11-beta-Hydroxysteroid Dehydrogenase Type 2
11-beta-Hydroxysteroid Dehydrogenase Type 1
3-alpha-Hydroxysteroid Dehydrogenase (B-Specific)
Molecular Sequence Data
Ketoglutarate Dehydrogenase Complex
Retinoic acid stimulates the expression of 11beta-hydroxysteroid dehydrogenase type 2 in human choriocarcinoma JEG-3 cells. (1/232)The syncytiotrophoblasts of the human placenta express high levels of 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2), the enzyme responsible for the inactivation of glucocorticoids. It has been proposed that the placental 11beta-HSD2 serves as a barrier to protect the fetus from high levels of maternal cortisol. To examine the hypothesis that nutritional signals regulate the expression of 11beta-HSD2 in placental syncytiotrophoblasts, we investigated the effects of retinoic acids (RAs), the major metabolites of vitamin A, on the expression of 11beta-HSD2 using human choriocarcinoma JEG-3 cells as a model. This trophoblast-like cell line displays a number of functional similarities to the syncytiotrophoblast. Treatment for 24 h with all-trans RA (1-1000 nM) resulted in a dose-dependent increase in 11beta-HSD2 activity with a maximal effect (increase to 3-fold) at 100 nM. The effect of all-trans RA (100 nM) was also time-dependent in that the effect was detectable at 6 h and reached its maximum by 48 h. Similar increases in 11beta-HSD2 activity were observed when the cells were treated with 9-cis RA. Results from semi-quantitative reverse transcription-polymerase chain reaction demonstrated that there was a corresponding increase in 11beta-HSD2 mRNA after RA treatment. Moreover, treatment with actinomycin D (100 ng/ml) abrogated the increase in 11beta-HSD2 mRNA induced by RA, indicating an effect on transcription. In conclusion, the present study has demonstrated for the first time that RA, at physiological concentrations, induces 11beta-HSD2 gene expression and enzyme activity in JEG-3 cells. If this occurs in vivo, the present finding suggests that high expression of 11beta-HSD2 in the human placenta may be maintained, at least in part, by dietary intake of vitamin A. (+info)
Developmental expression of sodium entry pathways in rat nephron. (2/232)During the past several years, sites of expression of ion transport proteins in tubules from adult kidneys have been described and correlated with functional properties. Less information is available concerning sites of expression during tubule morphogenesis, although such expression patterns may be crucial to renal development. In the current studies, patterns of renal axial differentiation were defined by mapping the expression of sodium transport pathways during nephrogenesis in the rat. Combined in situ hybridization and immunohistochemistry were used to localize the Na-Pi cotransporter type 2 (NaPi2), the bumetanide-sensitive Na-K-2Cl cotransporter (NKCC2), the thiazide-sensitive Na-Cl cotransporter (NCC), the Na/Ca exchanger (NaCa), the epithelial sodium channel (rENaC), and 11beta-hydroxysteroid dehydrogenase (11HSD). The onset of expression of these proteins began in post-S-shape stages. NKCC2 was initially expressed at the macula densa region and later extended into the nascent ascending limb of the loop of Henle (TAL), whereas differentiation of the proximal tubular part of the loop of Henle showed a comparatively retarded onset when probed for NaPi2. The NCC was initially found at the distal end of the nascent distal convoluted tubule (DCT) and later extended toward the junction with the TAL. After a period of changing proportions, subsegmentation of the DCT into a proximal part expressing NCC alone and a distal part expressing NCC together with NaCa was evident. Strong coexpression of rENaC and 11HSD was observed in early nascent connecting tubule (CNT) and collecting ducts and later also in the distal portion of the DCT. Ontogeny of the expression of NCC, NaCa, 11HSD, and rENaC in the late distal convolutions indicates a heterogenous origin of the CNT. These data present a detailed analysis of the relations between the anatomic differentiation of the developing renal tubule and the expression of tubular transport proteins. (+info)
Inhibition of 11 beta-hydroxysteroid dehydrogenase obtained from guinea pig kidney by some bioflavonoids and triterpenoids. (3/232)AIM: To study the inhibitory effect of some bioflavonoids and triterpenoids on 11 beta-hydroxysteroid dehydrogenase (11 beta-OHSD) from guinea pig kidney. METHOD: The 11 beta-OHSD of kidney cortex microsomes in addition of cortisol was incubated in the presence of NADP, Triton DF-18, and the test compounds at 37 degrees C for 1 h. The enzyme activity was assayed by measuring the rate of conversion of cortisol to cortisone eluted with HPLC gradient analysis. RESULTS: The IC50 (95% confidence limits) values of glycyrrhizic acid, naringenin, fisetin, emodin were 254 (202-320), 336 (270-418), 470 (392-564), and 527 (425-653) mumol.L-1, respectively. The inhibitory effect of oleanolic acid was 2-fold stronger than that of astramembranin I. The mode of action of naringenin was competitive inhibition. CONCLUSION: The test compounds inhibited the 11 beta-OHSD in kidney cortex with different potencies as glycyrrhizic acid did. (+info)
Hypertension in mice lacking 11beta-hydroxysteroid dehydrogenase type 2. (4/232)Deficiency of 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2) in humans leads to the syndrome of apparent mineralocorticoid excess (SAME), in which cortisol illicitly occupies mineralocorticoid receptors, causing sodium retention, hypokalemia, and hypertension. However, the disorder is usually incompletely corrected by suppression of cortisol, suggesting additional and irreversible changes, perhaps in the kidney. To examine this further, we produced mice with targeted disruption of the 11beta-HSD2 gene. Homozygous mutant mice (11beta-HSD2(-/-)) appear normal at birth, but approximately 50% show motor weakness and die within 48 hours. Both male and female survivors are fertile but exhibit hypokalemia, hypotonic polyuria, and apparent mineralocorticoid activity of corticosterone. Young adult 11beta-HSD2(-/-) mice are markedly hypertensive, with a mean arterial blood pressure of 146 +/- 2 mmHg, compared with 121 +/- 2 mmHg in wild-type controls and 114 +/- 4 mmHg in heterozygotes. The epithelium of the distal tubule of the nephron shows striking hypertrophy and hyperplasia. These histological changes do not readily reverse with mineralocorticoid receptor antagonism in adulthood. Thus, 11beta-HSD2(-/-) mice demonstrate the major features of SAME, providing a unique rodent model to study the molecular mechanisms of kidney resetting leading to hypertension. (+info)
