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.

High dietary potassium chloride intake augments rat renal mineralocorticoid receptor selectivity via 11beta-hydroxysteroid dehydrogenase. (1/271)

Glucocorticoid access to renal corticosteroid receptors is regulated by 11beta-hydroxysteroid dehydrogenases (11beta-HSDs), converting 11beta-hydroxyglucocorticoids into inactive 11-ketones. This mechanism plays a key role in maintaining normal salt-water homeostasis and blood pressure. To study whether renal cortical proximal and distal tubular 11beta-HSDs are modulated, upon shifting the electrolyte status (and may thereby contribute to adjusting the salt-water homeostasis), rats were treated for 14 days with diets with low (0.058 w/w%), normal (0.58%, which is the KCl content of standard European laboratory rat food) or high (5.8%) potassium chloride content. In proximal tubules, dietary KCl had no effect regarding corticosterone 11beta-oxidation in intact cells as well as 11beta-HSD1 and 11beta-HSD2 protein (Western blotting) and mRNA levels (semi-quantitative RT-PCR). In distal tubules, the low KCl diet also had no effect. However, distal tubules of rats fed the high KCl diet showed increased corticosterone 11beta-oxidation rates (1.6-fold, P<0.01) and 11beta-HSD2 protein (4-fold, P<0.01), whereas 11beta-HSD1 protein was decreased (no longer detected, P<0.05). Distal tubular 11beta-HSD mRNA levels were not changed upon dietary treatment. Our results suggest that upon dietary KCl loading distal tubular mineralocorticoid receptor selectivity for aldosterone is increased because of enhanced corticosterone 11beta-oxidation. This may contribute to the fine-tuning of salt-water homeostasis by the kidney.  (+info)

Full induction of rat myometrial 11beta-hydroxysteroid dehydrogenase type 1 in late pregnancy is dependent on intrauterine occupancy. (2/271)

The 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD-1) enzyme catalyses the conversion of the biologically inert glucocorticoid 11-dehydrocorticosterone to active corticosterone (11-oxoreductase activity) in vivo, and it is dramatically up-regulated in uterine myometrium in the days leading up to parturition. 11beta-HSD-1 is likely to enhance local concentrations of glucocorticoid within the myometrium and thus facilitate uterine contractility, but the stimulus for the increase in myometrial 11beta-HSD-1 is unknown. The objective of the present study was to test whether the induction of myometrial 11beta-HSD-1 is dependent on uterine occupancy or systemic hormonal signals of late pregnancy. This involved use of a unilateral pregnancy (ULP) model in which the gravid and nongravid uterine horns are both exposed to the normal systemic hormonal milieu of pregnancy. Western blot analysis showed that the 11beta-HSD-1 signal was only partially induced in the nongravid horn of ULP rats on Day 22 of pregnancy (term: Day 23). Moreover, artificial distension of this nongravid horn had no effect on myometrial 11beta-HSD-1 immunoreactivity or bioactivity at either Day 16 or Day 22 of pregnancy. Removal of fetuses and placentas on Day 18 reduced myometrial 11beta-HSD-1 bioactivity 4 days later, and this effect was not overcome by artificial maintenance of uterine distension. In contrast, after fetectomy at Day 18 (i.e., removal of the fetus but not placenta), myometrial 11beta-HSD-1 bioactivity was largely maintained on Day 22, indicative of placental support for myometrial 11beta-HSD-1 over this period. In conclusion, our data show that full induction of myometrial 11beta-HSD-1 expression and associated 11-oxoreductase bioactivity late in rat pregnancy is dependent upon intrauterine occupancy. Although the hormonal milieu of late pregnancy appears to stimulate myometrial 11beta-HSD-1 marginally, full induction clearly requires an additional stimulus. Manipulations involving fetectomy and artificial uterine distension indicate that the placenta provides at least part of this stimulus, but uterine stretch does not appear to play a role.  (+info)

Role of 11beta-hydroxysteroid dehydrogenase in nongenomic aldosterone effects in human arteries. (3/271)

The aim of the present study was to demonstrate rapid effects of aldosterone on the Na(+)-H(+) exchanger in strips of human vascular vessels and to determine whether 11beta-hydroxysteroid dehydrogenase enzyme (11beta-HSD) could play a protective role in this response, such as that described for the classic type I mineralocorticoid receptor (MR). The activity of 11beta-HSD isoforms 1 and 2 were measured in fetal and adult arteries. Both isoforms are present in adult and fetal vessels. However, a significant difference in the proportion of each isoform was found. Isoform 1 activity (in pmol x min(-1) x 100 mg(-1) protein) was 42+/-5 in fetal vessels and 29+/-2 in adult arteries, and isoform 2 activity was 78+/-7 in fetal and 12+/-2 in adult tissue. The nongenomic effect of aldosterone on Na(+)-H(+) exchanger activity was measured in strips of chorionic and radial uterine arteries loaded with the pH-sensitive dye 2',7'-bis(2-carboxyethyl)-5,6-carboxyfluorescein. Recordings of intracellular pH (pH(i)) were made by videofluorescence microscopy. Aldosterone (0.5 nmol/L) rapidly increased pH(i), with a half-maximal effect between 2 and 3 nmol/L in both fetal and adult vessels. Ethylisopropylamiloride, a specific inhibitor of the Na(+)-H(+) exchanger, inhibited this effect. The hormone-mediated increase in pH(i) was unaffected by spironolactone, a classic antagonist of MR, but was completely blocked by RU28318. Cortisol (up to 1 micromol/L) had no effect on pH(i), but when applied in the presence of carbenoxolone, a dramatic increase in Na(+)-H(+) exchanger activity was evident. The increments on pH(i) for each cortisol concentration were similar to those observed for aldosterone. These findings suggest that vascular 11beta-HSD plays an active role in maintaining the specificity of the rapid effects of aldosterone.  (+info)

Novel nuclear corticosteroid binding in rat small intestinal epithelia. (4/271)

When small intestinal epithelial cells are incubated with [(3)H]corticosterone, nuclear binding is displaced neither by aldosterone nor RU-28362, suggesting that [(3)H]corticosterone is binding to a site distinct from mineralocorticoid receptor and glucocorticoid receptor. Saturation and Scatchard analysis of nuclear [(3)H]corticosterone binding demonstrate a single saturable binding site with a relatively low affinity (49 nM) and high capacity (5 fmol/microg DNA). Competitive binding assays indicate that this site has a unique steroid binding specificity, which distinguishes it from other steroid receptors. Steroid specificity of nuclear binding mirrors inhibition of the low 11beta-dehydrogenase activity, suggesting that binding may be to an 11beta-hydroxysteroid dehydrogenase (11betaHSD) isoform, although 11betaHSD1 is not present in small intestinal epithelia and 11betaHSD2 does not colocalize intracellularly with the binding site. In summary, a nuclear [(3)H]corticosterone binding site is present in small intestinal epithelia that is distinct from other steroid receptors and shares steroid specificity characteristics with 11betaHSD2 but is distinguishable from the latter by its distinct intracellular localization.  (+info)

