, P<0.05). In contrast, aortic ET-1 protein levels were enhanced by GA (308+/-38 versus 497+/-47 pg/mg tissue, P<0.05). Both spironolactone and eplerenone normalized blood pressure in animals on GA (142+/-9 and 143+/-9 mm Hg, respectively, versus 189+/-8 mm Hg in the placebo group; P<0.01), restored endothelium-dependent relaxation (96+/-3% and 97+/-3%, respectively, P<0.01 versus placebo), blunted the decrease in vascular eNOS protein content and nitrate tissue levels, and normalized vascular ET-1 levels. This is the first study to demonstrate that aldosterone receptor antagonism normalizes blood pressure, prevents upregulation of vascular ET-1, restores NO-mediated endothelial dysfunction, and thus, may advance as a novel and specific therapeutic approach in 11beta-HSD2-deficient hypertension.  (+info)

Expression of 11 beta-hydroxysteroid dehydrogenase isozymes and corticosteroid hormone receptors in primary cultures of human trophoblast and placental bed biopsies. (5/205)

Interconversion of active and inactive glucocorticoids, e.g. cortisol (F) and cortisone (E) is catalysed by 11 beta-hydroxysteroid dehydrogenase (11 beta-HSD) which exists as two isoforms. We have used human placental bed biopsies and an in-vitro cytotrophoblast cell culture system to examine the expression and activity of the 11 beta-HSD isoforms along with that of the glucocorticoid and mineralocorticoid receptors (GR and MR). Immunohistochemistry localized 11 beta-HSD1 to decidualized stromal cells and 11 beta-HSD2 to villous cytotrophoblast, syncytiotrophoblasts and trophoblast cells invading the placental bed and maternal vasculature. In primary cultures of human cytotrophoblast, 11 beta-HSD2, GR and MR mRNA were expressed. Low levels of 11 beta-HSD1 mRNA were noted in these cultured cells, but could be explained on the basis of contaminating, vimentin-positive decidual stromal cells (< or =5%). Enzyme activity studies confirmed the presence of a high-affinity, NAD-dependent dehydrogenase activity (K(m) 137 nmol/l and V(max) 128 pmol E/h/mg protein), indicative of the 11 beta-HSD2 isoform. No reductase activity was observed. The presence of functional MR and GR was determined using Scatchard analyses of dexamethasone and aldosterone binding (MR K(d) 1.4 nmol/l B(max) 3.0; GR K(d) 6.6 nmol/l B(max) 16.2 fmol/ng protein). The expression of 11 beta-HSD1 in maternal decidua and 11 beta-HSD2 in adjacent trophoblast suggests an important role for glucocorticoids in determining trophoblast invasion. The presence of the MR within trophoblast indicates that some of the effects of cortisol could be MR- rather than GR-mediated.  (+info)

The intracellular localization of the mineralocorticoid receptor is regulated by 11beta-hydroxysteroid dehydrogenase type 2. (6/205)

11beta-hydroxysteroid dehydrogenase (11beta-HSD) type 2 has been considered to protect the mineralocorticoid receptor (MR) by converting 11beta-hydroxyglucocorticoids into their inactive 11-keto forms, thereby providing specificity to the MR for aldosterone. To investigate the functional protection of the MR by 11beta-HSD2, we coexpressed epitope-tagged MR and 11beta-HSD2 in HEK-293 cells lacking 11beta-HSD2 activity and analyzed their subcellular localization by fluorescence microscopy. When expressed alone in the absence of hormones, the MR was both cytoplasmic and nuclear. However, when coexpressed with 11beta-HSD2, the MR displayed a reticular distribution pattern, suggesting association with 11beta-HSD2 at the endoplasmic reticulum membrane. The endoplasmic reticulum membrane localization of the MR was observed upon coexpression only with 11beta-HSD2, but not with 11beta-HSD1 or other steroid-metabolizing enzymes. Aldosterone induced rapid nuclear translocation of the MR, whereas moderate cortisol concentrations (10-200 nm) did not activate the receptor, due to 11beta-HSD2-dependent oxidation to cortisone. Compromised 11beta-HSD2 activity (due to genetic mutations, the presence of inhibitors, or saturating cortisol concentrations) led to cortisol-induced nuclear accumulation of the MR. Surprisingly, the 11beta-HSD2 product cortisone blocked the aldosterone-induced MR activation by a strictly 11beta-HSD2-dependent mechanism. Our results provide evidence that 11beta-HSD2, besides inactivating 11beta-hydroxyglucocorticoids, functionally interacts with the MR and directly regulates the magnitude of aldosterone-induced MR activation.  (+info)

Increased ACTH levels do not alter renal 11beta-hydroxysteroid dehydrogenase type 2 gene expression in the sheep. (7/205)

The regulation of renal 11beta-hydroxysteroid dehydrogenase type 2 (11betaHSD2) gene expression is poorly understood. Inhibition of expression can result in hypertension. An example of this is in ectopic adrenocorticotropin (ACTH) syndrome (EAS). Inhibition of 11betaHSD2 activity is suggested by the observed increased ratio of cortisol to cortisone in both plasma and urine. To investigate whether ACTH or ACTH-dependent steroids can modulate renal 11betaHSD2 gene expression we analysed renal 11betaHSD2 mRNA levels after treatment with ACTH of 1 H and 24 H and demonstrated no change in the levels of gene expression. We have demonstrated in this study that the expression of 11betaHSD2 in the kidney is unaltered by ACTH. The reduced inactivation of cortisol by 11betaHSD2 observed in EAS is likely to be in part due to end product inhibition or substrate overload of the enzyme by endogenous substrates (cortisol, corticosterone, etc) rather than inhibition of 11betaHSD2 at the transcriptional level by either ACTH or ACTH regulated steroids.  (+info)

Course of placental 11beta-hydroxysteroid dehydrogenase type 2 and 15-hydroxyprostaglandin dehydrogenase mRNA expression during human gestation. (8/205)

BACKGROUND: During human pregnancy, 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2) plays an important role in protecting the fetus from high maternal glucocorticoid concentrations by converting cortisol to inactive cortisone. Furthermore, 11beta-HSD2 is indirectly involved in the regulation of the prostaglandin inactivating enzyme 15-hydroxyprostaglandin dehydrogenase (PGDH), because cortisol reduces the gene expression and enzyme activity of PGDH in human placental cells. OBJECTIVE: To examine developmental changes in placental 11beta-HSD2 and PGDH gene expression during the 2nd and 3rd trimesters of human pregnancies. METHODS: In placental tissue taken from 20 healthy women with normal pregnancy and 20 placentas of 17 mothers giving birth to premature babies, 11beta-HSD2 and PGDH mRNA expression was determined using quantitative real-time PCR. RESULTS: Placental mRNA expression of 11beta-HSD2 and PGDH increased significantly with gestational age (r=0.55, P=0.0002 and r=0.42, P=0.007). In addition, there was a significant correlation between the two enzymes (r=0.58, P<0.0001). CONCLUSIONS: In the course of pregnancy there is an increase in 11beta-HSD2 and PGDH mRNA expression in human placental tissue. This adaptation of 11beta-HSD2 prevents increasing maternal cortisol concentrations from transplacental passage and is exerted at the gene level. 11beta-HSD2 up-regulation may also lead to an increase in PGDH mRNA concentrations that, until term, possibly delays myometrial contractions induced by prostaglandins.  (+info)

Hydroxysteroid dehydrogenases (HSDs) are a group of enzymes that play a crucial role in steroid hormone metabolism. They catalyze the oxidation and reduction reactions of hydroxyl groups on the steroid molecule, which can lead to the activation or inactivation of steroid hormones. HSDs are involved in the conversion of various steroids, including sex steroids (e.g., androgens, estrogens) and corticosteroids (e.g., cortisol, cortisone). These enzymes can be found in different tissues throughout the body, and their activity is regulated by various factors, such as hormones, growth factors, and cytokines. Dysregulation of HSDs has been implicated in several diseases, including cancer, diabetes, and cardiovascular disease.

11-Beta-Hydroxysteroid Dehydrogenase Type 1 (11β-HSD1) is an enzyme that plays a crucial role in the metabolism of steroid hormones, particularly cortisol, in the body. Cortisol is a glucocorticoid hormone produced by the adrenal glands that helps regulate various physiological processes such as metabolism, immune response, and stress response.

11β-HSD1 is primarily expressed in liver, fat, and muscle tissues, where it catalyzes the conversion of cortisone to cortisol. Cortisone is a biologically inactive form of cortisol that is produced when cortisol levels are high, and it needs to be converted back to cortisol for the hormone to exert its effects.

By increasing the availability of active cortisol in these tissues, 11β-HSD1 has been implicated in several metabolic disorders, including obesity, insulin resistance, and type 2 diabetes. Inhibitors of 11β-HSD1 are currently being investigated as potential therapeutic agents for the treatment of these conditions.

11-Beta-Hydroxysteroid Dehydrogenase Type 2 (11β-HSD2) is an enzyme that plays a crucial role in the regulation of steroid hormones, particularly cortisol and aldosterone. It is primarily found in tissues such as the kidneys, colon, and salivary glands.

The main function of 11β-HSD2 is to convert active cortisol into inactive cortisone, which helps to prevent excessive mineralocorticoid receptor activation by cortisol. This is important because cortisol can bind to and activate mineralocorticoid receptors, leading to increased sodium reabsorption and potassium excretion in the kidneys, as well as other effects on blood pressure and electrolyte balance.

By converting cortisol to cortisone, 11β-HSD2 helps to protect mineralocorticoid receptors from being overstimulated by cortisol, allowing aldosterone to bind and activate these receptors instead. This is important for maintaining normal blood pressure and electrolyte balance.

Deficiencies or mutations in the 11β-HSD2 enzyme can lead to a condition called apparent mineralocorticoid excess (AME), which is characterized by high blood pressure, low potassium levels, and increased sodium reabsorption in the kidneys. This occurs because cortisol is able to bind to and activate mineralocorticoid receptors in the absence of 11β-HSD2 activity.

17-Hydroxysteroid dehydrogenases (17-HSDs) are a group of enzymes that play a crucial role in steroid hormone biosynthesis. They are involved in the conversion of 17-ketosteroids to 17-hydroxy steroids or vice versa, by adding or removing a hydroxyl group (–OH) at the 17th carbon atom of the steroid molecule. This conversion is essential for the production of various steroid hormones, including cortisol, aldosterone, and sex hormones such as estrogen and testosterone.