Glucocorticoids and insulin resistance: old hormones, new targets. (5/232)Insulin resistance has been proposed as a mediator of the association between risk factors for cardiovascular disease in the population. The clinical syndrome of glucocorticoid excess (Cushing's syndrome) is associated with glucose intolerance, obesity and hypertension. By opposing the actions of insulin, glucocorticoids could contribute to insulin resistance and its association with other cardiovascular risk factors. In this review, we describe briefly the known mechanisms of insulin resistance and highlight the potential mechanisms for the effect of glucocorticoids. We then discuss factors which modulate the influence of glucocorticoids on insulin sensitivity; this highlights a novel therapeutic strategy to manipulate glucocorticoid action which may prove to be a useful tool in treating subjects with insulin resistance. Finally, we describe evidence from human studies that glucocorticoids make an important contribution to the pathophysiology of insulin resistance in the population. (+info)
Targeting proteins to the lumen of endoplasmic reticulum using N-terminal domains of 11beta-hydroxysteroid dehydrogenase and the 50-kDa esterase. (6/232)Previous studies identified two intrinsic endoplasmic reticulum (ER) proteins, 11beta-hydroxysteroid dehydrogenase, isozyme 1 (11beta-HSD) and the 50-kDa esterase (E3), sharing some amino acid sequence motifs in their N-terminal transmembrane (TM) domains. Both are type II membrane proteins with the C terminus projecting into the lumen of the ER. This finding implied that the N-terminal TM domains of 11beta-HSD and E3 may constitute a lumenal targeting signal (LTS). To investigate this hypothesis we created chimeric fusions using the putative targeting sequences and the reporter gene, Aequorea victoria green fluorescent protein. Transfected COS cells expressing LTS-green fluorescent protein chimeras were examined by fluorescent microscopy and electron microscopic immunogold labeling. The orientation of expressed chimeras was established by immunocytofluorescent staining of selectively permeabilized COS cells. In addition, protease protection assays of membranes in the presence and absence of detergents was used to confirm lumenal or the cytosolic orientation of the constructed chimeras. To investigate the general applicability of the proposed LTS, we fused the N terminus of E3 to the N terminus of the NADH-cytochrome b5 reductase lacking the myristoyl group and N-terminal 30-residue membrane anchor. The orientation of the cytochrome b5 reductase was reversed, from cytosolic to lumenal projection of the active domain. These observations establish that an amino acid sequence consisting of short basic or neutral residues at the N terminus, followed by a specific array of hydrophobic residues terminating with acidic residues, is sufficient for lumenal targeting of single-pass proteins that are structurally and functionally unrelated. (+info)
NAD- and NADP-dependent 11 beta-hydroxysteroid dehydrogenase isoforms in guinea pig kidney with gossypol inhibition. (7/232)AIM: To study the mechanism of gossypol-induced hypokalemia. METHODS: The 11 beta-hydroxysteroid dehydrogenase (11 beta-OHSD) protein was prepared from guinea pig kidney. The activity of 11 beta-OHSD with NAD or NADP as the coenzyme was measured by HPLC in both control and gossypol treatment. RESULTS: The Vmax and K(m) were 0.64 mmol.h-1/g protein and 0.07 mumol (cortisol) for NAD-dependent 11 beta-OHSD, 1.75 mmol.h-1/g protein and 0.21 mumol (cortisol) for NADP-dependent 11 beta-OHSD, respectively when 80 micrograms of enzyme protein was used. The inhibitory effects of gossypol on these two 11 beta-OHSD isoforms were different. The IC50 (95% confidence limits) were 50.2 (48.3-52.0) mumol of gossypol for NAD-dependent 11 beta-OHSD and 1143 (1098-1188) mumol of gossypol for NADP-dependent 11 beta-OHSD. The Ki was gossypol 96 mmol.L-1 for the former and 340 mmol.L-1 for the latter. CONCLUSION: The NAD-dependent 11 beta-OHSD is a more critical physiologic mechanism than NADP-dependent 11 beta-OHSD for hypokalemia caused by gossypol. (+info)
Glucocorticoid resistance caused by reduced expression of the glucocorticoid receptor in cells from human vascular lesions. (8/232)Mechanisms that control the balance between cell proliferation and death are important in the development of vascular lesions. Rat primary smooth muscle cells were 80% inhibited by low microgram doses of hydrocortisone (HC) and 50% inhibited by nanogram concentrations of transforming growth factor-beta1 (TGF-beta1), although some lines acquired resistance in late passage. However, comparable doses of HC, or TGF-beta1, failed to inhibit most human lesion-derived cell (LDC) lines. In sensitive LDC, HC (10 microg/mL) inhibited proliferation by up to 50%, with obvious apoptosis in some lines, and TGF-beta1 inhibited proliferation by more than 90%. Collagen production, as measured by [3H]proline incorporation or RIA for type III pro-collagen, was either unaffected or increased in the LDCs by HC. These divergent responses between LDC lines were partially explained by the absence of the glucocorticoid receptor (GR) and heat shock protein 90 mRNA in 10 of 12 LDC lines, but the presence of the mineralocorticoid receptor and 11beta-hydroxysteroid dehydrogenase type II. Western blot analysis confirmed the absence of the GR protein in cells lacking GR mRNA. Immunohistochemistry of human carotid lesions showed high levels of GR in the tunica media, but large areas lacking GR in the fibrous lesion. Considering the absence of the GR in most lines, the effects of HC may be elicited through the mineralocorticoid receptor. Functional resistance to the antiproliferative and antifibrotic effects of HC may contribute to excessive wound repair in atherosclerosis and restenosis. (+info)
Hydroxysteroid dehydrogenases (HSDs) are a group of enzymes that play a crucial role in the metabolism of steroid hormones in the body. These enzymes catalyze the conversion of one form of a steroid hormone to another by removing or adding a hydroxyl group. There are several types of HSDs, each with a specific function and localization in the body. For example, some HSDs are found in the liver, where they help regulate the levels of sex hormones such as estrogen and testosterone. Other HSDs are found in the brain, where they play a role in the regulation of mood and behavior. HSDs are also involved in the metabolism of other types of hormones, such as cortisol and aldosterone. Dysfunction of HSDs can lead to a variety of medical conditions, including hormonal imbalances, mood disorders, and metabolic disorders.