Peroxisome proliferator-activated receptor-gamma ligands inhibit adipocyte 11beta -hydroxysteroid dehydrogenase type 1 expression and activity. (5/271)

Peroxisome proliferator-activated receptor-gamma (PPARgamma) has been shown to play an important role in the regulation of expression of a subclass of adipocyte genes and to serve as the molecular target of the thiazolidinedione (TZD) and certain non-TZD antidiabetic agents. Hypercorticosteroidism leads to insulin resistance, a variety of metabolic dysfunctions typically seen in diabetes, and hypertrophy of visceral adipose tissue. In adipocytes, the enzyme 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD-1) converts inactive cortisone into the active glucocorticoid cortisol and thereby plays an important role in regulating the actions of corticosteroids in adipose tissue. Here, we show that both TZD and non-TZD PPARgamma agonists markedly reduced 11beta-HSD-1 gene expression in 3T3-L1 adipocytes. This diminution correlated with a significant decrease in the ability of the adipocytes to convert cortisone to cortisol. The half-maximal inhibition of 11beta-HSD-1 mRNA expression by the TZD, rosiglitazone, occurred at a concentration that was similar to its K(d) for binding PPARgamma and EC(50) for inducing adipocyte differentiation thereby indicating that this action was PPARgamma-dependent. The time required for the inhibitory action of the TZD was markedly greater for 11beta-HSD-1 gene expression than for leptin, suggesting that these genes may be down-regulated by different molecular mechanisms. Furthermore, whereas regulation of PPARgamma-inducible genes such as phosphoenolpyruvate carboxykinase was maintained when cellular protein synthesis was abrogated, PPARgamma agonist inhibition of 11beta-HSD-1 and leptin gene expression was ablated, thereby supporting the conclusion that PPARgamma affects the down-regulation of 11beta-HSD-1 indirectly. Finally, treatment of diabetic db/db mice with rosiglitazone inhibited expression of 11beta-HSD-1 in adipose tissue. This decrease in enzyme expression correlated with a significant decline in plasma corticosterone levels. In sum, these data indicate that some of the beneficial effects of PPARgamma antidiabetic agents may result, at least in part, from the down-regulation of 11beta-HSD-1 expression in adipose tissue.  (+info)

Functional expression, characterization, and purification of the catalytic domain of human 11-beta -hydroxysteroid dehydrogenase type 1. (6/271)

11-beta-hydroxysteroid dehydrogenase type 1 catalyzes the conversion of cortisone to hormonally active cortisol and has been implicated in the pathogenesis of a number of disorders including insulin resistance and obesity. The enzyme is a glycosylated membrane-bound protein that has proved difficult to purify in an active state. Extracted enzyme typically loses the reductase properties seen in intact cells and shows principally dehydrogenase activity. The C-terminal catalytic domain is known to contain a disulfide bond and is located within the lumen of the endoplasmic reticulum, anchored to the membrane by a single N-terminal transmembrane domain. We report here the functional expression of the catalytic domain of the human enzyme, without the transmembrane domain and the extreme N terminus, in Escherichia coli. Moderate levels of soluble active protein were obtained using an N-terminal fusion with thioredoxin and a 6xHis tag. In contrast, the inclusion of a 6xHis tag at the C terminus adversely affected protein solubility and activity. However, the highest levels of active protein were obtained using a construct expressing the untagged catalytic domain. Nonreducing electrophoresis revealed the presence of both monomeric and dimeric disulfide bonded forms; however, mutation of a nonconserved cysteine residue resulted in a recombinant protein with no intermolecular disulfide bonds but full enzymatic activity. Using the optimal combination of plasmid construct and E. coli host strain, the recombinant protein was purified to apparent homogeneity by single step affinity chromatography. The purified protein possessed both dehydrogenase and reductase activities with a K(m) of 1.4 micrometer for cortisol and 9.5 micrometer for cortisone. This study indicates that glycosylation, the N-terminal region including the transmembrane helix, and intermolecular disulfide bonds are not essential for enzyme activity and that expression in bacteria can provide active recombinant protein for future structural and functional studies.  (+info)

A transgenic model of visceral obesity and the metabolic syndrome. (7/271)

The adverse metabolic consequences of obesity are best predicted by the quantity of visceral fat. Excess glucocorticoids produce visceral obesity and diabetes, but circulating glucocorticoid levels are normal in typical obesity. Glucocorticoids can be produced locally from inactive 11-keto forms through the enzyme 11beta hydroxysteroid dehydrogenase type 1 (11beta HSD-1). We created transgenic mice overexpressing 11beta HSD-1 selectively in adipose tissue to an extent similar to that found in adipose tissue from obese humans. These mice had increased adipose levels of corticosterone and developed visceral obesity that was exaggerated by a high-fat diet. The mice also exhibited pronounced insulin-resistant diabetes, hyperlipidemia, and, surprisingly, hyperphagia despite hyperleptinemia. Increased adipocyte 11beta HSD-1 activity may be a common molecular etiology for visceral obesity and the metabolic syndrome.  (+info)

Correlation between decrease of 11beta-hydroxysteroid dehydrogenase activity and hypokalemia induced by furosemide in rats. (8/271)

AIM: To investigate the correlation between decrease of 11beta-hydroxysteroid dehydrogenase (11beta-HSD) activity and hypokalemia induced by furosemide (Fur) in rats. METHODS: SD rats were given single dose or successive doses of Fur by gavage. The activity of 11beta-HSD was evaluated by measuring the ratio of 11-dehydrocorticosterone (A) and corticosterone (B) in urine and conversion rate of B to A in renal cortex microsome preparation was determined with HPLC. RESULTS: After giving single dose of Fur (40, 100, and 250 mg/kg) or multiple doses of Fur (10, 20, and 100 mg/kg, bid x 20 d), the ratio of A/B was reduced by 29.0 %, 58.6 %, and 60.9 % at 0 - 2 h; 14.4 %, 36.0 %, and 44.9 %, respectively; the conversion rate of B to A was decreased by 29 %, 33 %, and 37 %; 6 %, 17 %, and 23 %, respectively. The serum potassium was significantly reduced by multiple doses of Fur (20 and 100 mg/kg, bid x 20 d) (P < 0.01). The reduction in serum potassium was positively correlated with the lowering of A/B ratio and the conversion of B to A (P < 0.01). CONCLUSION: The inhibition of renal 11beta-HSD activity may be another new biochemical mechanism for hypokalemia induced by Fur.  (+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.