There are several isoforms of 17-HSDs, each with distinct substrate specificities, tissue distributions, and functions:

1. 17-HSD type 1 (17-HSD1): This isoform primarily catalyzes the conversion of estrone (E1) to estradiol (E2), an active form of estrogen. It is mainly expressed in the ovary, breast, and adipose tissue.
2. 17-HSD type 2 (17-HSD2): This isoform catalyzes the reverse reaction, converting estradiol (E2) to estrone (E1). It is primarily expressed in the placenta, prostate, and breast tissue.
3. 17-HSD type 3 (17-HSD3): This isoform is responsible for the conversion of androstenedione to testosterone, an essential step in male sex hormone biosynthesis. It is predominantly expressed in the testis and adrenal gland.
4. 17-HSD type 4 (17-HSD4): This isoform catalyzes the conversion of dehydroepiandrosterone (DHEA) to androstenedione, an intermediate step in steroid hormone biosynthesis. It is primarily expressed in the placenta.
5. 17-HSD type 5 (17-HSD5): This isoform catalyzes the conversion of cortisone to cortisol, a critical step in glucocorticoid biosynthesis. It is predominantly expressed in the adrenal gland and liver.
6. 17-HSD type 6 (17-HSD6): This isoform catalyzes the conversion of androstenedione to testosterone, similar to 17-HSD3. However, it has a different substrate specificity and is primarily expressed in the ovary.
7. 17-HSD type 7 (17-HSD7): This isoform catalyzes the conversion of estrone (E1) to estradiol (E2), similar to 17-HSD1. However, it has a different substrate specificity and is primarily expressed in the ovary.
8. 17-HSD type 8 (17-HSD8): This isoform catalyzes the conversion of DHEA to androstenedione, similar to 17-HSD4. However, it has a different substrate specificity and is primarily expressed in the testis.
9. 17-HSD type 9 (17-HSD9): This isoform catalyzes the conversion of estrone (E1) to estradiol (E2), similar to 17-HSD1. However, it has a different substrate specificity and is primarily expressed in the placenta.
10. 17-HSD type 10 (17-HSD10): This isoform catalyzes the conversion of DHEA to androstenedione, similar to 17-HSD4. However, it has a different substrate specificity and is primarily expressed in the testis.
11. 17-HSD type 11 (17-HSD11): This isoform catalyzes the conversion of estrone (E1) to estradiol (E2), similar to 17-HSD1. However, it has a different substrate specificity and is primarily expressed in the placenta.
12. 17-HSD type 12 (17-HSD12): This isoform catalyzes the conversion of DHEA to androstenedione, similar to 17-HSD4. However, it has a different substrate specificity and is primarily expressed in the testis.
13. 17-HSD type 13 (17-HSD13): This isoform catalyzes the conversion of estrone (E1) to estradiol (E2), similar to 17-HSD1. However, it has a different substrate specificity and is primarily expressed in the placenta.
14. 17-HSD type 14 (17-HSD14): This isoform catalyzes the conversion of DHEA to androstenedione, similar to 17-HSD4. However, it has a different substrate specificity and is primarily expressed in the testis.
15. 17-HSD type 15 (17-HSD15): This isoform catalyzes the conversion of estrone (E1) to estradiol (E2), similar to 17-HSD1. However, it has a different substrate specificity and is primarily expressed in the placenta.
16. 17-HSD type 16 (17-HSD16): This isoform catalyzes the conversion of DHEA to androstenedione, similar to 17-HSD4. However, it has a different substrate specificity and is primarily expressed in the testis.
17. 17-HSD type 17 (17-HSD17): This isoform catalyzes the conversion of estrone (E1) to estradiol (E2), similar to 17-HSD1. However, it has a different substrate specificity and is primarily expressed in the placenta.
18. 17-HSD type 18 (17-HSD18): This isoform catalyzes the conversion of DHEA to androstenedione, similar to 17-HSD4. However, it has a different substrate specificity and is primarily expressed in the testis.
19. 17-HSD type 19 (17-HSD19): This isoform catalyzes the conversion of estrone (E1) to estradiol (E2), similar to 17-HSD1. However, it has a different substrate specificity and is primarily expressed in the placenta.
20. 17-HSD type 20 (17-HSD20): This isoform catalyzes the conversion of DHEA to androstenedione, similar to 17-HSD4. However, it has a different substrate specificity and is primarily expressed in the testis.
21. 17-HSD type 21 (17-HSD21): This isoform catalyzes the conversion of estrone (E1) to estradiol (E2), similar to 17-HSD1. However, it has a different substrate specificity and is primarily expressed in the placenta.
22. 17-HSD type 22 (17-HSD22): This isoform catalyzes the conversion of DHEA to androstenedione, similar to 17-HSD4. However, it has a different substrate specificity and is primarily expressed in the testis.
23. 17-HSD type 23 (17-HSD23): This isoform catalyzes the conversion of estrone (E1) to estradiol (E2), similar to 17-HSD1. However, it has a different substrate specificity and is primarily expressed in the placenta.
24. 17-HSD type 24 (17-HSD24): This isoform catalyzes the conversion of DHEA to androstenedione, similar to 17-HSD4. However, it has a different substrate specificity and is primarily expressed in the testis.
25. 17-HSD type 25 (17-HSD25): This isoform catalyzes the conversion of estrone (E1) to estradiol (E2), similar to 17-HSD1. However, it has a different substrate specificity and is primarily expressed in the placenta.
26. 17-HSD type 26 (17-HSD26): This isoform catalyzes the conversion of DHEA to androstenedione, similar to 17-HSD4. However

3-Hydroxysteroid dehydrogenases (3-HSDs) are a group of enzymes that play a crucial role in steroid hormone biosynthesis. These enzymes catalyze the conversion of 3-beta-hydroxy steroids to 3-keto steroids, which is an essential step in the production of various steroid hormones, including progesterone, cortisol, aldosterone, and sex hormones such as testosterone and estradiol.

There are several isoforms of 3-HSDs that are expressed in different tissues and have distinct substrate specificities. For instance, 3-HSD type I is primarily found in the ovary and adrenal gland, where it catalyzes the conversion of pregnenolone to progesterone and 17-hydroxyprogesterone to 17-hydroxycortisol. On the other hand, 3-HSD type II is mainly expressed in the testes, adrenal gland, and placenta, where it catalyzes the conversion of dehydroepiandrosterone (DHEA) to androstenedione and androstenedione to testosterone.

Defects in 3-HSDs can lead to various genetic disorders that affect steroid hormone production and metabolism, resulting in a range of clinical manifestations such as adrenal insufficiency, ambiguous genitalia, and sexual development disorders.

11-Beta-Hydroxysteroid dehydrogenases (11-β-HSDs) are a group of enzymes that play a crucial role in the metabolism of steroid hormones, particularly cortisol and cortisone, which belong to the class of glucocorticoids. These enzymes exist in two isoforms: 11-β-HSD1 and 11-β-HSD2.

1. 11-β-HSD1: This isoform is primarily located within the liver, adipose tissue, and various other peripheral tissues. It functions as a NADPH-dependent reductase, converting inactive cortisone to its active form, cortisol. This enzyme helps regulate glucocorticoid action in peripheral tissues, influencing glucose and lipid metabolism, insulin sensitivity, and inflammation.
2. 11-β-HSD2: This isoform is predominantly found in mineralocorticoid target tissues such as the kidneys, colon, and salivary glands. It functions as a NAD+-dependent dehydrogenase, converting active cortisol to its inactive form, cortisone. By doing so, it protects the mineralocorticoid receptor from being overstimulated by cortisol, ensuring aldosterone specifically binds and activates this receptor to maintain proper electrolyte and fluid balance.

Dysregulation of 11-β-HSDs has been implicated in several disease states, including metabolic syndrome, type 2 diabetes, hypertension, and psychiatric disorders. Therefore, understanding the function and regulation of these enzymes is essential for developing novel therapeutic strategies to treat related conditions.

20-Hydroxysteroid Dehydrogenases (20-HSDs) are a group of enzymes that play a crucial role in the metabolism of steroid hormones. These enzymes catalyze the conversion of steroid hormone precursors to their active forms by adding or removing a hydroxyl group at the 20th carbon position of the steroid molecule.

There are several isoforms of 20-HSDs, each with distinct tissue distribution and substrate specificity. The most well-known isoforms include 20-HSD type I and II, which have opposing functions in regulating the activity of cortisol, a glucocorticoid hormone produced by the adrenal gland.

Type I 20-HSD, primarily found in the liver and adipose tissue, converts inactive cortisone to its active form, cortisol. In contrast, type II 20-HSD, expressed mainly in the kidney, brain, and immune cells, catalyzes the reverse reaction, converting cortisol back to cortisone.

Dysregulation of 20-HSDs has been implicated in various medical conditions, such as metabolic disorders, inflammatory diseases, and cancers. Therefore, understanding the function and regulation of these enzymes is essential for developing targeted therapies for these conditions.

Steroid 17-alpha-hydroxylase, also known as CYP17A1, is a cytochrome P450 enzyme that plays a crucial role in steroid hormone biosynthesis. It is located in the endoplasmic reticulum of cells in the adrenal glands and gonads. This enzyme catalyzes the 17-alpha-hydroxylation and subsequent lyase cleavage of pregnenolone and progesterone, converting them into dehydroepiandrosterone (DHEA) and androstenedione, respectively. These steroid intermediates are essential for the biosynthesis of both glucocorticoids and sex steroids, including cortisol, aldosterone, estrogens, and testosterone.

Defects in the CYP17A1 gene can lead to several disorders, such as congenital adrenal hyperplasia (CAH) due to 17-alpha-hydroxylase deficiency, which is characterized by decreased production of cortisol and sex steroids and increased mineralocorticoid levels. This condition results in sexual infantilism, electrolyte imbalances, and hypertension.

Hydrocortisone is a synthetic glucocorticoid, which is a class of steroid hormones. It is identical to the naturally occurring cortisol, a hormone produced by the adrenal gland that helps regulate metabolism and helps your body respond to stress. Hydrocortisone has anti-inflammatory effects and is used to treat various inflammatory conditions such as allergies, skin disorders, and autoimmune diseases. It works by suppressing the immune system's response to reduce swelling, redness, itching, and other symptoms caused by inflammation.

Hydrocortisone is available in different forms, including oral tablets, topical creams, lotions, gels, and ointments, as well as injectable solutions. The specific use and dosage depend on the condition being treated and the individual patient's medical history and current health status.

As with any medication, hydrocortisone can have side effects, especially when used in high doses or for extended periods. Common side effects include increased appetite, weight gain, mood changes, insomnia, and skin thinning. Long-term use of hydrocortisone may also increase the risk of developing osteoporosis, diabetes, cataracts, and other health problems. Therefore, it is essential to follow your healthcare provider's instructions carefully when using this medication.

Estradiol dehydrogenases are a group of enzymes that are involved in the metabolism of estradiols, which are steroid hormones that play important roles in the development and maintenance of female reproductive system and secondary sexual characteristics. These enzymes catalyze the oxidation or reduction reactions of estradiols, converting them to other forms of steroid hormones.

There are two main types of estradiol dehydrogenases: 1) 3-alpha-hydroxysteroid dehydrogenase (3-alpha HSD), which catalyzes the conversion of estradi-17-beta to estrone, and 2) 17-beta-hydroxysteroid dehydrogenase (17-beta HSD), which catalyzes the reverse reaction, converting estrone back to estradiol.

These enzymes are widely distributed in various tissues, including the ovaries, placenta, liver, and adipose tissue, and play important roles in regulating the levels of estradiols in the body. Abnormalities in the activity of these enzymes have been associated with several medical conditions, such as hormone-dependent cancers, polycystic ovary syndrome, and hirsutism.

Cortisone is a type of corticosteroid hormone that is produced naturally in the body by the adrenal gland. It is released in response to stress and helps to regulate metabolism, reduce inflammation, and suppress the immune system. Cortisone can also be synthetically produced and is often used as a medication to treat a variety of conditions such as arthritis, asthma, and skin disorders. It works by mimicking the effects of the natural hormone in the body and reducing inflammation and suppressing the immune system. Cortisone can be administered through various routes, including oral, injectable, topical, and inhalational.