11-beta-Hydroxysteroid Dehydrogenase Type 2 (11β-HSD2) is an enzyme that plays a crucial role in regulating the levels of cortisol, a hormone produced by the adrenal gland. It is primarily found in the liver, kidney, and adipose tissue. The primary function of 11β-HSD2 is to convert cortisol to its inactive form, cortisone. This process helps to prevent cortisol from exerting its effects on various tissues throughout the body, including the brain, muscles, and immune system. In the medical field, 11β-HSD2 is of particular interest because of its role in the development of metabolic disorders such as obesity, insulin resistance, and type 2 diabetes. Studies have shown that individuals with reduced activity of 11β-HSD2 are less likely to develop these conditions, suggesting that the enzyme may play a protective role against metabolic disease. In addition, 11β-HSD2 has been implicated in the development of certain psychiatric disorders, such as depression and anxiety. Research has shown that individuals with reduced activity of 11β-HSD2 may be more susceptible to the effects of stress and may be at increased risk for developing these conditions. Overall, 11β-HSD2 is a critical enzyme that plays a key role in regulating cortisol levels and maintaining metabolic and psychiatric health.
3-Hydroxysteroid dehydrogenases (3-HSDs) are a group of enzymes that play a crucial role in the metabolism of steroid hormones in the body. These enzymes are responsible for converting 3-hydroxysteroids, which are derivatives of cholesterol, into their corresponding 3-ketosteroids. There are several types of 3-HSDs, including NAD-dependent and NADP-dependent enzymes, which are found in different tissues throughout the body. For example, the NAD-dependent 3-HSD is found in the liver and is involved in the metabolism of cortisol, aldosterone, and other glucocorticoids. The NADP-dependent 3-HSD is found in the adrenal gland and is involved in the metabolism of androgens and estrogens. Disruptions in the activity of 3-HSDs can lead to a variety of medical conditions, including hormonal imbalances, metabolic disorders, and reproductive problems. For example, mutations in the gene encoding the NAD-dependent 3-HSD can cause a rare genetic disorder called 3-beta-hydroxysteroid dehydrogenase deficiency, which can lead to the accumulation of 3-hydroxysteroids in the body and cause a range of symptoms, including adrenal insufficiency, ambiguous genitalia, and adrenal hyperplasia.
11-beta-Hydroxysteroid Dehydrogenase Type 1 (11β-HSD1) is an enzyme that plays a crucial role in regulating the levels of cortisol, a hormone produced by the adrenal gland. It is expressed in various tissues throughout the body, including the liver, muscle, adipose tissue, and brain. The primary function of 11β-HSD1 is to convert inactive cortisone to its active form, cortisol. This conversion occurs in the liver and adipose tissue, where 11β-HSD1 is highly expressed. Cortisol is a key hormone involved in the body's stress response and plays a role in regulating metabolism, immune function, and blood pressure. In addition to its role in cortisol metabolism, 11β-HSD1 has also been implicated in the development of various diseases, including obesity, diabetes, cardiovascular disease, and depression. For example, increased activity of 11β-HSD1 in adipose tissue has been linked to insulin resistance and the development of type 2 diabetes. Similarly, increased activity of 11β-HSD1 in the brain has been linked to depression and anxiety. Overall, 11β-HSD1 is a critical enzyme involved in regulating cortisol metabolism and has important implications for the development of various diseases.
17-Hydroxysteroid dehydrogenases (17-HSDs) are a group of enzymes that play a crucial role in the metabolism of sex hormones in the human body. These enzymes are responsible for converting one form of a sex hormone into another, which can affect the hormone's activity and impact various physiological processes. There are several types of 17-HSDs, each with a specific function. For example, 17-HSD1 is involved in the conversion of estradiol to estrone, while 17-HSD2 is involved in the conversion of testosterone to dihydrotestosterone. These enzymes are found in various tissues throughout the body, including the liver, adrenal glands, and reproductive organs. Abnormalities in the activity of 17-HSDs can lead to various medical conditions, such as polycystic ovary syndrome (PCOS), which is characterized by hormonal imbalances and irregular menstrual cycles. In addition, some forms of cancer, such as breast and ovarian cancer, have been linked to changes in the activity of 17-HSDs. Overall, 17-HSDs play a critical role in regulating sex hormone metabolism and are an important area of research in the field of endocrinology.
11-beta-Hydroxysteroid dehydrogenases (11β-HSDs) are a group of enzymes that play a crucial role in regulating the levels of active glucocorticoids in the body. These enzymes are found in various tissues, including the liver, adipose tissue, and the brain. There are two main isoforms of 11β-HSD: 11β-HSD1 and 11β-HSD2. 11β-HSD1 converts inactive cortisone to its active form, cortisol, in the liver and adipose tissue. This enzyme is involved in the regulation of glucose metabolism, insulin sensitivity, and inflammation. On the other hand, 11β-HSD2 converts active cortisol to its inactive form, cortisone, in the kidneys and other tissues. This enzyme helps to protect the body from the harmful effects of excess cortisol, such as weight gain, insulin resistance, and high blood pressure. Dysregulation of 11β-HSD activity has been implicated in various diseases, including obesity, diabetes, cardiovascular disease, and depression. Therefore, understanding the role of 11β-HSDs in the body and developing drugs that target these enzymes may have therapeutic potential for the treatment of these diseases.