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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 ... dopamine beta-hydroxylase MeSH D08.811.682.690.708.392 - fatty acid desaturases MeSH D08.811.682.690.708.392.312 - beta- ... 20-hydroxysteroid dehydrogenases MeSH D08.811.682.047.436.400.074 - 20alpha-hydroxysteroid dehydrogenase MeSH D08.811.682.047. ...
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"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 ...
... 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- ...
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42 (1): 1-23. doi:10.1016/j.jchemneu.2011.05.003. PMC 3148274. PMID 21605659. Dong, HW; Petrovich, GD; Watts, AG; Swanson, LW ( ... 1115 (1): 54-64. doi:10.1016/j.brainres.2006.07.091. PMID 16935272. Geerling, JC; Kawata, M; Loewy, AD (Jan 20, 2006). " ... Geerling, JC; Engeland, WC; Kawata, M; Loewy, AD (Jan 11, 2006). "Aldosterone target neurons in the nucleus tractus solitarius ... Geerling, JC; Loewy, AD (Aug 1, 2006). "Aldosterone-sensitive neurons in the nucleus of the solitary tract: bidirectional ...
3(or+17)beta-hydroxysteroid+dehydrogenase at the U.S. National Library of Medicine Medical Subject Headings (MeSH) Portal: ... Soubhye J, Alard IC, van Antwerpen P, Dufrasne F (2015). "Type 2 17-β hydroxysteroid dehydrogenase as a novel target for the ... Has 3α-HSDTooltip 3α-hydroxysteroid dehydrogenase and 20α-HSDTooltip 20α-hydroxysteroid dehydrogenase activity in addition to ... Yang SY, He XY, Isaacs C, Dobkin C, Miller D, Philipp M (2014). "Roles of 17β-hydroxysteroid dehydrogenase type 10 in ...
... type 2 deficiency 17 alpha hydroxylase deficiency 17 beta hydroxysteroide dehydrogenase deficiency 17-beta-hydroxysteroid ... type 3, rare (NIH) 3 beta hydroxysteroid dehydrogenase deficiency 3 hydroxyisobutyric aciduria 3 hydroxyisobutyric aciduria, ... dehydrogenase deficiency, rare (NIH) 17q21.31 microdeletion syndrome 18-Hydroxylase deficiency, rare (NIH) 18p deletion ... 3 methylglutaconyl coa hydratase deficiency 3-hydroxy 3-methyl glutaryl-coa lyase deficiency 3-hydroxyacyl-coa dehydrogenase ...
Rheault P, Dufort I, Soucy P, Luu-The V (1999). "Assignment of HSD17B5 encoding type 5 17 beta-hydroxysteroid dehydrogenase to ... 3-alpha hydroxysteroid dehydrogenase, type II)". Theisen, J. Graham; Sundaram, Viji; Filchak, Mary S.; Chorich, Lynn P.; ... also known as 17β-hydroxysteroid dehydrogenase type 5 (17β-HSD5, HSD17B5) is a key steroidogenic enzyme that in humans is ... "Structural basis of the multispecificity demonstrated by 17beta-hydroxysteroid dehydrogenase types 1 and 5". Molecular and ...
... 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 ...
This type of receptor becomes activated upon ligand binding. After a hormone binds to the corresponding receptor, the newly ... 1 (1). doi:10.15347/wjm/2014.005. ISSN 2002-4436. Omar, HR; Komarova, I; El-Ghonemi, M; Fathy, A; Rashad, R; Abdelmalak, HD; ... This enzyme, 11-beta hydroxysteroid dehydrogenase type II (Protein:HSD11B2), catalyzes the deactivation of glucocorticoids to ... 11 ed)., Saunders Elsevier, Philadelphia, pp. 445-504. Bennett PN and Brown MJ (2008) "Adrenal corticosteroids, antagonists, ...
... 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- ...
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Soubhye J, Alard IC, van Antwerpen P, Dufrasne F (2015). "Type 2 17-β hydroxysteroid dehydrogenase as a novel target for the ... Sam KM, Auger S, Luu-The V, Poirier D (1995). "Steroidal spiro-gamma-lactones that inhibit 17 beta-hydroxysteroid dehydrogenase ... Poirier D (2003). "Inhibitors of 17 beta-hydroxysteroid dehydrogenases". Curr. Med. Chem. 10 (6): 453-77. doi:10.2174/ ... "Spironolactone-related inhibitors of type II 17beta-hydroxysteroid dehydrogenase: chemical synthesis, receptor binding ...
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 ...
... 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 ...
"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 ... 40 (1): 4075-4076. doi:10.1002/ajmg.1320400114. PMID 1909490. Nieschlag E, Behre H, Wieacker P, Meschede D, Kamischke A, ...
"Human placental 17 beta-estradiol dehydrogenase and 20 alpha-hydroxysteroid dehydrogenase. Two activities at a single enzyme ... Akinola LA, Poutanen M, Vihko R, Vihko P (July 1997). "Expression of 17beta-hydroxysteroid dehydrogenase type 1 and type 2, ... 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, ...
The 17-beta-hydroxysteroid dehydrogenase enzyme (EC 1.1.1.62) oxidizes or reduces estrogens and androgens in mammals and ... Ohnesorg T, Adamski J (2005). "Promoter analyses of human and mouse 17beta-hydroxysteroid dehydrogenase type 7". J. Steroid ... "Entrez Gene: HSD17B7 hydroxysteroid (17-beta) dehydrogenase 7". Mendoza-Hernández G, Rendón JL, Díaz-Zagoya JC (1985). "A ... "Two 17beta-hydroxysteroid dehydrogenases (17HSDs) of estradiol biosynthesis: 17HSD type 1 and type 7". J Steroid Biochem Mol ...
17 beta-dihydroxy-17-methyl-1, 4-androstadien-3-one and related compounds". Steroids. 43 (3): 271-82. doi:10.1016/0039-128x(84) ... 27 (3 Pt 1): 421-5. doi:10.1161/01.hyp.27.3.421. PMID 8698448. Fürstenberger C, Vuorinen A, Da Cunha T, Kratschmar DV, Saugy M ... In accordance, 11α- and 11β-hydroxyprogesterone are known to be potent inhibitors of 11β-hydroxysteroid dehydrogenase (11β-HSD ... ISBN 978-1-4757-2085-3. Felippone F, Resnati G, Scolastico C, Tronconi G (1984). "Synthesis of 2-carboxy-11 beta, ...
REVERSAL OF THE 3-BETA-HYDROXYSTEROID DEHYDROGENASE-ISOMERASE REACTIONS. CONVERSION OF ANDROST-4-ENE-3,17-DIONE-4-14C TO 3-BETA ... That is why, in practice, agents labeled with these compounds of this type turned out to be falsified, because they contained, ... Lommer D, Dorfman RI, Forchelli E. Reversal of the 3 -hydroxysteroid dehydrogenase-isomerase reactions in rat adrenals. ... In situations like ones described above the purchaser of this fake substance knows neither the type nor the dosage of the ...