Sulfotransferases (STs) are a group of enzymes that play a crucial role in the process of sulfoconjugation, which is the transfer of a sulfo group (-SO3H) from a donor molecule to an acceptor molecule. These enzymes are widely distributed in nature and are found in various organisms, including humans.

In humans, STs are involved in the metabolism and detoxification of numerous xenobiotics, such as drugs, food additives, and environmental pollutants, as well as endogenous compounds, such as hormones, neurotransmitters, and lipids. The sulfoconjugation reaction catalyzed by STs can increase the water solubility of these compounds, facilitating their excretion from the body.

STs can be classified into several families based on their sequence similarity and cofactor specificity. The largest family of STs is the cytosolic sulfotransferases, which use 3'-phosphoadenosine 5'-phosphosulfate (PAPS) as a cofactor to transfer the sulfo group to various acceptor molecules, including phenols, alcohols, amines, and steroids.

Abnormalities in ST activity have been implicated in several diseases, such as cancer, cardiovascular disease, and neurological disorders. Therefore, understanding the function and regulation of STs is essential for developing new therapeutic strategies to treat these conditions.

Alcohol oxidoreductases are a class of enzymes that catalyze the oxidation of alcohols to aldehydes or ketones, while reducing nicotinamide adenine dinucleotide (NAD+) to NADH. These enzymes play an important role in the metabolism of alcohols and other organic compounds in living organisms.

The most well-known example of an alcohol oxidoreductase is alcohol dehydrogenase (ADH), which is responsible for the oxidation of ethanol to acetaldehyde in the liver during the metabolism of alcoholic beverages. Other examples include aldehyde dehydrogenases (ALDH) and sorbitol dehydrogenase (SDH).

These enzymes are important targets for the development of drugs used to treat alcohol use disorder, as inhibiting their activity can help to reduce the rate of ethanol metabolism and the severity of its effects on the body.

Steroids, also known as corticosteroids, are a type of hormone that the adrenal gland produces in your body. They have many functions, such as controlling the balance of salt and water in your body and helping to reduce inflammation. Steroids can also be synthetically produced and used as medications to treat a variety of conditions, including allergies, asthma, skin conditions, and autoimmune disorders.

Steroid medications are available in various forms, such as oral pills, injections, creams, and inhalers. They work by mimicking the effects of natural hormones produced by your body, reducing inflammation and suppressing the immune system's response to prevent or reduce symptoms. However, long-term use of steroids can have significant side effects, including weight gain, high blood pressure, osteoporosis, and increased risk of infections.

It is important to note that anabolic steroids are a different class of drugs that are sometimes abused for their muscle-building properties. These steroids are synthetic versions of the male hormone testosterone and can have serious health consequences when taken in large doses or without medical supervision.

NAD (Nicotinamide Adenine Dinucleotide) is a coenzyme found in all living cells. It plays an essential role in cellular metabolism, particularly in redox reactions, where it acts as an electron carrier. NAD exists in two forms: NAD+, which accepts electrons and becomes reduced to NADH. This pairing of NAD+/NADH is involved in many fundamental biological processes such as generating energy in the form of ATP during cellular respiration, and serving as a critical cofactor for various enzymes that regulate cellular functions like DNA repair, gene expression, and cell death.

Maintaining optimal levels of NAD+/NADH is crucial for overall health and longevity, as it declines with age and in certain disease states. Therefore, strategies to boost NAD+ levels are being actively researched for their potential therapeutic benefits in various conditions such as aging, neurodegenerative disorders, and metabolic diseases.

Carbohydrate dehydrogenases are a group of enzymes that catalyze the oxidation of carbohydrates, including sugars and sugar alcohols. These enzymes play a crucial role in cellular metabolism by helping to convert these molecules into forms that can be used for energy or as building blocks for other biological compounds.

During the oxidation process, carbohydrate dehydrogenases remove hydrogen atoms from the carbohydrate substrate and transfer them to an electron acceptor, such as NAD+ or FAD. This results in the formation of a ketone or aldehyde group on the carbohydrate molecule and the reduction of the electron acceptor to NADH or FADH2.

Carbohydrate dehydrogenases are classified into several subgroups based on their substrate specificity, cofactor requirements, and other factors. Some examples include glucose dehydrogenase, galactose dehydrogenase, and sorbitol dehydrogenase.

These enzymes have important applications in various fields, including biotechnology, medicine, and industry. For example, they can be used to detect or quantify specific carbohydrates in biological samples, or to produce valuable chemical compounds through the oxidation of renewable resources such as plant-derived sugars.

In the context of medicine and pharmacology, "kinetics" refers to the study of how a drug moves throughout the body, including its absorption, distribution, metabolism, and excretion (often abbreviated as ADME). This field is called "pharmacokinetics."

1. Absorption: This is the process of a drug moving from its site of administration into the bloodstream. Factors such as the route of administration (e.g., oral, intravenous, etc.), formulation, and individual physiological differences can affect absorption.

2. Distribution: Once a drug is in the bloodstream, it gets distributed throughout the body to various tissues and organs. This process is influenced by factors like blood flow, protein binding, and lipid solubility of the drug.

3. Metabolism: Drugs are often chemically modified in the body, typically in the liver, through processes known as metabolism. These changes can lead to the formation of active or inactive metabolites, which may then be further distributed, excreted, or undergo additional metabolic transformations.

4. Excretion: This is the process by which drugs and their metabolites are eliminated from the body, primarily through the kidneys (urine) and the liver (bile).

Understanding the kinetics of a drug is crucial for determining its optimal dosing regimen, potential interactions with other medications or foods, and any necessary adjustments for special populations like pediatric or geriatric patients, or those with impaired renal or hepatic function.

The liver is a large, solid organ located in the upper right portion of the abdomen, beneath the diaphragm and above the stomach. It plays a vital role in several bodily functions, including:

1. Metabolism: The liver helps to metabolize carbohydrates, fats, and proteins from the food we eat into energy and nutrients that our bodies can use.
2. Detoxification: The liver detoxifies harmful substances in the body by breaking them down into less toxic forms or excreting them through bile.
3. Synthesis: The liver synthesizes important proteins, such as albumin and clotting factors, that are necessary for proper bodily function.
4. Storage: The liver stores glucose, vitamins, and minerals that can be released when the body needs them.
5. Bile production: The liver produces bile, a digestive juice that helps to break down fats in the small intestine.
6. Immune function: The liver plays a role in the immune system by filtering out bacteria and other harmful substances from the blood.

Overall, the liver is an essential organ that plays a critical role in maintaining overall health and well-being.

Testosterone is a steroid hormone that belongs to androsten class of hormones. It is primarily secreted by the Leydig cells in the testes of males and, to a lesser extent, by the ovaries and adrenal glands in females. Testosterone is the main male sex hormone and anabolic steroid. It plays a key role in the development of masculine characteristics, such as body hair and muscle mass, and contributes to bone density, fat distribution, red cell production, and sex drive. In females, testosterone contributes to sexual desire and bone health. Testosterone is synthesized from cholesterol and its production is regulated by luteinizing hormone (LH) and follicle-stimulating hormone (FSH).

L-Lactate Dehydrogenase (LDH) is an enzyme found in various tissues within the body, including the heart, liver, kidneys, muscles, and brain. It plays a crucial role in the process of energy production, particularly during anaerobic conditions when oxygen levels are low.

In the presence of the coenzyme NADH, LDH catalyzes the conversion of pyruvate to lactate, generating NAD+ as a byproduct. Conversely, in the presence of NAD+, LDH can convert lactate back to pyruvate using NADH. This reversible reaction is essential for maintaining the balance between lactate and pyruvate levels within cells.

Elevated blood levels of LDH may indicate tissue damage or injury, as this enzyme can be released into the circulation following cellular breakdown. As a result, LDH is often used as a nonspecific biomarker for various medical conditions, such as myocardial infarction (heart attack), liver disease, muscle damage, and certain types of cancer. However, it's important to note that an isolated increase in LDH does not necessarily pinpoint the exact location or cause of tissue damage, and further diagnostic tests are usually required for confirmation.

Androsterone is a weak androgen and an endogenous steroid hormone. It's produced in the liver from dehydroepiandrosterone (DHEA) and is converted into androstenedione, another weak androgen. Androsterone is excreted in urine as a major metabolite of testosterone. It plays a role in male sexual development and function, although its effects are much weaker than those of testosterone. In clinical contexts, androsterone levels may be measured to help diagnose certain hormonal disorders or to monitor hormone therapy.

Alcohol dehydrogenase (ADH) is a group of enzymes responsible for catalyzing the oxidation of alcohols to aldehydes or ketones, and reducing equivalents such as NAD+ to NADH. In humans, ADH plays a crucial role in the metabolism of ethanol, converting it into acetaldehyde, which is then further metabolized by aldehyde dehydrogenase (ALDH) into acetate. This process helps to detoxify and eliminate ethanol from the body. Additionally, ADH enzymes are also involved in the metabolism of other alcohols, such as methanol and ethylene glycol, which can be toxic if allowed to accumulate in the body.

Tetrahydrocortisol (THF) is a metabolite of cortisol, which is a natural hormone produced by the adrenal gland in response to stress. Cortisol has various functions in the body, including regulating metabolism, immune response, and stress reaction.

Tetrahydrocortisol is formed when cortisol undergoes reduction in the liver by the enzyme 5β-reductase. It is a weak glucocorticoid with minimal biological activity compared to cortisol. Tetrahydrocortisol is primarily used as a biomarker for assessing cortisol production and metabolism in research and clinical settings, particularly in the diagnosis of disorders related to the adrenal gland or hypothalamic-pituitary-adrenal (HPA) axis.

There are two major types of tetrahydrocortisol: 5β-tetrahydrocortisol (5β-THF) and 5α-tetrahydrocortisol (5α-THF). The ratio of these two forms can provide additional information about cortisol metabolism, as the activity of 5β-reductase may vary in different individuals or under certain conditions.

Aldehyde dehydrogenase (ALDH) is a class of enzymes that play a crucial role in the metabolism of alcohol and other aldehydes in the body. These enzymes catalyze the oxidation of aldehydes to carboxylic acids, using nicotinamide adenine dinucleotide (NAD+) as a cofactor.

There are several isoforms of ALDH found in different tissues throughout the body, with varying substrate specificities and kinetic properties. The most well-known function of ALDH is its role in alcohol metabolism, where it converts the toxic aldehyde intermediate acetaldehyde to acetate, which can then be further metabolized or excreted.

Deficiencies in ALDH activity have been linked to a number of clinical conditions, including alcohol flush reaction, alcohol-induced liver disease, and certain types of cancer. Additionally, increased ALDH activity has been associated with chemotherapy resistance in some cancer cells.

Tetrahydrocortisone is a physiological inactive end product of cortisol metabolism. It's a type of steroid hormone that is produced by the adrenal gland and plays a role in the response to stress, the regulation of metabolism, and the immune system.

Tetrahydrocortisone is formed when cortisol, also known as hydrocortisone, is metabolized in the liver by the enzyme 3α-hydroxysteroid dehydrogenase (3α-HSD). This reaction converts cortisol to tetrahydrocortisone, which is then conjugated with glucuronic acid and excreted in the urine.

Tetrahydrocortisone has no known biological activity, and its measurement in the body is primarily used as a marker for cortisol metabolism. Abnormal levels of tetrahydrocortisone may indicate disorders of cortisol metabolism or adrenal gland function.

Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is an enzyme that plays a crucial role in the metabolic pathway of glycolysis. Its primary function is to convert glyceraldehyde-3-phosphate (a triose sugar phosphate) into D-glycerate 1,3-bisphosphate, while also converting nicotinamide adenine dinucleotide (NAD+) into its reduced form NADH. This reaction is essential for the production of energy in the form of adenosine triphosphate (ATP) during cellular respiration. GAPDH has also been implicated in various non-metabolic processes, including DNA replication, repair, and transcription regulation, due to its ability to interact with different proteins and nucleic acids.

Carbenoxolone is a synthetic derivative of glycyrrhizin, which is found in the root of the licorice plant. It has been used in the treatment of gastric and duodenal ulcers due to its ability to increase the mucosal resistance and promote healing. Carbenoxolone works by inhibiting the enzyme 11-beta-hydroxysteroid dehydrogenase, which leads to an increase in the levels of cortisol and other steroids in the body. This can have various effects on the body, including anti-inflammatory and immunosuppressive actions.

However, long-term use of carbenoxolone has been associated with serious side effects such as hypertension, hypokalemia (low potassium levels), and edema (fluid retention). Therefore, its use is generally limited to short-term treatment of gastric and duodenal ulcers.

Medical Definition: Carbenoxolone

A synthetic derivative of glycyrrhizin, used in the treatment of gastric and duodenal ulcers due to its ability to increase mucosal resistance and promote healing. It is an inhibitor of 11-beta-hydroxysteroid dehydrogenase, leading to increased levels of cortisol and other steroids in the body, with potential anti-inflammatory and immunosuppressive effects. However, long-term use is associated with serious side effects such as hypertension, hypokalemia, and edema.

Medical Definition:

Mineralocorticoid Receptors (MRs) are a type of nuclear receptor protein that are activated by the binding of mineralocorticoid hormones, such as aldosterone. These receptors are expressed in various tissues and cells, including the kidneys, heart, blood vessels, and brain.

When activated, MRs regulate gene expression related to sodium and potassium homeostasis, water balance, and electrolyte transport. This is primarily achieved through the regulation of ion channels and transporters in the distal nephron of the kidney, leading to increased sodium reabsorption and potassium excretion.

Abnormalities in mineralocorticoid receptor function have been implicated in several diseases, including hypertension, heart failure, and primary aldosteronism.

20-α-Hydroxysteroid Dehydrogenase (20-α-HSD) is an enzyme that catalyzes the conversion of steroids, specifically the oxidation of 20α-hydroxysteroids to 20-keto steroids. This enzyme plays a crucial role in the metabolism and regulation of steroid hormones, such as corticosteroids and progestogens.

In the adrenal gland, 20-α-HSD is involved in the biosynthesis and interconversion of various corticosteroids, including cortisol, cortisone, and aldosterone. By catalyzing the conversion of cortisol to cortisone or vice versa, this enzyme helps maintain a balance between active and inactive forms of these hormones, which is essential for proper physiological functioning.

In the reproductive system, 20-α-HSD is involved in the metabolism of progestogens, such as progesterone and its derivatives. This enzyme can convert active forms of progestogens into their inactive counterparts, thereby regulating their levels and activity within the body.

Dysregulation or mutations in 20-α-HSD have been implicated in several medical conditions, including adrenal insufficiency, congenital adrenal hyperplasia, and certain reproductive disorders.

Inosine Monophosphate Dehydrogenase (IMDH or IMPDH) is an enzyme that is involved in the de novo biosynthesis of guanine nucleotides. It catalyzes the conversion of inosine monophosphate (IMP) to xanthosine monophosphate (XMP), which is the rate-limiting step in the synthesis of guanosine triphosphate (GTP).

There are two isoforms of IMPDH, type I and type II, which are encoded by separate genes. Type I IMPDH is expressed in most tissues, while type II IMPDH is primarily expressed in lymphocytes and other cells involved in the immune response. Inhibitors of IMPDH have been developed as immunosuppressive drugs to prevent rejection of transplanted organs. Defects in the gene encoding IMPDH type II have been associated with retinal degeneration and hearing loss.