20-Hydroxysteroid dehydrogenases (20-HSDs) are a group of enzymes that play a crucial role in the metabolism of various hormones, including cortisol, aldosterone, and androgens. These enzymes are responsible for converting the active forms of these hormones into their inactive forms, which are then excreted from the body. In the medical field, 20-HSDs are often studied in the context of various diseases and disorders, including Cushing's syndrome, Addison's disease, and polycystic ovary syndrome (PCOS). In Cushing's syndrome, for example, the overproduction of cortisol is often caused by a malfunction in the 20-HSD enzyme responsible for converting cortisol to its inactive form. In Addison's disease, the deficiency of this enzyme can lead to a deficiency in cortisol production. In PCOS, the activity of 20-HSD enzymes has been shown to be altered, leading to an imbalance in the levels of androgens and estrogens. This can contribute to the development of symptoms such as irregular menstrual cycles, excess hair growth, and infertility. Overall, 20-HSDs play a critical role in regulating hormone levels in the body, and their dysfunction can have significant implications for various medical conditions.
Steroid 17-alpha-hydroxylase is an enzyme that plays a crucial role in the biosynthesis of steroid hormones in the human body. It is located in the mitochondria of various steroidogenic cells, including the adrenal cortex, gonads, and placenta. The enzyme catalyzes the conversion of cholesterol to pregnenolone, which is the precursor to all other steroid hormones. Specifically, it adds a hydroxyl group to the 17th carbon atom of cholesterol, forming pregnenolone. This reaction is the first and rate-limiting step in the biosynthesis of all steroid hormones, including cortisol, aldosterone, and sex hormones such as testosterone and estrogen. Mutations in the gene encoding steroid 17-alpha-hydroxylase can lead to a deficiency in the enzyme, resulting in a rare genetic disorder called 17-alpha-hydroxylase deficiency. This condition can cause a range of symptoms, including adrenal insufficiency, ambiguous genitalia in newborns, and infertility in adults. Treatment typically involves hormone replacement therapy to replace the deficient hormones.
Hydrocortisone is a synthetic glucocorticoid hormone that is used in the medical field to treat a variety of conditions. It is a potent anti-inflammatory and immunosuppressive agent that can help reduce inflammation, swelling, and redness in the body. Hydrocortisone is also used to treat conditions such as allergies, asthma, eczema, and psoriasis, as well as to reduce the symptoms of adrenal insufficiency, a condition in which the body does not produce enough of the hormone cortisol. It is available in a variety of forms, including oral tablets, topical creams, and injections.
Estradiol dehydrogenases are a group of enzymes that are involved in the metabolism of estradiol, a type of estrogen hormone. These enzymes are responsible for converting estradiol into other forms of estrogen, such as estrone and estriol, or into non-estrogenic compounds. There are several different types of estradiol dehydrogenases, including 17β-hydroxysteroid dehydrogenase (17β-HSD) and aromatase. 17β-HSD is responsible for converting estradiol into estrone, while aromatase is responsible for converting androgens (male hormones) into estrogens. Estradiol dehydrogenases play an important role in regulating estrogen levels in the body. Imbalances in these enzymes can lead to hormonal imbalances and a variety of health problems, including infertility, osteoporosis, and certain types of cancer.
Sulfotransferases are a group of enzymes that transfer a sulfate group from a donor molecule to an acceptor molecule. These enzymes play important roles in the metabolism of many drugs, hormones, and other substances in the body. They are also involved in the detoxification of harmful substances, such as environmental pollutants and toxins. Sulfotransferases are found in many tissues throughout the body, including the liver, kidney, and brain. They are classified into different families based on their substrate specificity and mechanism of action. Some of the most well-known families of sulfotransferases include the cytosolic sulfotransferases (SULTs) and the membrane-bound sulfotransferases (SULTs). In the medical field, sulfotransferases are important for understanding the metabolism and pharmacology of drugs. They can affect the efficacy and toxicity of drugs by modifying their chemical structure and altering their interactions with receptors and enzymes. Sulfotransferases are also being studied as potential targets for the development of new drugs for the treatment of various diseases, including cancer, cardiovascular disease, and neurological disorders.
Cortisone is a synthetic form of the hormone cortisol, which is produced by the adrenal glands. It is a corticosteroid medication that is used to treat a variety of inflammatory and autoimmune conditions, such as rheumatoid arthritis, lupus, and psoriasis. Cortisone can also be used to treat allergies, asthma, and other respiratory conditions, as well as to reduce swelling and inflammation in the body. It is available in various forms, including tablets, injections, and creams. Cortisone is a potent medication and should only be used under the guidance of a healthcare professional.
Alcohol oxidoreductases are a group of enzymes that catalyze the oxidation of alcohols. In the medical field, these enzymes are of particular interest because they play a key role in the metabolism of alcohol in the body. There are several different types of alcohol oxidoreductases, including alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH). ADH is responsible for converting alcohol (ethanol) into acetaldehyde, a toxic substance that can cause a range of symptoms when present in high concentrations, including headache, nausea, and dizziness. ALDH is responsible for converting acetaldehyde into acetate, a non-toxic substance that can be further metabolized by the body. Alcohol oxidoreductases are found in a variety of tissues throughout the body, including the liver, brain, and lungs. In the liver, ADH and ALDH are particularly important for metabolizing alcohol, as this organ is responsible for processing a large amount of the alcohol that is consumed. Disruptions in the activity of alcohol oxidoreductases can lead to a range of health problems, including alcohol dependence, liver disease, and certain types of cancer. For example, individuals who are unable to effectively metabolize alcohol due to a deficiency in ADH or ALDH may be more susceptible to the negative effects of alcohol consumption, such as liver damage and addiction.
In the medical field, steroids refer to a class of drugs that are derived from the natural hormone cortisol, which is produced by the adrenal gland. Steroids are used to treat a wide range of medical conditions, including inflammatory diseases, autoimmune disorders, allergies, and certain types of cancer. There are two main types of steroids: corticosteroids and anabolic steroids. Corticosteroids are used to reduce inflammation and suppress the immune system, while anabolic steroids are used to build muscle mass and increase strength. Steroids can be administered in various forms, including oral tablets, injections, creams, and inhalers. They can have a range of side effects, including weight gain, mood changes, high blood pressure, and increased risk of infections. It is important to note that the use of steroids is closely monitored by healthcare professionals, and they are typically prescribed only for specific medical conditions and under the guidance of a doctor.。
NAD stands for nicotinamide adenine dinucleotide, which is a coenzyme found in all living cells. It plays a crucial role in various metabolic processes, including energy production, DNA repair, and regulation of gene expression. In the medical field, NAD is often used as a supplement to support cellular health and improve overall well-being. It is also being studied for its potential therapeutic applications in treating conditions such as depression, anxiety, and chronic pain.