Therapeutic inhibition of 11beta-HSD1 reductase activity in patients with obesity and the metabolic syndrome, as well as in ... In this review, we discuss both the genetic and enzymatic characterization of 11beta-HSD1, as well as describing its role in ... The molecular basis of cortisone reductase deficiency, the putative 11beta-HSD1 knockout state in humans, has been defined ... We speculate that hexose-6-phosphate dehydrogenase activity and therefore reduced nicotinamide-adenine dinucleotide phosphate ...
... beta-hydroxysteroid dehydrogenase isoforms using reverse-transcriptase-polymerase chain reaction and localization of the 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 ... "11beta-Hydroxysteroid dehydrogenase types 1 and 2 are up- and downregulated in cortisol-secreting adrenal adenomas". Journal of ...
11beta-hydroxysteroid dehydrogenase type 1: a tissue-specific regulator of glucocorticoid response. Endocr Rev. 2004 Oct. 25(5 ... Thomas A Wilson, MD is a member of the following medical societies: Endocrine Society, Pediatric Endocrine Society, Phi Beta ... Alternative splicing of the primary transcript gives rise to the 2 mRNA and protein isoforms, hGR-alpha and hGR-beta. (B) ... Alternative splicing of the primary transcript gives rise to the 2 mRNA and protein isoforms, hGR-alpha and hGR-beta. (B) ...
17-Beta-Hydroxysteroid Dehydrogenase Type 14) ELISA Kit. Human HSD17b14(17-Beta-Hydroxysteroid Dehydrogenase Type 14) ELISA Kit ... Description: A sandwich ELISA for quantitative measurement of Rat 17 beta hydroxysteroid dehydrogenase type 1 in samples from ... Description: A sandwich ELISA for quantitative measurement of Rat 17 beta hydroxysteroid dehydrogenase type 1 in samples from ... Description: A sandwich ELISA for quantitative measurement of Rat 17 beta hydroxysteroid dehydrogenase type 1 in samples from ...
PDB Compounds: (B:) 11beta-hydroxysteroid dehydrogenase type 1. SCOPe Domain Sequences for d1xseb_:. Sequence; same for both ... also known as short-chain dehydrogenases and SDR family. parallel beta-sheet is extended by 7th strand, order 3214567; left- ... PDB Description: crystal structure of guinea pig 11beta-hydroxysteroid dehydrogenase type 1 ... core: 3 layers, a/b/a; parallel beta-sheet of 6 strands, order 321456. The nucleotide-binding modes of this and the next two ...
11beta-hydroxysteroid dehydrogenase type 1 [Rattus norvegicus] None gi,37361816 Rattus norvegicus gi,37361816,gb,AAQ91021.1, ... Displaying results 1 to 4 of 4... MS=Mass Spectrometry Y2H=Yeast Two-Hybrid PSP=Protein Structure Micro=Fluorescence Microscopy ... Corticosteroid 11-beta-dehydrogenase isozyme 1 OS=Rattus norvegicus GN=Hsd11b1 PE=1 SV=2 None ... Search results for: 11-beta-hydroxysteroid dehydrogenase (NADP+) activity (Exact Annotation) ...
For other types of ligands, e.g. longer nucleotides and peptides, a manually drawn representation of the molecule may be ... Comment: AZD8329 is an inhibitor of 11-beta-hydroxysteroid dehydrogenase type 1 (11β-HSD1). This compound is included in ...
... type 2 diabetes mellitus, diabetic nephropathy, diabetic cognitive dysfunction, type 2 diabetes mellitus with fatty liver ... type 2 diabetes mellitus, diabetic nephropathy, diabetic cognitive dysfunction, type 2 diabetes mellitus with fatty liver ... The molecular targets of these effects mainly contains GLUTs, SGLT1, GLP-1, FoxO1, TNF-α, IL-6, caspase-3, bcl-2, MDA, SOD, ... type saponins to treat diabetes and its complications, including type 1 diabetes mellitus, ...
Synonyms: 11beta-hydroxysteroid dehydrogenase type 1, 11beta-HSD-1. Type: Gene. Species: Mus musculus (mouse) ... Name: inhibin beta-A. Synonyms: activin beta-A. Type: Gene. Species: Mus musculus (mouse) ... When maintaining a live colony, heterozygous mice may be bred together, bred with wild-type siblings, or bred with C57BL/6J ... 1 The distribution fee covers the expense of rederiving mice from a live mouse; you will receive the resulting litter. The ...
01013798484 ELISA kit for Human Transforming Growth factor β1,TGF-β1 Info Pariselements PR-S10113 1 kit/96-wells plate Ask Ask ... 04012487525 11-Beta-Hydroxysteroid Dehydrogenase Type 1 (HSD11b1) Polyclonal Antibody Info bioma CAU24477 200 μg Ask Ask ... 01014298201 Rapid Adenovirus Viditest Info Vidia tests ODZ-285 1 cassette x 20 tests in kit Ask Ask ... 01014296945 Anti-AB IgM, 1 viall of 10ml, 200 tests Info Tody laboratories 620010 10ml Ask Ask ...
Effects of an 11beta-hydroxysteroid dehydrogenase type 1 inhibitor, MK-0916, in patients with type 2 diabetes mellitus and ... beta-hydroxysteroid dehydrogenase type 1 inhibitor INCB13739 improves hyperglycemia in patients with type 2 diabetes ... hydroxysteroid dehydrogenase type 1 (11 - HSD1), GPR119, TGR5, sirtuin 1 (SIRT1), the sodium-glucose co-transporter 2 (SGLT2), ... Present and Future Challenges in Type 2 Diabetes. 26 August 2011 , By Dr Lesley J Millatt, Dr Rmy Hanf and Dr Dean W Hum , ...
Corticosteroids have been shown to have a wide range of effects on multiple cell types (eg mast cells, eosinophils, neutrophils ... GH inhibits 11-beta-HSD-1. Consequently, individuals with untreated GH deficiency have relative increases in 11-beta-HSD-1 and ... GH inhibits 11-beta-HSD-1. Consequently, individuals with untreated GH deficiency have relative increases in 11-beta-HSD-1 and ... GH inhibits 11-beta-HSD-1. Consequently, individuals with untreated GH deficiency have relative increases in 11-beta-HSD-1 and ...
... study on the effect of vitamin A on 11beta-hydroxysteroid dehydrogenase type 1 activity in liver and visceral fat of WNIN/Ob ... If you want to try harnessing Vitamin A for fat loss, we recommend supplementing with a mixture of Vitamin A and beta-carotene ... The Type 1 isoform (11 ? -HSD1) of this enzyme is responsible for converting inactive cortisone to active cortisol, whereas the ... or increasing that of Type 2, which either reduces the production of cortisol or increases the rate of its inactivation. ...
Bezafibrate regulates the expression and enzyme activity of 11beta-hydroxysteroid dehydrogenase type 1 in murine adipose tissue ... Dreyer C, Krey G, Keller H, Givel F, Helftenbein G, Wahli W. Control of the peroxisomal beta-oxidation pathway by a novel ... Effect of rosiglitazone on insulin sensitivity and body composition in type 2 diabetic patients (corrected). Obes Res. 2002;10: ... Effect of pioglitazone on abdominal fat distribution and insulin sensitivity in type 2 diabetic patients. J Clin Endocrinol ...