497 (2): 223-50. doi:10.1002/cne.20993. PMID 16705681. Shin, JW; Geerling, JC; Loewy, AD (Dec 10, 2008). "Inputs to the ... 26 (2): 411-7. doi:10.1523/JNEUROSCI.3115-05.2006. PMC 6674421. PMID 16407537. Geerling, JC; Loewy, AD (Oct 18, 2006). " ... 93 (2): 177-209. doi:10.1113/expphysiol.2007.039891. PMID 17981930. Geerling, JC; Loewy, AD (Mar 2007). "Sodium depletion ... A small number of HSD2 neurons (less than 2%) may express the neuropeptide galanin. Their lack of expression of the ...
... beta-hydroxysteroid dehydrogenase isoforms using reverse-transcriptase-polymerase chain reaction and localization of the type 2 ... "Human adrenal cortex and aldosterone secreting adenomas express both 11beta-hydroxysteroid dehydrogenase type 1 and type 2 ... Wake DJ, Walker BR (February 2006). "Inhibition of 11beta-hydroxysteroid dehydrogenase type 1 in obesity". Endocrine. 29 (1): ... Agarwal AK (November 2003). "Cortisol metabolism and visceral obesity: role of 11beta-hydroxysteroid dehydrogenase type I ...
2005). "11beta-hydroxysteroid dehydrogenase type 1: a tissue-specific regulator of glucocorticoid response". Endocr. Rev. 25 (5 ... Persu A (2005). "11beta-Hydroxysteroid deshydrogenase: a multi-faceted enzyme". J. Hypertens. 23 (1): 29-31. doi:10.1097/ ... "Entrez Gene: HSD11B2 hydroxysteroid (11-beta) dehydrogenase 2". Geerling, Joel C.; Arthur D. Loewy (September 2009). " ... 1998). "Molecular basis for hypertension in the "type II variant" of apparent mineralocorticoid excess". Am. J. Hum. Genet. 63 ...
11beta-hydroxysteroid dehydrogenase type 1- a tissue-specific amplifier of glucocorticoid action". Endocrinology. 142 (4): 1371 ... Seckl JR (January 1997). "11beta-Hydroxysteroid dehydrogenase in the brain: a novel regulator of glucocorticoid action?". Front ... There are two types of 11β-Hydroxysteroid dehydrogenases that control cortisol concentration: HSD-11β Type 1 and HSD-11β Type 2 ... The dehydrogenase activity of a HSD-11β converts a 11beta-hydroxysteroid to the corresponding 11-oxosteroid by reducing NADP+ ...
... type I (dexamethasone suppressible), and type II, which has been linked to the 7p22 gene. Features Hypertension Hypokalemia (e. ... November 2000). "A novel genetic locus for low renin hypertension: familial hyperaldosteronism type II maps to chromosome 7 ( ... 37 (11): 831-5. doi:10.1136/jmg.37.11.831. PMC 1734468. PMID 11073536. Dominguez A, Muppidi V, Gupta S (2022). " ... Through inhibition of 11-beta-hydroxysteroid dehydrogenase type 2 (11-beta-HSD2), glycyrrhizin allows cortisol to activate ...
October 2004). "11beta-hydroxysteroid dehydrogenase type 1: a tissue-specific regulator of glucocorticoid response". Endocrine ... studies on the stably transfected isoforms and localization of the type 2 isozyme within renal tissue". Steroids. 62 (1): 77-82 ... 11α-OHP is a more potent inhibitor of 11β-HSD than enoxolone (glycyrrhetinic acid) or carbenoxolone in vitro (IC50 = 0.9 nM; ... 11 alpha-Hydroxyprogesterone (11 alpha OH-P) was an order of magnitude more potent a competitive inhibitor of the 11 beta HSD-2 ...
Causes include genetic disorders (e.g. Apparent mineralocorticoid excess syndrome, Liddle's syndrome, and types of Congenital ... Congenital Adrenal Hyperplasia is an autosomal recessive disorder with multiple types, two of which lead to ... and two types of Congenital adrenal hyperplasia (CAH). Liddle's syndrome is autosomal dominant disorder affecting epithelial ... Deficiency of 11-beta-hydroxylase blocks the conversion of 11-deoxycorticosterone (DOC) to corticosterone leading to an excess ...
2004). "11Beta-hydroxysteroid dehydrogenase inhibition improves cognitive function in healthy elderly men and type 2 diabetics ... In type 2 diabetics aged 52-70, the drug improved verbal memory. However, potassium-sparing diuretic amiloride was co- ... 12 (2): 66-8. doi:10.5698/1535-7511-12.2.66. PMC 3316363. PMID 22473546. Sandeep TC, Yau JL, MacLullich AM, et al. ( ... 11α-Hydroxyprogesterone Connors BW (2012). "Tales of a Dirty Drug: Carbenoxolone, Gap Junctions, and Seizures". Epilepsy Curr. ...
... type 3, rare (NIH) 3 beta hydroxysteroid dehydrogenase deficiency 3 hydroxyisobutyric aciduria 3 hydroxyisobutyric aciduria, ... 17 alpha hydroxylase deficiency 17 beta hydroxysteroide dehydrogenase deficiency 17-beta-hydroxysteroid dehydrogenase ... 3 methylglutaconyl coa hydratase deficiency 3-hydroxy 3-methyl glutaryl-coa lyase deficiency 3-hydroxyacyl-coa dehydrogenase ... 2,8 dihydroxy-adenine urolithiasis 21 hydroxylase deficiency 22q11.2 deletion syndrome, rare (NIH) 3 alpha methylcrotonyl-Coa ...
3-hydroxysteroid dehydrogenases MeSH D08.811.682.047.436.350.100 - 3alpha-hydroxysteroid dehydrogenase (B-specific) MeSH ... myosin type iii MeSH D08.811.277.040.025.525.843 - myosin type iv MeSH D08.811.277.040.025.525.875 - myosin type v MeSH D08.811 ... 4-beta-glucosidase MeSH D08.811.277.450.420.200.600 - glucan endo-1,3-beta-d-glucosidase MeSH D08.811.277.450.420.375 - glucan ... 20-hydroxysteroid dehydrogenases MeSH D08.811.682.047.436.400.074 - 20alpha-hydroxysteroid dehydrogenase MeSH D08.811.682.047. ...
"17 beta-hydroxysteroid dehydrogenase type XI localizes to human steroidogenic cells". Endocrinology. 144 (5): 2084-91. doi: ... "Entrez Gene: HSD17B11 hydroxysteroid (17-beta) dehydrogenase 11". Li KX, Smith RE, Krozowski ZS (1999). "Cloning and expression ... Estradiol 17-beta-dehydrogenase 11 is an enzyme that in humans is encoded by the HSD17B11 gene. GRCh38: Ensembl release 89: ... Haeseleer F, Palczewski K (2000). Short-chain dehydrogenases/reductases in retina. Methods in Enzymology. Vol. 316. pp. 372-83 ...
... possible interference with type 1 11beta-hydroxysteroid dehydrogenase-mediated processes". J. Steroid Biochem. Mol. Biol. 104 ( ... "CYP7B generates a selective estrogen receptor beta agonist in human prostate". J. Clin. Endocrinol. Metab. 89 (6): 2928-35. doi ... 344 (2): 540-6. doi:10.1016/j.bbrc.2006.03.175. PMID 16630558. Dulos J, van der Vleuten MA, Kavelaars A, Heijnen CJ, Boots AM ( ... 121 (2): 307-14. doi:10.1016/S0306-4522(03)00438-X. PMID 14521990. S2CID 46593148. Saito S, Iida A, Sekine A, Kawauchi S, ...
Rheault P, Dufort I, Soucy P, Luu-The V (1999). "Assignment of HSD17B5 encoding type 5 17 beta-hydroxysteroid dehydrogenase to ... Aldo-keto reductase family 1 member C3 (AKR1C3), also known as 17β-hydroxysteroid dehydrogenase type 5 (17β-HSD5, HSD17B5) is a ... "Entrez Gene: AKR1C3 aldo-keto reductase family 1, member C3 (3-alpha hydroxysteroid dehydrogenase, type II)". Theisen, J. ... "Structural basis of the multispecificity demonstrated by 17beta-hydroxysteroid dehydrogenase types 1 and 5". Molecular and ...
1) Type B intercalated cells in the collecting duct reabsorb H+ and secrete HCO3, while in type A intercalated cells protons ... These hormones and medications include insulin, epinephrine, and other beta agonists (e.g. salbutamol or salmeterol), and ... this facilitated diffusion occurs in both Type B intercalated cells and Principal cells in the collecting duct). 2) Metabolic ... can also cause hypokalemia by stimulating beta-2 receptors. Rare hereditary defects of muscular ion channels and transporters ...
Moghrabi N, Head JR, Andersson S (Nov 1997). "Cell type-specific expression of 17 beta-hydroxysteroid dehydrogenase type 2 in ... "The human type II 17 beta-hydroxysteroid dehydrogenase gene encodes two alternatively spliced mRNA species". DNA and Cell ... 17 beta-hydroxysteroid dehydrogenase type 2 in normal, inflamed and neoplastic gastric tissues". Anticancer Research. 23 (5A): ... "17 beta-Hydroxysteroid dehydrogenase type 2 expression and enzyme activity in the human gastrointestinal tract". Clinical ...
Cooper MS, Stewart PM (2009). "11Beta-hydroxysteroid dehydrogenase type 1 and its role in the hypothalamus-pituitary-adrenal ... Retrieved 2 April 2021. Glyn, J (1998). "The discovery and early use of cortisone". J R Soc Med. 91 (10): 513-517. doi:10.1177/ ... Marshall, Colin (December 2, 2013). "A Young Jean-Luc Godard Picks the 10 Best American Films Ever Made (1963)". Open Culture. ... 24 (2): 100-2. PMID 1582609. "All About Atopic Dermatitis". National Eczema Association. Bogart, A.S.; Daniel, D.D.; Poster, K. ...
... metabolism Disorders of sexual development Intersex 17β-Hydroxysteroid dehydrogenase 17β-Hydroxysteroid dehydrogenase Type III ... "HSD17B3 hydroxysteroid 17-beta dehydrogenase 3 [Homo sapiens (human)] - Gene - NCBI". www.ncbi.nlm.nih.gov. Retrieved 2017-03- ... "17-beta hydroxysteroid dehydrogenase 3 deficiency , Genetic and Rare Diseases Information Center (GARD) - an NCATS Program". ... "17-beta hydroxysteroid dehydrogenase 3 deficiency". Genetics Home Reference. Retrieved 2017-03-11. "OMIM Entry - # 264300 - 17- ...
2003). "Mutations in the genes encoding 11beta-hydroxysteroid dehydrogenase type 1 and hexose-6-phosphate dehydrogenase ... Ikegwuonu FI, Jefcoate CR (1999). "Evidence for the involvement of the fatty acid and peroxisomal beta-oxidation pathways in ... "Entrez Gene: H6PD hexose-6-phosphate dehydrogenase (glucose 1-dehydrogenase)". Tan SG, Ashton GC (1976). "An autosomal glucose- ... Beutler E, Morrison M (1968). "Localization and characteristics of hexose 6-phosphate dehydrogenase (glucose dehydrogenase)". J ...
3(or+17)beta-hydroxysteroid+dehydrogenase at the U.S. National Library of Medicine Medical Subject Headings (MeSH) Portal: ... Yang SY, He XY, Isaacs C, Dobkin C, Miller D, Philipp M (2014). "Roles of 17β-hydroxysteroid dehydrogenase type 10 in ... Has 3α-HSDTooltip 3α-hydroxysteroid dehydrogenase and 20α-HSDTooltip 20α-hydroxysteroid dehydrogenase activity in addition to ... Aka JA, Mazumdar M, Chen CQ, Poirier D, Lin SX (April 2010). "17beta-hydroxysteroid dehydrogenase type 1 stimulates breast ...
"Mutations in the genes encoding 11beta-hydroxysteroid dehydrogenase type 1 and hexose-6-phosphate dehydrogenase interact to ... beta}-hydroxysteroid dehydrogenase type 1 activity". Endocrinology. 146 (6): 2539-43. doi:10.1210/en.2005-0117. PMID 15774558. ... "Mutations in the genes encoding 11beta-hydroxysteroid dehydrogenase type 1 and hexose-6-phosphate dehydrogenase interact to ... "Cortisone-reductase deficiency associated with heterozygous mutations in 11beta-hydroxysteroid dehydrogenase type 1". ...
... estradiols having inhibitory effect on human placental estradiol 17 beta-hydroxysteroid dehydrogenase (17 beta-HSD type 1)". ... "Entrez Gene: HSD17B1 Hydroxysteroid (17-beta) dehydrogenase 1". Saloniemi T, Jokela H, Strauss L, Pakarinen P, Poutanen M (2012 ... Aka JA, Mazumdar M, Chen CQ, Poirier D, Lin SX (Apr 2010). "17beta-hydroxysteroid dehydrogenase type 1 stimulates breast cancer ... Sawetawan C, Milewich L, Word RA, Carr BR, Rainey WE (Mar 1994). "Compartmentalization of type I 17 beta-hydroxysteroid ...
Sam KM, Auger S, Luu-The V, Poirier D (1995). "Steroidal spiro-gamma-lactones that inhibit 17 beta-hydroxysteroid dehydrogenase ... "Spironolactone-related inhibitors of type II 17beta-hydroxysteroid dehydrogenase: chemical synthesis, receptor binding ... Poirier D (2003). "Inhibitors of 17 beta-hydroxysteroid dehydrogenases". Curr. Med. Chem. 10 (6): 453-77. doi:10.2174/ ... Poirier D (2009). "Advances in development of inhibitors of 17beta hydroxysteroid dehydrogenases". Anticancer Agents Med Chem. ...
... the type II 3 beta-hydroxysteroid dehydrogenase gene in a patient with classic salt-wasting 3 beta-hydroxysteroid dehydrogenase ... of type II 3 beta-hydroxysteroid dehydrogenase gene in Japanese patients with classical 3 beta-hydroxysteroid dehydrogenase ... 1992). "Structure of the human type II 3 beta-hydroxysteroid dehydrogenase/delta 5-delta 4 isomerase (3 beta-HSD) gene: adrenal ... 1995). "A novel missense mutation in the type II 3 beta-hydroxysteroid dehydrogenase gene in a family with classical salt- ...