L-Lactate Dehydrogenase (LDH) is an enzyme that plays a crucial role in the metabolism of lactate, a byproduct of cellular respiration. In the medical field, LDH is often used as a diagnostic marker for various diseases and conditions, including liver and heart diseases, cancer, and muscle injuries. LDH is found in many tissues throughout the body, including the liver, heart, muscles, kidneys, and red blood cells. When these tissues are damaged or injured, LDH is released into the bloodstream, which can be detected through blood tests. In addition to its diagnostic use, LDH is also used as a prognostic marker in certain diseases, such as cancer. High levels of LDH in the blood can indicate a more aggressive form of cancer or a poorer prognosis for the patient. Overall, LDH is an important enzyme in the body's metabolism and plays a critical role in the diagnosis and management of various medical conditions.
Testosterone is a hormone that is primarily produced in the testicles in males and in smaller amounts in the ovaries and adrenal glands in females. It is responsible for the development of male sexual characteristics, such as the growth of facial hair, deepening of the voice, and muscle mass. Testosterone also plays a role in bone density, red blood cell production, and the regulation of the body's metabolism. In the medical field, testosterone is often used to treat conditions related to low testosterone levels, such as hypogonadism (a condition in which the body does not produce enough testosterone), delayed puberty, and certain types of breast cancer in men. It can also be used to treat conditions related to low estrogen levels in women, such as osteoporosis and menopause symptoms. Testosterone therapy can be administered in various forms, including injections, gels, patches, and pellets. However, it is important to note that testosterone therapy can have side effects, such as acne, hair loss, and an increased risk of blood clots, and should only be prescribed by a healthcare professional.
Androsterone is a naturally occurring androgenic hormone that is produced in the human body. It is a derivative of testosterone and is found in both males and females, although it is present in higher concentrations in males. Androsterone is produced in the adrenal glands and is also synthesized in the gonads and other tissues throughout the body. In the medical field, androsterone is sometimes used as a marker of male sexual development and function. It is also used as a diagnostic tool in the evaluation of certain medical conditions, such as congenital adrenal hyperplasia and polycystic ovary syndrome. Androsterone has also been studied for its potential therapeutic effects in the treatment of certain conditions, such as osteoporosis and prostate cancer.
Alcohol dehydrogenase (ADH) is an enzyme that plays a key role in the metabolism of alcohol in the human body. It is found in many tissues, including the liver, brain, and stomach, but it is particularly abundant in the liver. When alcohol is consumed, it is absorbed into the bloodstream and eventually reaches the liver, where it is metabolized by ADH. ADH catalyzes the conversion of alcohol (ethanol) into acetaldehyde, a toxic substance that can cause a range of symptoms, including nausea, headache, and dizziness. Once acetaldehyde is formed, it is further metabolized by another enzyme called aldehyde dehydrogenase (ALDH) into acetate, a non-toxic substance that can be easily eliminated from the body in the form of carbon dioxide and water. ADH is also involved in the metabolism of other substances, including some drugs and toxins. In some cases, ADH activity can be affected by factors such as genetics, age, gender, and chronic alcohol consumption, which can impact the body's ability to metabolize alcohol and other substances.
Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) is an enzyme that plays a crucial role in cellular metabolism. It is involved in the glycolytic pathway, which is the process by which cells convert glucose into energy. GAPDH catalyzes the conversion of glyceraldehyde-3-phosphate to 1,3-bisphosphoglycerate, which is an important step in the breakdown of glucose. In addition to its role in glycolysis, GAPDH has also been implicated in a variety of other cellular processes, including apoptosis (programmed cell death), inflammation, and the regulation of gene expression. It is also a commonly used biomarker in research and clinical settings, as it is expressed in many different types of cells and tissues and is relatively stable under a variety of conditions. GAPDH is a highly conserved enzyme, meaning that it is found in many different species and has a similar structure and function across these species. It is a homotetramer, meaning that it is composed of four identical subunits, and it is found in the cytoplasm of cells.
20-alpha-Hydroxysteroid dehydrogenase (20α-HSD) is an enzyme that plays a crucial role in the metabolism of various hormones, including cortisol, aldosterone, and androgens. It catalyzes the conversion of 20α-hydroxy steroids to their corresponding 11-keto steroids. This enzyme is primarily found in the adrenal gland, gonads, and placenta. In the context of medical research, 20α-HSD has been studied in relation to various diseases and conditions, including Cushing's syndrome, Addison's disease, and polycystic ovary syndrome (PCOS). In Cushing's syndrome, the overproduction of cortisol is often due to an excess of 20α-HSD activity in the adrenal gland. In Addison's disease, the deficiency of 20α-HSD can lead to a decrease in cortisol production. In PCOS, the increased activity of 20α-HSD in the ovaries can contribute to the overproduction of androgens. In addition, 20α-HSD has been studied as a potential therapeutic target for the treatment of various diseases, including cancer, cardiovascular disease, and osteoporosis.
Aldehyde dehydrogenase (ALDH) is an enzyme that plays a crucial role in the metabolism of aldehydes, which are toxic compounds that can be produced during the breakdown of certain drugs, alcohol, and other substances. ALDH catalyzes the oxidation of aldehydes to their corresponding carboxylic acids, which are less toxic and can be further metabolized by other enzymes in the body. In the medical field, ALDH is important for detoxifying the body and preventing the accumulation of toxic aldehydes. Deficiency in ALDH can lead to a condition called aldehyde dehydrogenase deficiency, which can cause sensitivity to certain drugs and alcohol, as well as other health problems. ALDH is also a target for the development of new drugs for the treatment of various diseases, including cancer, neurodegenerative disorders, and alcohol addiction.