Depending on the type of cell the steroids are in, this activation can change how certain genes behave - especially the ones ... Comment: Microsomal enzyme 11-beta-hydroxysteroid dehydrogenase type 1 (11-beta-HSD-1) required for cortisone conversion to its ... only the compound to break through cells were cotransfected with increasing concentrations of an expression vector for SRC-1 in ...
Using RT-PCR, our results showed that mouse microglia expressed mRNA for 17beta-hydroxysteroid dehydrogenase type 1 and steroid ... A conditional knockout of mir-10b in KIT+-cells or depletion of KIT+-cells in mice leads to degeneration of beta cells and ICCs ... than other cell types tested. These experiments highlight the pivotal role of 3beta-hydroxysteroid dehydrogenase/ketoisomerase ... Chimeras (wild type host/EYFP+ bone marrow) suggest that the increase of EYFP+ cells in the aging brain is in part due to an ...
Here, we use aqueous two-phase partitioning for the isolation of membrane bound 11beta-hydroxysteroid dehydrogenase type 1 ( ... as well as a batch metal affinity capture step of 6xHis tagged 11beta-HSD1 in the two-phase system. The use of detergent/ ... 11beta-HSD1). Different detergents were used to find optimal conditions regarding solubilization and retaining target protein ... 1) of the target membrane protein compared to a conventional purification protocol where a specific enzyme activity of 1440 ...
Selective Inhibition of 11beta-Hydroxysteroid Dehydrogenase Type 1: A Novel Treatment for the Metabolic Syndrome. Tomlinson, J ... Assessing the Therapeutic Efficacy of an 11Beta-Hydroxysteroid Dehydrogenase Type 1 Inhibitor (AZD4017) in Idiopathic ... Investigating Hexose-6-Phosphate Dehydrogenase in the Control of Skeletal Muscle Function and Carbohydrate Metabolism. Lavery, ... Glucocorticoids and 11β-HSD1 are major regulators of intramyocellular protein metabolism. In: Journal of Endocrinology. 2016 ; ...
This study aimed to examine the mechanism of actions of 11β-HSD1 in lipopolysaccharide (LPS)-induced THP-1 cells.Materials and ... The protein expression of IL-1β in cell supernatants was detected via ELISA. Oxidative stress and mitochondrial membrane ... Overall, the results indicate that 11β-HSD1 amplifies inflammatory responses by activating the NF-κB and MAPK signaling ... However, the role of 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), which catalyzes the conversion of inactive cortisone ...
11beta-HSD1), which generates active glucocorticoids within cells, CORT-mediated induction of 11beta-HSD1 mRNA levels was more ... These data suggest that CORT-inducible 11beta-HSD1 expression in fat contributes to the adverse cardiometabolic effects of CORT ... Despite lower basal expression of 11beta-hydroxysteroid dehydrogenase type 1 ( ... Despite lower basal expression of 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1), which generates active ...
AAK83653.1 11-BETA HYDROXYSTEROID DEHYDROGENASE TYPE 1 [HOMO SAPIENS]. FASTA Sequence. ...
Estrogen promotes apoptosis of murine osteoclasts mediated by TGF-beta. Nat Med. 1996;2:1132-6 ... Osteoblastic 11beta-hydroxysteroid dehydrogenase type 1 activity increases with age and glucocorticoid exposure. J Bone Miner ... 11beta-Hydroxysteroid dehydrogenase type 1 selective inhibitor BVT.2733 protects osteoblasts against endogenous glucocorticoid ... Malunowicz EM, Romer TE, Urban M, Bossowski A. 11beta-hydroxysteroid dehydrogenase type 1 deficiency (apparent cortisone ...
... particularly to address beta-cell preservation and its sensitivity to glucose; while minimising hypoglycaemia. Most of these ... On the Horizon : New Oral Therapies for Type 2 Diabetes Mellitus : Review ... On the Horizon : New Oral Therapies for Type 2 Diabetes Mellitus : Review ... and 11-beta hydroxysteroid dehydrogenase type 1 inhibitors (11-beta HSD1 inhibitors). Various molecules; including some enzymes ...
G6P availability directly modulates the activity of 11β-hydroxysteroid dehydrogenase type 1 (11βHSD1), an ER-bound enzyme ... Inhibition of 11beta-hydroxysteroid dehydrogenase type 1 reduces food intake and weight gain but maintains energy expenditure ... and lipoprotein profile and show increased expression of hepatic mRNAs encoding regulators of fatty acid beta-oxidation. These ... 11beta-Hydroxysteroid Dehydrogenase Type 1 Regulation by Intracellular Glucose 6-Phosphate Provides Evidence for a Novel Link ...
Dy J, Guan H, Sampath-Kumar R, Richardson BS, Yang K (2008) Placental 11beta-hydroxysteroid dehydrogenase type 2 in pregnancies ... Differences in expression and activity of 11beta-hydroxysteroid dehydrogenase type 1 and 2 in human placentas in term ... physical inactivity and season independently associated with midnight salivary cortisol in type 1 diabetes. BMC Endocr Disord ... Table 1. Maternal and pregnancy characteristics of cases of preterm birth, low birth weight, and small-for-gestational age and ...
BACKGROUND: 11ß-hydroxysteroid dehydrogenase type 2 enzyme (11ß-HSD2) inactivates cortisol (F) to cortisone (E); its impairment ... BACKGROUND: Familial hyperaldosteronism type I (FH-I) is caused by the unequal recombination between the 11beta-hydroxylase ( ... 11ß-hydroxysteroid dehydrogenase type 2 polymorphisms and activity in a Chilean essential hypertensive and normotensive cohort ... BACKGROUND: The impairment of 11ß-hydroxysteroid dehydrogenase type 2 enzyme (11ßHSD2) results in an inefficient conversion of ...
Two 1 mg vials must be reconstituted with the provided diluent (Sterile Water for Injection) as follows to provide the 2-mg ... 1-888-227-6469 © 2023 PDR, LLC. All rights reserved. , Terms of Service , California Residents , Supplemental Privacy Notice , ... Place the 1/2-inch 27-gauge safety injection needle onto the syringe.. Use reconstituted solution immediately. If injection in ... Place a new 1/2-inch 30-gauge needle onto the syringe.. Administer dose immediately after reconstitution, and discard any ...