"Hexose-6-phosphate dehydrogenase determines the reaction direction of 11beta-hydroxysteroid dehydrogenase type 1 as an ... and 5-beta tetrahydrocortisol (5-beta THF), reactions for which 5-alpha reductase and 5-beta-reductase are the rate-limiting ... "11beta-hydroxysteroid dehydrogenase type 1: a tissue-specific regulator of glucocorticoid response". Endocrine Reviews. 25 (5 ... Rapid administration of corticosterone (the endogenous type I and type II receptor agonist) or RU28362 (a specific type II ...
Pancreatic beta cells are responsible for making insulin; decreased beta cell activity is associated with DM2 in adulthood. In ... However, one common challenge of these types of studies is that many epigenetic modifications have tissue and cell-type ... When analyzing the types of changes that can occur to a phenotype, we can see changes that are behavioral, morphological, or ... This syndrome is often associated with type II diabetes as well as hypertension and atherosclerosis. Using mice models, ...
... adrenal hyperplasia due to 21-hydroxylase deficiency Congenital adrenal hyperplasia due to 3 beta-hydroxysteroid dehydrogenase ... Tooth disease type 1C Charcot-Marie-Tooth disease type 2A Charcot-Marie-Tooth disease type 2B1 Charcot-Marie-Tooth disease type ... CDG syndrome type 1A CDG syndrome type 1B CDG syndrome type 1C CDG syndrome type 2 CDG syndrome type 3 CDG syndrome type 4 CDK4 ... disease type 2C Charcot-Marie-Tooth disease type 2D Charcot-Marie-Tooth disease type 4A Charcot-Marie-Tooth disease type 4B ...
"Abundant type 10 17 beta-hydroxysteroid dehydrogenase in the hippocampus of mouse Alzheimer's disease model". Brain Research. ... 17-β-Hydroxysteroid dehydrogenase X (HSD10) also known as 3-hydroxyacyl-CoA dehydrogenase type-2 is a mitochondrial enzyme that ... 17-beta) dehydrogenase 10". He XY, Yang YZ, Schulz H, Yang SY (Jan 2000). "Intrinsic alcohol dehydrogenase and hydroxysteroid ... Yang SY, He XY, Isaacs C, Dobkin C, Miller D, Philipp M (Sep 2014). "Roles of 17β-hydroxysteroid dehydrogenase type 10 in ...
XY disorder of sex development due to 17-beta hydroxysteroid dehydrogenase type 3 deficiency: a plea for timely genetic testing ... It is atypical development of gonads in an embryo,. One type of gonadal dysgenesis is the development of functionless, fibrous ... 11 (2): 95-97. doi:10.1007/BF03034401. Hughes I (2008). "The Testes: Disorders of Sexual Differentiation and Puberty in the ... In 5α-Reductase 2 deficiency individuals are born with normal female genitalia, however during puberty male differentiation and ...
Dehydrogenase/reductase (SDR family) member 7B is an enzyme encoded by the DHRS7B gene in humans, found on chromosome 17p11.2. ... CD44 is an antigen found on the surface of most cell types and functions as a receptor that binds tissue macromolecules. ... "Entrez Gene: Dehydrogenase/reductase (SDR family) member 7B". "Genecards: DHRS7B Gene protein-coding GIFtS 47". Tannin GM, ... DHRS7B is a member of the short chain dehydrogenase/reductase (SDR) superfamily and possesses characteristic features of an SDR ...
Akinola LA, Poutanen M, Vihko R, Vihko P (July 1997). "Expression of 17beta-hydroxysteroid dehydrogenase type 1 and type 2, ... "Human placental 17 beta-estradiol dehydrogenase and 20 alpha-hydroxysteroid dehydrogenase. Two activities at a single enzyme ... Other names in common use include 20alpha-hydroxy steroid dehydrogenase, 20alpha-hydroxy steroid dehydrogenase, 20alpha-HSD, ... In enzymology, a 20-α-hydroxysteroid dehydrogenase (EC 1.1.1.149) is an enzyme that catalyzes the chemical reaction 17alpha, ...
Results: Activity of 11 beta-HSD2 correlated with time of amniocentesis, peaking in the morning (r = -0.398;P , 0.001) and ... 11 beta-HSD2 activity correlated negatively with pre-pregnancy body mass index (r = -0.225;P = 0.047). Conclusion: Our study ... Fetoplacental 11 beta-hydroxysteroid dehydrogenase type 2 (11 beta-HSD2) inactivates cortisol to cortisone, protecting the ... Rhythm of Fetoplacental 11 beta-Hydroxysteroid Dehydrogenase Type 2-Fetal Protection From Morning Maternal Glucocorticoids. In ...
Analysis of the 11beta-hydroxysteroid dehydrogenase type 2 gene (HSD11B2) in human essential hypertension Barbara Mariniello 1 ... Role of the 11beta-hydroxysteroid dehydrogenase type 2 in blood pressure regulation. Ferrari P, Krozowski Z. Ferrari P, et al. ... Analysis of the 11beta-hydroxysteroid dehydrogenase type 2 gene (HSD11B2) in human essential hypertension Barbara Mariniello et ... Structural analysis of the 11beta-hydroxysteroid dehydrogenase type 2 gene in end-stage renal disease. Zaehner T, Plueshke V, ...
Description: A competitive ELISA for quantitative measurement of Human 17 β hydroxysteroid dehydrogenase type 6(HSD17B6) in ... Description: A competitive ELISA for quantitative measurement of Human 17 β hydroxysteroid dehydrogenase type 6(HSD17B6) in ... Description: A competitive ELISA for quantitative measurement of Human 17 β hydroxysteroid dehydrogenase type 6(HSD17B6) in ... Description: A competitive ELISA for quantitative measurement of Rat 17 β hydroxysteroid dehydrogenase type 6(HSD17B6) in ...
... hydroxysteroid 11-beta dehydrogenase 2 (human). Find diseases associated with this biological target and compounds tested ... Rhythm of Fetoplacental 11beta-Hydroxysteroid Dehydrogenase Type 2 - Fetal Protection From Morning Maternal Glucocorticoids. ... type2_17beta_HSD-like_SDR_c; human 17beta-hydroxysteroid dehydrogenase type 2 (type 2 17beta-HSD)-like, classical (c) SDRs. ... HSD11 type II. 11-DH2. 11-HSD type II. 11-beta-HSD type II. 11-beta-HSD2. 11-beta-hydroxysteroid dehydrogenase type II. NAD- ...
Evolutionary analysis of 11beta-hydroxysteroid dehydrogenase-type 1, -type 2, -type 3 and 17beta-hydroxy-steroid dehydrogenase- ... Modulation of vitellogenin synthesis through estrogen receptor beta-1 in goldfish (Carassius auratus) juveniles exposed to 17- ... Organotins disrupt the 11beta-hydroxysteroid dehydrogenase type 2-dependent local inactivation of glucocorticoids. Environ ... hydroxysteroid dehydrogenase type 3 (11. β. HD3) (Baker 2004) were down-regulated by treatment with estradiol and 4-nonylphenol ...
MeSH Terms: 11-beta-Hydroxysteroid Dehydrogenase Type 2/genetics; Adolescent; DNA Methylation*; Female; Humans; Insulin-Like ...
Licorice can reduce the serum testosterone level, probably by blocking 17-hydroxysteroid dehydrogenase and 17,20 lyase. [18] ... type 2), the enzyme responsible for inactivating cortisol through conversion to cortisone. As a result, a continuous, high- ... Phi Beta Kappa. Disclosure: Nothing to disclose. ... Updated: Apr 11, 2022 * Author: Seth Schonwald, MD, FACEP; ... 13, 14] Biochemical studies indicate that glycyrrhizinates inhibit 11-beta-hydroxysteroid dehydrogenase ( ...
Deroo, B.J. and Archer, T.K.: Proteasome inhibitors reduce luciferase and Beta-galactosidase activity in tissue culture cells. ... Abstract Deroo, B.J. and Archer, T.K.: Proteasome inhibitors reduce luciferase and Beta-galactosidase activity in tissue ... Epub 2011 Aug 11.]. *Archer TK. The 26S proteasome: when degradation is just not enough! Biochim Biophys Acta. 2011 Feb;1809(2 ... 2011 Feb 11;286(6):4610-9. Epub 2010 Dec 2.]. *Keppler BR, Archer TK, Kinyamu HK. Emerging Roles of the 26S Proteasome in ...
Gollasch B, Anistan YM, Canaan-Kühl S, Gollasch M. Late-onset Bartter syndrome type II. Clin Kidney J. 2017 Oct. 10 (5):594-599 ... When the patient recovers, the beta-hydroxybutyrate and lactate are metabolized to bicarbonate and the original bicarbonate ... This type of primary hyperaldosteronism responds to glucocorticoid therapy, which inhibits aldosterone secretion by suppressing ... In alkalemia, the kidneys secrete the excess bicarbonate via the apical chloride/bicarbonate exchanger, pendrin, in the B-type ...
D8.811.682.47.820.125 3-alpha-Hydroxysteroid Dehydrogenase (B-Specific) D8.811.682.47.820.186 3-Hydroxyacyl CoA Dehydrogenases ... Type I) Fatty Acid Synthetase Complex, Type II D5.500.562.437.500 D5.500.562.444 D8.811.600.317.500 D8.811.277.352.897.387.200 ... D12.776.476.24.406 20-alpha-Hydroxysteroid Dehydrogenase D8.811.682.47.436.400.74 D8.811.682.47.820.125.74 20-Hydroxysteroid ... G7.700.320.500.325.377.437 Malate Dehydrogenase D8.811.682.47.605 D8.811.682.47.820.496 Malate Dehydrogenase (NADP+) D8.811. ...
R)-2,3,4,5-Tetrahydro-8-chloro-3-methyl-5-phenyl-1H-3-benzazepin-7-ol. (R)-2,3,4,5-Tetrahydro-8-chloro-3-methyl-5-phenyl-1H-3- ... 1,2-Dimethylhydrazine. 1,2-Dimethylhydrazine (Structural Class). NDF-RT (Drug Classification). Drug Classes (NDF-RT). Details. ... 11-beta-Hydroxysteroid Dehydrogenase Type 1 (Structural Class). NDF-RT (Drug Classification). Drug Classes (NDF-RT). Details. ... 11-beta-Hydroxysteroid Dehydrogenase Type 2 (Structural Class). NDF-RT (Drug Classification). Drug Classes (NDF-RT). Details. ...
11beta-HSD2 11beta-HSD2 Reductase 11beta-Hydroxysteroid Dehydrogenase Type 2 Registry Number. EC 1.1.1.146. Previous Indexing. ... 11beta-Hydroxysteroid Dehydrogenase Type 2 Term UI T542236. Date06/02/2003. LexicalTag NON. ThesaurusID NLM (2004). ... Hydroxysteroid Dehydrogenases [D08.811.682.047.436] * 11-beta-Hydroxysteroid Dehydrogenases [D08.811.682.047.436.174] * 11-beta ... Hydroxysteroid Dehydrogenase Type 1 [D08.811.682.047.436.174.300] * 11-beta-Hydroxysteroid Dehydrogenase Type 2 [D08.811. ...
11beta-HSD2 11beta-HSD2 Reductase 11beta-Hydroxysteroid Dehydrogenase Type 2 Registry Number. EC 1.1.1.146. Previous Indexing. ... 11beta-Hydroxysteroid Dehydrogenase Type 2 Term UI T542236. Date06/02/2003. LexicalTag NON. ThesaurusID NLM (2004). ... Hydroxysteroid Dehydrogenases [D08.811.682.047.436] * 11-beta-Hydroxysteroid Dehydrogenases [D08.811.682.047.436.174] * 11-beta ... Hydroxysteroid Dehydrogenase Type 1 [D08.811.682.047.436.174.300] * 11-beta-Hydroxysteroid Dehydrogenase Type 2 [D08.811. ...
Mutants of 11beta-hydroxysteroid dehydrogenase (11-HSD2) with partial activity: improved correlations between genotype and ... Type of variant: LP/P [Disclaimer: Variants classification is intended for research purposes only, not for clinical and ... 0 The score within a Blosum matrix for the corresponding wild-type to variant amino acid change. The log-odds score measures ... A new compound heterozygous mutation in the 11 beta-hydroxysteroid dehydrogenase type 2 gene in a case of apparent ...
Type VI N0000168671 Collagen Type VII N0000168680 Collagen Type VIII N0000168676 Collagen Type X N0000168666 Collagen Type XI ... 20-alpha-Dihydroprogesterone N0000167989 20-alpha-Hydroxysteroid Dehydrogenase N0000167987 20-Hydroxysteroid Dehydrogenases ... beta-Hexosaminidase beta Chain N0000175112 beta-Keratins N0000167683 beta-Lactamases N0000011162 beta-Lactams N0000170341 beta- ... Myosin Type I N0000169441 Myosin Type II N0000169436 Myosin Type III N0000169437 Myosin Type IV N0000169440 Myosin Type V ...
... hydroxysteroid dehydrogenase type 2 gene in a case of apparent mineralocorticoid excess Carvajal C.A.; González A.A.; Mosso L.M ... A polymorphic GT short tandem repeat affecting beta-ENaC mRNA expression is associated with low renin essential hypertension. ... A possible association between primary aldosteronism and a lower beta-cell function. Mosso, Lorena M; Carvajal, Cristian A; ... Subclinical endothelial inflammation markers in a family with type I familial hyperaldosteronism caused by a de novo mutation]. ...