Glutamate dehydrogenase (GDH) is an enzyme that plays a crucial role in the metabolism of amino acids, particularly glutamate. It catalyzes the reversible conversion of glutamate to alpha-ketoglutarate, which is a key intermediate in the citric acid cycle. GDH is found in a variety of tissues, including the liver, kidney, and brain, and is involved in a number of metabolic processes, including gluconeogenesis, amino acid catabolism, and the regulation of nitrogen metabolism. In the medical field, GDH is often measured as a diagnostic marker for liver and kidney function, and it may also be used as a target for the development of new drugs for the treatment of various diseases, including cancer and neurological disorders.
Glucosephosphate dehydrogenase (GPD) is an enzyme that plays a crucial role in the metabolism of glucose. It is involved in the pentose phosphate pathway, which is a metabolic pathway that generates reducing equivalents in the form of NADPH and ribose-5-phosphate. In the context of the medical field, GPD deficiency is a rare genetic disorder that affects the production of NADPH, which is essential for the functioning of various bodily processes, including the production of red blood cells. GPD deficiency can lead to a range of symptoms, including anemia, jaundice, and neurological problems. In addition, GPD is also used as a diagnostic tool in the medical field, particularly in the diagnosis of certain types of cancer. High levels of GPD activity have been observed in certain types of cancer cells, including breast, ovarian, and lung cancer. This has led to the development of diagnostic tests that measure GPD activity in patient samples, which can help in the early detection and diagnosis of cancer.
Malate dehydrogenase (MDH) is an enzyme that plays a crucial role in cellular metabolism. It catalyzes the conversion of malate, a four-carbon compound, to oxaloacetate, a five-carbon compound, in the citric acid cycle. This reaction is reversible and can occur in both directions, depending on the cellular needs and the availability of energy. In the medical field, MDH is often studied in the context of various diseases and disorders. For example, mutations in the MDH gene have been associated with certain forms of inherited metabolic disorders, such as Leigh syndrome and MELAS (mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes). In addition, MDH has been implicated in the development of certain types of cancer, such as breast and prostate cancer, and may play a role in the progression of these diseases. Overall, MDH is an important enzyme in cellular metabolism and its dysfunction can have significant implications for human health.
Isocitrate dehydrogenase (IDH) is an enzyme that plays a critical role in the citric acid cycle, also known as the Krebs cycle or tricarboxylic acid cycle. It catalyzes the conversion of isocitrate to alpha-ketoglutarate (α-KG) in the presence of NAD+ as a cofactor. This reaction is an important step in the production of energy in the form of ATP through cellular respiration. In the medical field, IDH is of particular interest because mutations in the IDH1 and IDH2 genes have been implicated in the development of certain types of cancer, including gliomas, acute myeloid leukemia, and chondrosarcoma. These mutations result in the production of an abnormal form of the enzyme that has altered activity and can lead to the accumulation of alpha-ketoglutarate, which can promote tumor growth and progression. As a result, IDH mutations are now considered important biomarkers for the diagnosis and prognosis of certain types of cancer, and targeted therapies that inhibit the activity of mutant IDH enzymes are being developed for their treatment.
Phosphoadenosine phosphosulfate (PAPS) is a molecule that plays a crucial role in the metabolism of sulfur-containing amino acids and other sulfur-containing compounds in the body. It is synthesized from adenosine triphosphate (ATP) and sulfate, and is involved in the formation of various sulfur-containing molecules, such as glutathione, coenzyme A, and sulfated glycosaminoglycans. In the medical field, PAPS is often studied in the context of various diseases and disorders, including cystic fibrosis, where it is involved in the metabolism of the amino acid cysteine. PAPS is also involved in the metabolism of drugs and xenobiotics, and its levels can be used as a biomarker for certain diseases, such as liver disease and cancer. Additionally, PAPS is a target for the development of new drugs for the treatment of various diseases, including cancer and inflammatory disorders.
Arylsulfotransferase (AST) is an enzyme that plays a role in the metabolism of various substances in the body, including drugs, hormones, and toxins. It catalyzes the transfer of a sulfate group from adenosine 5'-phosphosulfate (APS) to an aromatic compound, such as a phenol or a benzene ring. This reaction is an important step in the detoxification of many substances that are harmful to the body. In the medical field, AST is often measured in blood tests as a marker of liver function. High levels of AST in the blood can indicate liver damage or disease, such as hepatitis or cirrhosis. AST is also used as a diagnostic tool in the evaluation of certain types of cancer, such as liver cancer and colon cancer. Additionally, AST is an important enzyme in the synthesis of some drugs, and its activity is often monitored in the development and testing of new medications.
Ketosteroids are a group of hormones produced by the adrenal glands, which are located on top of the kidneys. They are also known as glucocorticoids because they help regulate glucose metabolism in the body. The most well-known ketosteroid is cortisol, which plays a crucial role in the body's response to stress, regulates metabolism, and helps maintain blood pressure and blood sugar levels. Other ketosteroids include corticosterone, cortisone, and aldosterone. In the medical field, ketosteroids are often prescribed to treat a variety of conditions, including: 1. Inflammation: Corticosteroids are effective at reducing inflammation and swelling in the body, making them useful for treating conditions such as asthma, allergies, and rheumatoid arthritis. 2. Autoimmune disorders: Corticosteroids can help suppress the immune system, making them useful for treating conditions such as lupus and multiple sclerosis. 3. Skin conditions: Corticosteroids are often used to treat skin conditions such as eczema, psoriasis, and acne. 4. Cancer: Corticosteroids can help reduce the side effects of cancer treatments such as chemotherapy and radiation therapy. However, long-term use of corticosteroids can have side effects, including weight gain, high blood pressure, and osteoporosis. Therefore, they are typically prescribed for short-term use only and in carefully monitored doses.
NADP stands for Nicotinamide Adenine Dinucleotide Phosphate. It is a coenzyme that plays a crucial role in various metabolic processes in the body, including the metabolism of carbohydrates, fats, and proteins. NADP is involved in the conversion of glucose to glycogen, the breakdown of fatty acids, and the synthesis of amino acids. It is also involved in the process of photosynthesis in plants, where it acts as a carrier of electrons. In the medical field, NADP is often used as a supplement to support various metabolic processes and to enhance energy production in the body.