Association studies between the HSD11B2 gene (encoding human 11beta-hydroxysteroid dehydrogenase type 2), type 1 diabetes ... 11ß-Hydroxysteroid dehydrogenase type 2 in hypertension: comparison of phenotype and genotype analysis. Journal of human ... hydroxysteroid dehydrogenase type 2 deficiency. Proceedings of the National Academy of Sciences of the United States of America ... Association between a variant in the 11 beta-hydroxysteroid dehydrogenase type 2 gene and primary hypertension. Journal of ...
Another paper11 published in July 2020, this one a case series, also hints at the usefulness of fibrinolytic enzymes for COVID ... 1. Lumbrokinase - A highly effective antithrombotic agent that reduces blood viscosity and platelet aggregation20 while also ... Aspirin (acetylsalicylic acid) was introduced in 1899 as an alternative to sodium salicylate,1 a pain reliever and anti- ... and directly by inhibiting the enzyme 11-beta-hydroxysteroid dehydrogenase Type 1. This enzyme synthesizes active cortisol from ...
  • 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) interconverts inactive cortisone and active cortisol. (ox.ac.uk)
  • Comment: Microsomal enzyme 11-beta-hydroxysteroid dehydrogenase type 1 (11-beta-HSD-1) required for cortisone conversion to its active metabolite, cortisol, in hepatic and adipose tissue. (sideload.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)
  • 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)
  • 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) is a key enzyme that transform cortisone to cortisol, which activates the endogenous glucocorticoid function. (ijbs.com)
  • 11βHSD1 is an ER-bound enzyme catalyzing the conversion of inactive cortisone in active cortisol in humans. (biomedcentral.com)
  • 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)
  • Importantly, aspirin will also lower your baseline cortisol - indirectly by lowering inflammation, and directly by inhibiting the enzyme 11-beta-hydroxysteroid dehydrogenase Type 1. (wekerle100.eu)
  • This could be explained by a reduction in cortisol clearance rate: urinary free cortisol/cortisone ratios were not different but A-ring-reduced metabolites of cortisol were higher in winter, suggesting that conversion of cortisone to cortisol by hepatic 11 beta-hydroxysteroid dehydrogenase 1 is enhanced. (nih.gov)
  • The human body regulates cortisol by employing an enzyme called 11 beta-hydroxysteroid dehydrogenase-type 1 or 11beta-HSD1, which catalyzes the synthesis of cortisol in liver and fat cells. (scienceblog.com)
  • That makes the fish a potentially useful analog for cortisol studies, including discovering the purpose and function of 11 beta-HSD3 in human brains, which may be an evolutionary precursor to 11 beta-HSD1. (scienceblog.com)
  • Description: A sandwich ELISA kit for detection of Glypican 1 from Mouse in samples from blood, serum, plasma, cell culture fluid and other biological fluids. (jemsec.com)
  • Description: Quantitativesandwich ELISA kit for measuring Rat glypican 1 (GPC1) in samples from serum, plasma, tissue homogenates. (jemsec.com)
  • The molecular basis of cortisone reductase deficiency, the putative "11beta-HSD1 knockout state" in humans, has been defined and is caused by intronic mutations in HSD11B1 that decrease gene transcription together with mutations in hexose-6-phosphate dehydrogenase, an endoluminal enzyme that provides reduced nicotinamide-adenine dinucleotide phosphate as cofactor to 11beta-HSD1 to permit reductase activity. (ox.ac.uk)
  • These data suggest that CORT-inducible 11beta-HSD1 expression in fat contributes to the adverse cardiometabolic effects of CORT in POMC deficiency, whereas higher GR levels may be more important in liver. (cam.ac.uk)
  • hydroxysteroid dehydrogenase type 2 deficiency. (cdc.gov)
  • In congenital adrenal hyperplasia (CAH), the DHEA level varies with the type of the enzymatic deficiency. (medscape.com)
  • 11β-Hydroxysteroid dehydrogenase type 1, also known as cortisone reductase, is an NADPH-dependent enzyme highly expressed in key metabolic tissues including liver, adipose tissue, and the central nervous system. (wikipedia.org)
  • More recent incretin-based treatment strategies include glucagon-like peptide-1 (GLP-1) mimetics and inhibitors of the enzyme that degrades GLP-1, dipeptidyl peptidase-4 (DPP-4). (ddw-online.com)
  • The use of detergent/polymer two-phase systems resulted in a specific enzyme activity of 3840 nmol mg(-1) min(-1) of the target membrane protein compared to a conventional purification protocol where a specific enzyme activity of 1440 nmol mg(-1) min(-1) was achieved. (ox.ac.uk)
  • 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)
  • Increased insulin secretion is also obtained by incubation with the inactive glucocorticoid dehydrocorticosterone, pointing to an important role of the enzyme 11beta-hydroxysteroid dehydrogenase type 1 in mediating glucocorticoid effects in beta-cells. (ox.ac.uk)
  • A related enzyme known as 11 beta-HSD-type3 or 11 beta-HSD3 is expressed in the brain, though its utility remains unknown. (scienceblog.com)
  • Interestingly, Baker found that the genomes of mice and rats do not contain 11 beta-HSD3, which means that inserting the appropriate gene for the enzyme in these animal models could provide additional avenues of investigation. (scienceblog.com)
  • Description: This is Double-antibody Sandwich Enzyme-linked immunosorbent assay for detection of Mouse Glypican 1 (GPC1) 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 Mouse Glypican 1 (GPC1) in samples from Serum, plasma, tissue homogenates and other biological fluids with no significant corss-reactivity with analogues from other species. (jemsec.com)
  • Description: This is Competitive Enzyme-linked immunosorbent assay for detection of Human Angiotensin 1-9 (Ang1-9) in serum, plasma, tissue homogenates, cell lysates, cell culture supernates and other biological fluids. (antibody-tech.com)
  • Description: Enzyme-linked immunosorbent assay based on the Competitive Inhibition method for detection of Human Angiotensin 1-9 (Ang1-9) in samples from serum, plasma, tissue homogenates, cell lysates, cell culture supernates and other biological fluids with no significant corss-reactivity with analogues from other species. (antibody-tech.com)