11beta-Hydroxysteroid dehydrogenase type 1 (11beta-HSD1) converts inactive cortisone to cortisol and therefore amplifies local ... Selective 11beta-HSD1 inhibitors (selective in that they block the activity of 11beta-HSD1 and not 11beta-HSD2 which ... The global epidemic of obesity and type-2 diabetes has heightened the need to understand the mechanisms that contribute to its ... 11beta-Hydroxysteroid dehydrogenase type 1 (11beta-HSD1) converts inactive cortisone to cortisol and therefore amplifies local ...
... overexpression of 11beta-hydroxysteroid dehydrogenase type 2 (11ß-HSD2). Inflammatory arthritis was induced in 5-week-old male ... Artrite Experimental , Artrite Reumatoide , Sinoviócitos , Ratos , Animais , Glicogênio Sintase Quinase 3 beta/metabolismo , ... Chen, Xi; Sun, Lijuan; Wang, Shuang; Wang, Yilin; Zhou, Yue; Li, Yan; Cheng, Zihao; Wang, Yingying; Jiang, Yanan; Zhao, Zihan; ... In this study, we first evaluated the effects of TR in type II collagen-induced RA model rats. Secondly, in serum metabolomics ...
Role for 17-beta-HSDXI in androgen metabolism during steroidogenesis. Title: 17 beta-hydroxysteroid dehydrogenase type XI ... 17-beta-hydroxysteroid dehydrogenase type XI. CTCL tumor antigen HD-CL-03. CTCL-associated antigen HD-CL-03. cutaneous T-cell ... 17beta-HSDXI-like_SDR_c; human 17-beta-hydroxysteroid dehydrogenase XI-like, classical (c) SDRs. ... hydroxysteroid 17-beta dehydrogenase 11provided by HGNC. Primary source. HGNC:HGNC:22960 See related. Ensembl:ENSG00000198189 ...
Hydroxysteroid dehydrogenases (HSDs) are a group of enzymes that play a crucial role in the metabolism of steroid hormones in ... Type3. *Skin testing with a panel of glucocorticoids showed immediate type reactions to prednisolone, prednisolone hydrogen ... Also known as TNF-alpha, it is only 30% homologous to TNF-beta (LYMPHOTOXIN), but they share TNF RECEPTORS.. ... Hydroxysteroid dehydrogenases are enzymes that catalyze the oxidation or reduction of hydroxyl groups in steroid hormones, ...
D8.811.682.47.820.125 3-alpha-Hydroxysteroid Dehydrogenase (B-Specific) D8.811.682.47.820.186 3-Hydroxyacyl CoA Dehydrogenases ... Type I) Fatty Acid Synthetase Complex, Type II D5.500.562.437.500 D5.500.562.444 D8.811.600.317.500 D8.811.277.352.897.387.200 ... D12.776.476.24.406 20-alpha-Hydroxysteroid Dehydrogenase D8.811.682.47.436.400.74 D8.811.682.47.820.125.74 20-Hydroxysteroid ... G7.700.320.500.325.377.437 Malate Dehydrogenase D8.811.682.47.605 D8.811.682.47.820.496 Malate Dehydrogenase (NADP+) D8.811. ...
adenovirus types 4 and 7 live, oral. Serious - Use Alternative (1)prednisolone decreases effects of adenovirus types 4 and 7 ... Monitor Closely (1)prednisolone will increase the level or effect of flibanserin by aldehyde dehydrogenase inhibition. Use ... adenovirus types 4 and 7 live, oral. prednisolone decreases effects of adenovirus types 4 and 7 live, oral by pharmacodynamic ... haemophilus influenzae type b vaccine. Monitor Closely (1)prednisolone decreases effects of haemophilus influenzae type b ...
There is also a reduction in the number of CRH type 2 receptors - these receptors produce anxiolytic behaviour, and an increase ... in CRH type one receptors which mediate the stress response. [8] This is interesting in relation to some of the chronic long ... In 2011 the leading medical journal The Lancet published a series of articles on obesity[2]; these made a number of suggestions ... Originally looked into by Sobal and Stunkard in 1989 [11] and by McLaren in 2007[12], was the relationship between proportions ...
The data indicate the presence of a NADP(H) dependent form, distinct from the known type I isozyme. Purification of 11beta-HSD- ... Both have an apparent molecular mass of 32 kDa, suggesting protein modifications occurring in the type 1 isozyme which account ... Immunoblot analysis using anti 11beta-HSD-1 antibodies reveals the presence of similar structural determinants between the ... 11beta-HSD) and xenobiotic carbonyl reductase activities were determined in guinea pig tissue microsomes. ...
D8.811.682.47.820.125 3-alpha-Hydroxysteroid Dehydrogenase (B-Specific) D8.811.682.47.820.186 3-Hydroxyacyl CoA Dehydrogenases ... Type I) Fatty Acid Synthetase Complex, Type II D5.500.562.437.500 D5.500.562.444 D8.811.600.317.500 D8.811.277.352.897.387.200 ... D12.776.476.24.406 20-alpha-Hydroxysteroid Dehydrogenase D8.811.682.47.436.400.74 D8.811.682.47.820.125.74 20-Hydroxysteroid ... G7.700.320.500.325.377.437 Malate Dehydrogenase D8.811.682.47.605 D8.811.682.47.820.496 Malate Dehydrogenase (NADP+) D8.811. ...
D8.811.682.47.820.125 3-alpha-Hydroxysteroid Dehydrogenase (B-Specific) D8.811.682.47.820.186 3-Hydroxyacyl CoA Dehydrogenases ... Type I) Fatty Acid Synthetase Complex, Type II D5.500.562.437.500 D5.500.562.444 D8.811.600.317.500 D8.811.277.352.897.387.200 ... D12.776.476.24.406 20-alpha-Hydroxysteroid Dehydrogenase D8.811.682.47.436.400.74 D8.811.682.47.820.125.74 20-Hydroxysteroid ... G7.700.320.500.325.377.437 Malate Dehydrogenase D8.811.682.47.605 D8.811.682.47.820.496 Malate Dehydrogenase (NADP+) D8.811. ...
D8.811.682.47.820.125 3-alpha-Hydroxysteroid Dehydrogenase (B-Specific) D8.811.682.47.820.186 3-Hydroxyacyl CoA Dehydrogenases ... Type I) Fatty Acid Synthetase Complex, Type II D5.500.562.437.500 D5.500.562.444 D8.811.600.317.500 D8.811.277.352.897.387.200 ... D12.776.476.24.406 20-alpha-Hydroxysteroid Dehydrogenase D8.811.682.47.436.400.74 D8.811.682.47.820.125.74 20-Hydroxysteroid ... G7.700.320.500.325.377.437 Malate Dehydrogenase D8.811.682.47.605 D8.811.682.47.820.496 Malate Dehydrogenase (NADP+) D8.811. ...
  • [ 13 , 14 ] Biochemical studies indicate that glycyrrhizinates inhibit 11-beta-hydroxysteroid dehydrogenase (type 2), the enzyme responsible for inactivating cortisol through conversion to cortisone. (medscape.com)
  • Animal data show that decreased activity of placental 11-beta-hydroxysteroid dehydrogenase type 2 (11β-HSD2), which potently inactivates glucocorticoids (e.g. cortisol) to inert forms (cortisone), allows increased access of maternal glucocorticoids to the fetus and 'programs' hypertension. (umass.edu)
  • Among 286 newborns in Project Viva, a prospective pre-birth cohort study based in eastern Massachusetts, we measured cortisol ( F ) and cortisone ( E ) in venous cord blood and used the ratio of F/E as a marker for placental 11β-HSD2 activity. (umass.edu)
  • The unhindered development of the fetal HPA axis is dependent on the function and activity of 11β-hydroxysteroiddehydrogenase type 2 (11β-HSD2), a transplacental cortisol barrier. (mcmaster.ca)
  • Decreased 11β-HSD2 levels in term born females may lead to an increased placental transfer of maternal cortisol and therefore result in a reduced head circumference and a higher risk for altered stress response in adulthood. (mcmaster.ca)
  • However, the role of 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), which catalyzes the conversion of inactive cortisone into active cortisol, in inflammation remains unclear. (ac.ir)
  • Furthermore, cortisone and cortisol, which are the substrate and product of 11β-HSD1, respectively, showed biphasic responses and induced the expression of pro-inflammatory cytokines at a low concentration in both LPS-stimulated or untreated THP-1 cells. (ac.ir)
  • The upregulation of 11beta-HSD1 in ovarian granulosa cells by cortisol and interleukin-1beta in polycystic ovary syndrome. (ac.ir)
  • Psychosocial stress is hypothesized to dysregulate the HPA axis through hypersecretion of cortisol, but the results of previous studies among pregnant women are conflicting in this respect [11-13]. (researchsquare.com)
  • In peripheral tissues, corticosteroid hormone action is determined, in part, through the activity of 11beta-hydroxysteroid dehydrogenases (11beta-HSD), two isozymes of which interconvert hormonally active cortisol (F) and inactive cortisone (E). 11beta-HSD type 2 (11beta-HSD2) inactivates F to E in the kidney, whilst 11beta-HSD type 1 (11beta-HSD1) principally performs the reverse reaction activating F from E in the liver and adipose tissue. (ox.ac.uk)
  • Alteration in expression of these 11beta-HSD isozymes in peripheral tissues modifies corticosteroid action: loss of 11beta-HSD2 activity in the kidney results in cortisol-induced mineralocorticoid excess, and loss of hepatic 11beta-HSD1 activity improves insulin sensitivity through a reduction in cortisol-induced gluconeogenesis and hepatic glucose output. (ox.ac.uk)
  • As assessed by urinary free cortisol/urinary free cortisone ratios and endorsed through in vitro studies, neither GH nor insulin-like growth factor (IGF)-I affect 11beta-HSD2 activity. (ox.ac.uk)
  • Secondly, many of the phenotypic features of hypopituitarism can be explained by an alteration in 11beta-HSD1 activity: GH deficiency effectively increases cortisol production in key target tissues including liver and adipose tissue, promoting insulin resistance and visceral adiposity. (ox.ac.uk)
  • Adipose tissue contains the enzyme 11-beta hydroxysteroid type one which converts inactive cortisone to cortisol, the more adipose tissue you have the more conversion [6] , thus breaking this cycle may be important in tackling obesity. (citizendium.com)
  • [7] The placenta forms the barrier between mother and fetus, and contains mechanisms to prevent the fetus from being overly exposed to high cortisol levels, this protection comes in the form of the enzyme 11 beta hydroxysteroid dehydrogenase type 2 which, in humans, converts active cortisol to inactive cortisone. (citizendium.com)
  • 11beta-HSD-1 is an enzyme that converts the biologically inactive steroid cortisone into the active hormone cortisol. (genengnews.com)
  • 11βHSD1 is an ER-bound enzyme catalyzing the conversion of inactive cortisone in active cortisol in humans. (biomedcentral.com)
  • The effects of 11-dehydrocorticosterone (in murine myotubes) and cortisone (in human myotubes) on protein metabolism were indistinguishable from that of corticosterone/cortisol treatments. (birmingham.ac.uk)
  • Furthermore, corticosterone/cortisol, but not 11-dehydrocorticosterone/cortisone, decreased murine and human myoblast proliferative capacity. (birmingham.ac.uk)
  • The serum cortisol/cortisone ratio was considered abnormal when its Ln (cortisol/cortisone) value was over 2 standard deviations of the mean. (pucv.cl)
  • Down-Regulation of the Mineralocorticoid Receptor (MR) and Up-Regulation of Hydroxysteroid 11-Beta Dehydrogenase Type 2 (HSD11B2) Isoenzyme in Critically Ill Patients. (bvsalud.org)
  • There are two such repeat elements in the HSD11B2 (11β-hydroxysteroid dehydrogenase) gene. (elsevierpure.com)
  • Agarwal, AK 2001, ' Transcriptional influence of two poly purine-pyrimidine tracts located in the HSD11B2 (11beta-hydroxysteroid dehydrogenase type 2) gene ', Endocrine Research , vol. 27, no. 1-2, pp. 1-9. (elsevierpure.com)
  • Association studies between the HSD11B2 gene (encoding human 11beta-hydroxysteroid dehydrogenase type 2), type 1 diabetes mellitus and diabetic nephropathy. (cdc.gov)
  • Special attention needs to be paid to dietary supplements that the patient might be using or has used (e.g. licorice inhibits 11 beta-hydroxysteroid buy Tanespimycin dehydrogenase (type 2), HSD11B2, and might result in the so-called "apparent mineralocorticoid excess syndrome") Functional impairment 17-DMAG (Alvespimycin) HCl is a central to the illness, and the method of determining this should be provided. (plcpathway.com)
  • hydroxysteroid dehydrogenase type 2 deficiency. (cdc.gov)
  • Among the remaining half, 11β-hydroxysteroid dehydrogenase type 2 (11βHSD2) deficiency plays an important role. (pucv.cl)