Dihydrolipoamide dehydrogenase (DLD) is an enzyme that plays a crucial role in the metabolism of carbohydrates and fatty acids in the body. It is also known as E3 of the pyruvate dehydrogenase complex (PDC) or dihydrolipoyl transacetylase. The PDC is a multi-enzyme complex that converts pyruvate, a product of glycolysis, into acetyl-CoA, which can then enter the citric acid cycle for further metabolism. DLD is the third enzyme in the PDC complex and is responsible for transferring electrons from dihydrolipoamide to ubiquinone, an electron carrier molecule that shuttles electrons to the electron transport chain for ATP production. DLD deficiency is a rare genetic disorder that can cause a range of symptoms, including muscle weakness, developmental delays, and neurological problems. It is caused by mutations in the DLD gene, which leads to a deficiency in the enzyme's activity. Treatment for DLD deficiency typically involves dietary modifications and supplements to support energy metabolism, as well as medications to manage symptoms.
Carbohydrate dehydrogenases are a group of enzymes that catalyze the oxidation of carbohydrates, such as glucose, fructose, and galactose, to produce aldehydes or ketones. These enzymes play important roles in various metabolic pathways, including glycolysis, the citric acid cycle, and the pentose phosphate pathway. There are several types of carbohydrate dehydrogenases, including glucose dehydrogenase, lactate dehydrogenase, and alcohol dehydrogenase. These enzymes are found in a variety of tissues, including the liver, muscle, and brain, and are involved in a range of physiological processes, such as energy metabolism, detoxification, and the synthesis of important molecules like nucleotides and amino acids. In the medical field, carbohydrate dehydrogenases are often used as diagnostic markers for various diseases and conditions. For example, elevated levels of lactate dehydrogenase in the blood can be an indicator of liver or muscle damage, while elevated levels of glucose dehydrogenase can be a sign of certain types of cancer or genetic disorders. Additionally, some carbohydrate dehydrogenases are used as targets for the development of new drugs and therapies.
Succinate dehydrogenase (SDH) is an enzyme that plays a crucial role in the citric acid cycle, also known as the Krebs cycle or tricarboxylic acid cycle. It is a complex enzyme that is composed of four protein subunits and one iron-sulfur flavoprotein subunit. In the citric acid cycle, SDH catalyzes the oxidation of succinate to fumarate, which is a key step in the production of energy in the form of ATP. This reaction also generates electrons that are used to reduce coenzyme Q, which is an electron carrier that is involved in the electron transport chain. SDH is found in the mitochondria of cells and is essential for the production of energy in the body. Mutations in the genes that encode the SDH subunits can lead to a group of rare inherited disorders known as succinate dehydrogenase deficiency (SDHD, SDHAF1, SDHB, SDHC, and SDHD2). These disorders can cause a range of symptoms, including muscle weakness, developmental delays, and neurological problems.
L-iditol 2-dehydrogenase is an enzyme that plays a role in the metabolism of L-iditol, a sugar alcohol that is found in some fruits and vegetables. This enzyme catalyzes the conversion of L-iditol to L-idonic acid, which is an intermediate in the metabolism of certain amino acids. L-iditol 2-dehydrogenase is found in a variety of organisms, including bacteria, fungi, and plants. In the medical field, this enzyme has been studied in relation to its potential role in the treatment of certain diseases, such as diabetes and obesity.
Dehydroepiandrosterone (DHEA) is a hormone produced by the adrenal glands, which are located on top of the kidneys. It is a precursor to other hormones, including testosterone and estrogen, and plays a role in a variety of bodily functions. In the medical field, DHEA is often measured in blood or saliva tests to assess adrenal function and diagnose conditions such as adrenal insufficiency or Cushing's syndrome. It is also sometimes used as a supplement to treat conditions such as low testosterone levels, osteoporosis, and depression, although the evidence for its effectiveness is mixed and more research is needed. However, it is important to note that DHEA supplements can have potential side effects and may interact with other medications, so they should only be used under the guidance of a healthcare professional.
Glycerolphosphate dehydrogenase (GPDH) is an enzyme that plays a role in the metabolism of glycerol-3-phosphate, a molecule involved in the breakdown of fats. In the medical field, GPDH is often studied in the context of diseases such as diabetes, where abnormal metabolism of fats can lead to complications such as cardiovascular disease. GPDH is also involved in the production of NADPH, a molecule that plays a role in the detoxification of harmful substances in the body. In addition, GPDH has been proposed as a potential target for the development of new drugs for the treatment of various diseases, including cancer and neurodegenerative disorders.
Glucose 1-dehydrogenase (G1DH) is an enzyme that plays a role in the metabolism of glucose in the body. It is involved in the conversion of glucose to glucose-6-phosphate, which is an important step in the process of glycolysis, the breakdown of glucose to produce energy. G1DH is found in a variety of tissues in the body, including the liver, muscle, and pancreas. In the liver, G1DH is involved in the production of glucose from non-carbohydrate sources, such as amino acids and fatty acids. In the pancreas, G1DH is involved in the regulation of blood glucose levels by converting glucose to glucose-6-phosphate, which can then be stored as glycogen or used for energy. G1DH is also involved in the metabolism of other sugars, such as galactose and fructose.
The Ketoglutarate Dehydrogenase Complex (KGDHC) is an enzyme complex that plays a crucial role in the citric acid cycle, also known as the Krebs cycle or TCA cycle. It is responsible for the oxidation of alpha-ketoglutarate, a molecule produced during the breakdown of amino acids, to succinyl-CoA, a molecule that enters the citric acid cycle. The KGDHC is a large multi-subunit enzyme complex that contains three different subunits: E1, E2, and E3. The E1 subunit catalyzes the oxidation of alpha-ketoglutarate to succinyl-CoA, while the E2 subunit catalyzes the transfer of electrons from the alpha-ketoglutarate to the E3 subunit. The E3 subunit then transfers the electrons to the electron transport chain, which generates ATP, the energy currency of the cell. The KGDHC is an important enzyme complex in the citric acid cycle because it is the first step in the cycle that requires oxygen. It is also a key enzyme in the metabolism of amino acids, as it is involved in the breakdown of glutamate, a major amino acid in the body. Disruptions in the function of the KGDHC can lead to a variety of metabolic disorders, including Leigh syndrome, a rare genetic disorder that affects the brain and muscles.