  • Description: This is Double-antibody Sandwich Enzyme-linked immunosorbent assay for detection of Rat Malate Dehydrogenase 1 (MDH1) in tissue homogenates, cell lysates, cell culture supernates and other biological fluids. (operatiebrp.nl)
  • AZD8329 is an inhibitor of 11-beta-hydroxysteroid dehydrogenase type 1 (11β-HSD1). (guidetopharmacology.org)
  • 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)
  • The human gene for 11 beta-hydroxysteroid dehydrogenase. (wikipedia.org)
  • The gene expression of 11β-HSD1 and pro-inflammatory cytokines was detected via RT-PCR. (ac.ir)
  • Association between a variant in the 11 beta-hydroxysteroid dehydrogenase type 2 gene and primary hypertension. (cdc.gov)
  • Association studies between the HSD11B2 gene (encoding human 11beta-hydroxysteroid dehydrogenase type 2), type 1 diabetes mellitus and diabetic nephropathy. (cdc.gov)
  • 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)
  • Variants in the SMCHD1 gene on chromosome 18, which encodes a protein known as structural maintenance of chromosomes flexible hinge domain containing 1, have been associated with FSHD2. (arkansasbluecross.com)
  • At least 1 commercial laboratory (Prevention Genetics, Marshfield, Wisconsin) was identified that offers testing for FSHD2 through sequencing of the SMCHD1 gene via bidirectional Sanger sequencing. (arkansasbluecross.com)
  • Therapeutic inhibition of 11beta-HSD1 reductase activity in patients with obesity and the metabolic syndrome, as well as in glaucoma and osteoporosis, remains an exciting prospect. (ox.ac.uk)
  • 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)
  • 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)
  • Description: A competitive inhibition quantitative ELISA assay kit for detection of Human Angiotensin 1-9 (Ang1-9) in samples from serum, plasma, tissue homogenates, cell lysates, cell culture supernates or other biological fluids. (antibody-tech.com)
  • It belongs to the family of short-chain dehydrogenases. (wikipedia.org)
  • Short-chain dehydrogenases/reductases (SDRs) constitute a large family of NAD(P)(H)-dependent oxidoreductases, sharing sequence motifs and displaying similar mechanisms. (researchgate.net)
  • We speculate that hexose-6-phosphate dehydrogenase activity and therefore reduced nicotinamide-adenine dinucleotide phosphate supply may be crucial in determining the directionality of 11beta-HSD1 activity. (ox.ac.uk)
  • 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)
  • However, the function of 11β-HSD1 in osteoclasts has not been elucidated. (ijbs.com)
  • Our data underscores the potential use of selective 11β-HSD1 inhibitors to ameliorate muscle-wasting effects associated with glucocorticoid excess. (birmingham.ac.uk)
  • Salicylate downregulates 11β-HSD1 expression in adipose tissue in obese mice and hence may explain why aspirin improves glycemic control in type 2 diabetes. (wikipedia.org)
  • 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)
  • A subset of persons with NAFLD progresses to nonalcoholic steatohepatitis (NASH), consisting of hepatic steatosis accompanied by inflammation and fibrosis (Figure 1 )[ 5 ]. (wjgnet.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)
  • 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)
  • Despite lower basal expression of 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1), which generates active glucocorticoids within cells, CORT-mediated induction of 11beta-HSD1 mRNA levels was more pronounced in adipose tissues of Pomc-/- mice. (cam.ac.uk)
  • Type 2 diabetes mellitus (T2DM) accounts for approximately 90% of the cases of diabetes. (ddw-online.com)
  • This altered glucose metabolism state is associated with an increased risk of developing T2DM (Figure 1), although other parameters including excess adiposity, inflammation and dyslipidemia are risk factors associated with the development of insulin resistance, loss of pancreatic function, worsening of hyperglycemia and progression to diabetes (1). (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)
  • High levels of the steroid have been linked to type 2 diabetes and may impair the brain's ability to store memories. (scienceblog.com)
  • The compound increases insulin release selectively at high glucose concentrations and is therefore of interest in type 2 diabetes. (researchgate.net)
  • Studies in animal models and in type 1 diabetes pa-tients have demonstrated multifaceted effects. (researchgate.net)
  • Alternative splicing of the primary transcript gives rise to the 2 mRNA and protein isoforms, hGR-alpha and hGR-beta. (medscape.com)
  • The human GR is a modular protein composed of distinct regions illustrated in panel B in the image below, as follows: (1) The amino-terminal A/B region, also called immunogenic or N-terminal domain (NTD) and (2) the C, D, and E regions, which correspond to the DNA-binding domain, the hinge region, and the ligand-binding domain, respectively. (medscape.com)
  • The AF-1 plays an important role in the interaction of the receptor with molecules necessary for the initiation of transcription, such as coactivators, chromatin modulators, and basal transcription factors, including RNA polymerase II, TATA-binding protein (TBP), and a host of TBP-associated proteins (TAFIIs). (medscape.com)
  • The protein expression of IL-1β in cell supernatants was detected via ELISA. (ac.ir)
  • In this study, we observed increased 11β-HSD1 expression in osteoclasts within an osteoporotic mice model (ovariectomized mice). (ijbs.com)
  • Then, 11β-HSD1 global knock-out or knock-in mice were employed to demonstrate its function in manipulating bone metabolism, showing significant bone volume decrease in 11β-HSD1 knock-in mice. (ijbs.com)
  • In contrast to animal models of insulin resistance, beta-cells from lean mice respond with an increased glucose-stimulated insulin secretion, with a peak effect around 18-24h of treatment. (ox.ac.uk)
  • Description: A competitive ELISA for quantitative measurement of Human 17 β hydroxysteroid dehydrogenase 14(HSD17B14) in samples from blood, plasma, serum, cell culture supernatant and other biological fluids. (glideruniversity.org)
  • Description: A sandwich ELISA for quantitative measurement of Human Butyrophilin subfamily 1 member A1(BTN1A1) in samples from blood, plasma, serum, cell culture supernatant and other biological fluids. (lipidx.org)