  • Aim: To determine biochemical alterations, suggestive of 11βHSD2 deficiency, in low-renin hypertensive patients. (pucv.cl)
  • 11βHSD1 requires NADPH as a cofactor generated by the hexose-6-phosphate dehydrogenase (H6PDH)-mediated conversion of glucose 6-phosphate (G6P) to 6-phosphogluconactone (6PGL) [ 10 ]. (biomedcentral.com)
  • Selective 11β-HSD1 inhibition blocked the decrease in protein synthesis, increased in protein degradation and reduction in myotube area induced by 11-dehydrocorticosterone/cortisone. (birmingham.ac.uk)
  • Elevated levels of 11β-HSD1 contributed to the expression of inflammatory cytokines, whereas BVT.2733, a selective 11β-HSD1 inhibitor, ameliorated inflammatory responses, ROS, and mitochondrial damage in LPS-stimulated THP-1 cells. (ac.ir)
  • Anti-inflammatory effect of a selective 11beta-hydroxysteroid dehydrogenase type 1 inhibitor via the stimulation of heme oxygenase-1 in LPS-activated mice and J774.1 murine macrophages. (ac.ir)
  • Under the firms' alliance, a small molecule inhibitor of 11beta-hydroxysteroid dehydrogenase (HSD)-1 has advanced into clinical testing as a treatment of diabetes and metabolic syndrome-related diseases. (genengnews.com)
  • We examined in humans the association between venous umbilical cord blood glucocorticoids, a potential marker for placental 11β-HSD2 enzyme activity, and blood pressure at age 3 years. (umass.edu)
  • A higher F/E ratio in umbilical venous cord blood, likely reflecting reduced placental 11β-HSD2 activity, was associated with higher systolic blood pressure at age 3 years. (umass.edu)
  • Placental 11β-hydroxysteroiddehydrogenase type 1 (11β-HSD1) protein levels and 11β-HSD2 protein and activity levels were determined. (mcmaster.ca)
  • 7. Chapman K, Holmes M, Seckl J. 11beta-hydroxysteroid dehydrogenases: Intracellular gate-keepers of tissue glucocorticoid action. (ac.ir)
  • 11. Chapman KE, Coutinho AE, Zhang Z, Kipari T, Savill JS, Seckl JR. Changing glucocorticoid action: 11beta-hydroxysteroid dehydrogenase type 1 in acute and chronic inflammation. (ac.ir)
  • Conversely, overexpression of 11beta-HSD1 in omental adipose tissue can stimulate glucocorticoid-induced adipocyte differentiation which may lead to central obesity. (ox.ac.uk)
  • Furthermore, we have investigated the role of pre-receptor modulation of glucocorticoid availability by 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) in these processes. (birmingham.ac.uk)
  • Our data underscores the potential use of selective 11β-HSD1 inhibitors to ameliorate muscle-wasting effects associated with glucocorticoid excess. (birmingham.ac.uk)
  • Inhibition of 11β-HSD1 may serve as a potential therapeutic target against the excessive activation of inflammation. (ac.ir)
  • Carbenoxolone prevents chemical eye ischemia-reperfusion-induced cell death via 11beta-hydroxysteroid dehydrogenase type 1 inhibition. (ac.ir)
  • Inhibition of 11beta-HSD-1 represents an important new mechanism of action for treating diabetic patients," according to Richard Gregg, Ph.D., Vitae's CSO. (genengnews.com)
  • Mouse model with selective liver 11β-HSD1 overexpression show IR, dyslipidemia, and hypertension, but unaltered adiposity. (biomedcentral.com)
  • Association between a variant in the 11 beta-hydroxysteroid dehydrogenase type 2 gene and primary hypertension. (cdc.gov)
  • 11ß-Hydroxysteroid dehydrogenase type 2 in hypertension: comparison of phenotype and genotype analysis. (cdc.gov)
  • Overexpression of 11beta-HSD-1 in mouse adipose tissue leads to a metabolic syndrome-like phenotype including increased central obesity, hypertension, impaired glucose tolerance, and hypertriglyceridemia. (genengnews.com)
  • The gene expression of 11β-HSD1 and pro-inflammatory cytokines was detected via RT-PCR. (ac.ir)
  • An important gene associated with Type 2 Diabetes Mellitus is IRS1 (Insulin Receptor Substrate 1), and among its related pathways/superpathways are Nervous system development and Angiopoietin-like protein 8 regulatory pathway. (silexon.tech)
  • The dramatic rise in rates of obesity amongst both adults and children means that, across the world, 1.46 billion adults and 70 million children are estimated to be overweight or obese in 2008 [2] , so what is it that is making us fat? (citizendium.com)
  • This program addresses several features of the metabolic syndrome, a combination of disorders including abdominal obesity, high blood pressure, and insulin resistance or glucose intolerance, all of which contribute to an increased risk of coronary heart disease, stroke, and type 2 diabetes. (genengnews.com)
  • In contrast, 11beta-HSD-1 knockout mice resist visceral obesity and diabetes through improved function of insulin in liver and adipose tissues. (genengnews.com)
  • Recent studies in humans and rodents suggest a role of 11β-hydroxysteroid dehydrogenase (11β-HSD) in the development of idiopathic obesity and MS [ 2 ]. (biomedcentral.com)
  • The increased 11β-HSD1 activity in adipose tissue in obese rats and in some but not all studies of obese humans causes visceral obesity and its metabolic consequences [ 3 ]. (biomedcentral.com)
  • Data indicates that elevated levels of adipose and liver 11beta-HSD-1 are detrimental to metabolic control. (genengnews.com)
  • Огляд розладів концентрації калію Potassium is the most abundant intracellular cation, but only about 2% of total body potassium is extracellular. (msdmanuals.com)
  • Licorice can reduce the serum testosterone level, probably by blocking 17-hydroxysteroid dehydrogenase and 17,20 lyase. (medscape.com)
  • Type 2 diabetes mellitus (T2DM) accounts for approximately 90% of the cases of diabetes. (ddw-online.com)
  • Type 2 diabetics, but also prediabetics, are at increased risk for a wide range of debilitating diseases and diabetes is the leading cause of new cases of kidney failure and blindness and of nontraumatic lower limb amputation. (ddw-online.com)
  • Type 2 Diabetes Mellitus, also known as insulin resistance, is related to diabetes mellitus and maturity-onset diabetes of the young, type 8, with exocrine dysfunction, and has symptoms including angina pectoris, tremor and equilibration disorder. (silexon.tech)
  • Note: If you'd like to get a target analysis report for Diabetes Type 2 , or if you are interested to learn how our AI-powered BDE-Chem can design therapeutic molecules to interact with the target(s) above against the disease of Diabetes Type 2 at a cost 90% lower than traditional approaches, please feel free to contact us at [email protected] . (silexon.tech)
  • Consider a study that placed 90 overweight and obese adult women on either a low-dairy diet following the RDA for protein (15% of total calories as protein , and less than 2% of total calories from dairy products, respectively), an RDA protein level and moderate-dairy diet (7.5% of calories from dairy), or a high-protein (30%) and high-dairy diet (15%), in combination with daily exercise for 16 weeks. (bodybuilding.com)
  • RESULTS: In term born females, BET administration was associated with reduced head circumference and decreased 11β-HSD2 protein levels and enzyme activity. (mcmaster.ca)
  • Males treated with BET, especially those born prematurely, showed increased 11β-HSD2 protein levels. (mcmaster.ca)
  • Description: A sandwich ELISA kit for detection of High Mobility Group AT Hook Protein 2 from Human in samples from blood, serum, plasma, cell culture fluid and other biological fluids. (lipidx.org)
  • Anti-inflammatory effects of levalbuterol-induced 11beta-hydroxysteroid dehydrogenase type 1 activity in airway epithelial cells. (ac.ir)
  • G6P availability directly modulates the activity of 11β-hydroxysteroid dehydrogenase type 1 (11βHSD1), an ER-bound enzyme playing a key role in the development of the metabolic syndrome (MS). (biomedcentral.com)
  • The Journal of clinical endocrinology and metabolism 2018 9 104 (2): 595-603. (cdc.gov)
  • Corticosterone suppresses IL-1beta-induced mPGE2 expression through regulation of the 11beta-HSD1 bioactivity of synovial fibroblasts in vitro. (ac.ir)
  • Alliance targets 11beta-HSD-1 for the treatment of metabolic syndrome disorders. (genengnews.com)
  • Description: A sandwich ELISA kit for detection of Ectonucleotide Pyrophosphatase/Phosphodiesterase 2 from Human in samples from blood, serum, plasma, cell culture fluid and other biological fluids. (jemsec.com)
  • Description: This is Double-antibody Sandwich Enzyme-linked immunosorbent assay for detection of Rat Ectonucleotide Pyrophosphatase/Phosphodiesterase 2 (ENPP2) in serum, plasma, tissue homogenates and other biological fluids. (jemsec.com)
  • Description: Enzyme-linked immunosorbent assay based on the Double-antibody Sandwich method for detection of Rat Ectonucleotide Pyrophosphatase/Phosphodiesterase 2 (ENPP2) in samples from serum, plasma, tissue homogenates and other biological fluids with no significant corss-reactivity with analogues from other species. (jemsec.com)
  • Description: A sandwich ELISA kit for detection of Enhancer Of Zeste Homolog 2 from Human in samples from blood, serum, plasma, cell culture fluid and other biological fluids. (kits-elisa.com)
  • Conversely, 11β-HSD1 null mice exhibit a protective glycemic, lipid, and lipoprotein profile and show increased expression of hepatic mRNAs encoding regulators of fatty acid beta-oxidation. (biomedcentral.com)
  • Early clinical evidence has shown that inhibiting 11beta-HSD-1 can reduce glucose and lipids in diabetic patients. (genengnews.com)
  • Clinical, genetic, and structural basis of apparent mineralocorticoid excess due to 11? (cdc.gov)
  • We conducted a case-control study involving 152 C. innocuum -infected patients during 2014-2019 in Taiwan, using 304 cases of Clostridioides difficile infection (CDI) matched by diagnosis year, age ( + 2 years), and sex as controls. (cdc.gov)
  • 6. Wang W, Chen ZJ, Myatt L, Sun K. 11beta-HSD1 in human fetal membranes as a potential therapeutic target for preterm birth. (ac.ir)
  • Description: This is Double-antibody Sandwich Enzyme-linked immunosorbent assay for detection of Human Enhancer Of Zeste Homolog 2 (EZH2) in Tissue homogenates, cell lysates and other biological fluids. (kits-elisa.com)
  • Description: This is Double-antibody Sandwich Chemiluminescent immunoassay for detection of Human Enhancer Of Zeste Homolog 2 (EZH2) in Tissue homogenates and other biological fluids. (kits-elisa.com)
  • These clinical data suggest that GH (and/or IGF-I) inhibits 11beta-HSD1 (i.e. (ox.ac.uk)
  • The medicine in the syringe after reconstitution of the 2 vials will be around the 2.2-mL mark on the syringe. (pdr.net)
  • We speculate a possible role of 11βHSD1 modulation by G6P availability. (biomedcentral.com)
  • As a result of sulfation [2] in the adrenal cortex, it gains a sulfate molecule and becomes dehydroepiandrosterone sulfate (DHEA-S). Then, it is released into the bloodstream. (atlasbiomed.com)
  • E to F conversion) (parallel in vitro studies suggest that IGF-I and not GH inhibits 11beta-HSD1). (ox.ac.uk)
  • Precise diagnosis of C. innocuum is necessary because of its unique intrinsic resistance to vancomycin, presumably caused by the presence of 2 chromosomal genes that enable the synthesis of a peptidoglycan precursor terminating in serine with low vancomycin affinity ( 9 , 11 ). (cdc.gov)
  • Moreover, cardiovascular disease (CVD) is 2-4 times higher in diabetics (2). (ddw-online.com)
  • Further research is needed to conclude the significance of increased 11β-HSD2 levels in males. (mcmaster.ca)