  • 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)
  • In conclusion, our study demonstrated the role of 11β-HSD1 in facilitating osteoclasts formation and maturation through the Hippo signaling, which is a new therapeutic target to manage osteoporosis. (ijbs.com)
  • Mouse model with selective liver 11β-HSD1 overexpression show IR, dyslipidemia, and hypertension, but unaltered adiposity. (biomedcentral.com)
  • 11ß-Hydroxysteroid dehydrogenase type 2 in hypertension: comparison of phenotype and genotype analysis. (cdc.gov)
  • In new findings to be published in the June 3 issue of FEBS Letters , Baker, a research professor of medicine who works in the division of nephrology-hypertension at UC San Diego's School of Medicine, reports that 11 beta-HSD3 (but not 11 beta-HSD1) is present in zebrafish, where it appears to serve an important role in fish endocrine physiology. (scienceblog.com)
  • Ensembl chr 1:96,598,647. (mcw.edu)
  • 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)
  • Description: A sandwich quantitative ELISA assay kit for detection of Mouse Enhancer Of Zeste Homolog 1 (EZH1) in samples from tissue homogenates or other biological fluids. (1elisakits.com)
  • An estimated 30% of adults and 10% of children and adolescents in the United States have nonalcoholic fatty liver disease (NAFLD), defined as liver fat content exceeding 5% (Figure 1 )[ 1 - 3 ]. (wjgnet.com)
  • Figure 1 Liver histology ranging from normal liver to steatohepatitis with fibrosis. (wjgnet.com)
  • The MDR superfamily with ~350-residue subunits contains the classical liver alcohol dehydrogenase (ADH), quinone reductase, leukotriene B4 dehydrogenase and many more forms. (researchgate.net)
  • Zinc binding to the peptide replica and analogs to residues 93-115 of horse liver alcohol dehydrogenase (ADH) was examined by competition of the peptides and the chromophoric chelator 4-(2- pyridylazo)resorcinol for zinc and X-ray absorption fine structure analysis of the zinc ligands. (researchgate.net)
  • GLP-1 is an intestinally-derived peptide that stimulates insulin secretion in response to food intake, as well as reducing the rate of gastric emptying, thus promoting satiety and weight loss. (ddw-online.com)
  • Meanwhile, we found 11β-HSD1 facilitated mature osteoclasts formation inhibited bone formation coupled H type vessel (CD31 hi Emcn hi ) growth through reduction of PDFG-BB secretion. (ijbs.com)
  • 11β-HSD1 has been observed to regulate skeletal metabolism, specifically within osteoblasts. (ijbs.com)
  • Purification of the human type 1 11beta-hydroxysteroid dehydrogenase. (ox.ac.uk)
  • Overall, the results indicate that 11β-HSD1 amplifies inflammatory responses by activating the NF-κB and MAPK signaling pathways. (ac.ir)
  • 5. Itoi S, Terao M, Murota H, Katayama I. 11beta-Hydroxysteroid dehydrogenase 1 contributes to the pro-inflammatory response of keratinocytes. (ac.ir)
  • Anti-inflammatory effects of levalbuterol-induced 11beta-hydroxysteroid dehydrogenase type 1 activity in airway epithelial cells. (ac.ir)
  • Aspirin (acetylsalicylic acid) was introduced in 1899 as an alternative to sodium salicylate, 1 a pain reliever and anti-inflammatory known for its unpleasant side effects such as stomach cramps, heartburn, nausea and vomiting. (wekerle100.eu)
  • Clinical, genetic, and structural basis of apparent mineralocorticoid excess due to 11? (cdc.gov)
  • In this review, we discuss both the genetic and enzymatic characterization of 11beta-HSD1, as well as describing its role in physiology and pathology in a tissue-specific manner. (ox.ac.uk)
  • We speculate a possible role of 11βHSD1 modulation by G6P availability. (biomedcentral.com)
  • Common adverse birth outcomes, including preterm birth, low birth weight, and small-for-gestational age (SGA), are associated with neonatal mortality and long-term health problems, including neurodevelopmental impairments, respiratory and gastrointestinal complications, and higher sympathetic activity, which is considered a risk factor for cardiovascular disease [1-4]. (researchsquare.com)
  • CONCLUSION: This study provides detailed insights on the oncological pharmaceutical expenditure for the treatment for solid tumors in the VHUH, based on real cost information from our hospital practice and for all antineoplastic therapies and types of solid tumors. (bvsalud.org)
  • For other types of ligands, e.g. longer nucleotides and peptides, a manually drawn representation of the molecule may be provided. (guidetopharmacology.org)
  • This was supported by decreased mRNA expression of IGF1, decreased activating phosphorylation of mTOR, decreased phosphorylation of 4E-BP1 and increased mRNA expression of key atrophy markers including: atrogin-1, FOXO3a, Mstn, MuRF1. (birmingham.ac.uk)
  • Series (Spanish-South American registry) comprised 25 patients,4 5 however, only the compound to break through cells were cotransfected with increasing concentrations of an expression vector for SRC-1 in the presence or absence of REA as indicated. (sideload.com)
  • Corticosterone suppresses IL-1beta-induced mPGE2 expression through regulation of the 11beta-HSD1 bioactivity of synovial fibroblasts in vitro. (ac.ir)
  • In vitro experiments showed the endogenous high expression of 11β-HSD1 lead to osteoclast formation and maturation. (ijbs.com)
  • Then, by suppression of YAP expression in Hippo signaling, we observed the redundant of osteoclasts formation even in 11β-HSD1 high expression conditions. (ijbs.com)
  • Despite a certain number of gastrointestinal side-effects, the GLP-1 mimetic exenatide was approved by the FDA in 2005, and its indication was extended in 2009 to standalone therapy for T2DM. (ddw-online.com)
  • Depending on the type of cell the steroids are in, this activation can change how certain genes behave - especially the ones that control the changes that happen during puberty. (sideload.com)
  • METHODS: This was a single-center retrospective cohort study of adult cancer patients attended in clinical practice at the Medical Oncology Department of VHUH between 1 January 2010 and 31 December 2019. (bvsalud.org)