Aldehyde oxidoreductases (ALDHs) are a group of enzymes that play a crucial role in the metabolism of aldehydes, which are toxic compounds that can be produced during normal cellular metabolism or as a result of environmental exposure. ALDHs are found in many tissues throughout the body, including the liver, lungs, and kidneys, and they help to detoxify aldehydes by converting them into less toxic compounds. There are several different types of ALDHs, each with its own specific substrate and activity. Some ALDHs are involved in the metabolism of ethanol, while others are involved in the metabolism of other aldehydes, such as acetaldehyde, formaldehyde, and acrolein. ALDHs are also involved in the metabolism of certain drugs and toxins, and they have been implicated in the development of certain diseases, such as cancer and neurodegenerative disorders. In the medical field, ALDHs are often studied as potential targets for the development of new drugs and therapies. For example, drugs that inhibit ALDH activity have been shown to be effective in the treatment of certain types of cancer, and ALDHs are also being studied as potential biomarkers for the early detection of certain diseases. Additionally, ALDHs are being investigated as potential targets for the development of new therapies for the treatment of alcoholism and other addictions.
11β-Hydroxysteroid dehydrogenase type 1
Corticosteroid 11-beta-dehydrogenase isozyme 2
Cortisone reductase deficiency
17β-Hydroxysteroid dehydrogenase III deficiency
List of diseases (0-9)
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Transcriptional influence of two poly purine-pyrimidine tracts located in the HSD11B2 (11beta-hydroxysteroid dehydrogenase type...
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- 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)
- 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)
- To ensure that every time you get a surge of cortisol you don't get a mineralocorticoid response God (you can substitute evolution if it makes you happier) created 11-beta-hydroxysteroid dehydrogenase. (medicine-opera.com)
- 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) is a key enzyme that transform cortisone to cortisol, which activates the endogenous glucocorticoid function. (ijbs.com)
- The unhindered development of the fetal HPA axis is dependent on the function and activity of 11β-hydroxysteroiddehydrogenase type 2 (11β-HSD2), a transplacental cortisol barrier. (mcmaster.ca)
- Decreased 11β-HSD2 levels in term born females may lead to an increased placental transfer of maternal cortisol and therefore result in a reduced head circumference and a higher risk for altered stress response in adulthood. (mcmaster.ca)
- 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)
- RESULTS: In term born females, BET administration was associated with reduced head circumference and decreased 11β-HSD2 protein levels and enzyme activity. (mcmaster.ca)
- 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)
- Down-Regulation of the Mineralocorticoid Receptor (MR) and Up-Regulation of Hydroxysteroid 11-Beta Dehydrogenase Type 2 (HSD11B2) Isoenzyme in Critically Ill Patients. (bvsalud.org)
- Association studies between the HSD11B2 gene (encoding human 11beta-hydroxysteroid dehydrogenase type 2), type 1 diabetes mellitus and diabetic nephropathy. (cdc.gov)
Observed increased 111
- In this study, we observed increased 11β-HSD1 expression in osteoclasts within an osteoporotic mice model (ovariectomized mice). (ijbs.com)
- The invention relates to "compounds, compositions, and methods for the study, diagnosis, and treatment of traits, diseases and conditions that respond to the modulation of 11 beta-hydroxysteroid dehydrogenase-1 gene expression and/or activity," the patent application's abstract states. (genomeweb.com)
- The invention "is also directed to compounds, compositions, and methods relating to traits, diseases and conditions that respond to the modulation of expression and/or activity of genes involved in 11 beta-hydroxysteroid dehydrogenase-1 gene expression pathways or other cellular processes that mediate the maintenance or development of such traits, diseases, and conditions. (genomeweb.com)
- Specifically, the invention relates to double stranded nucleic acid molecules … capable of mediating RNA interference against 11 beta-hydroxysteroid dehydrogenase-1 gene expression, including cocktails of such small nucleic acid molecules and lipid nanoparticle (LNP) formulations of such small nucleic acid molecules. (genomeweb.com)
- Association between a variant in the 11 beta-hydroxysteroid dehydrogenase type 2 gene and primary hypertension. (cdc.gov)
- hydroxysteroid dehydrogenase type 2 deficiency. (cdc.gov)
- Hydroxysteroid 11-beta dehydrogenase (HSD11B) isoenzymes regulate which ligand will bind to MR. In this study we aimed to evaluate the expression of the MR and the HSD11B isozymes in peripheral polymorphonuclear cells (PMNs) in critical illness for a 13-day period. (bvsalud.org)
- 11β-HSD1 has been observed to regulate skeletal metabolism, specifically within osteoblasts. (ijbs.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)
- Placental 11β-hydroxysteroiddehydrogenase type 1 (11β-HSD1) protein levels and 11β-HSD2 protein and activity levels were determined. (mcmaster.ca)
- 11ß-Hydroxysteroid dehydrogenase type 2 in hypertension: comparison of phenotype and genotype analysis. (cdc.gov)
- Precise diagnosis of C. innocuum is necessary because of its unique intrinsic resistance to vancomycin, presumably caused by the presence of 2 chromosomal genes that enable the synthesis of a peptidoglycan precursor terminating in serine with low vancomycin affinity ( 9 , 11 ). (cdc.gov)
- Licorice constituents reduce or reverse drug resistance in MRSA when combined with beta-lactam antibiotics. (interactionsguide.com)
- Clinical, genetic, and structural basis of apparent mineralocorticoid excess due to 11? (cdc.gov)
- 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)
- Furthermore, specifically knock out 11β-HSD1 in osteoclasts, by crossing cathepsin-cre mice with 11β-HSD1 flox/flox mice, presented significant protecting effect of skeleton when they underwent ovariectomy surgery. (ijbs.com)
- 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)
- However, the function of 11β-HSD1 in osteoclasts has not been elucidated. (ijbs.com)
- 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)
- Since biology operates under the rule that anything that can go wrong will go wrong, patients have been described with a genetic defect in 11-beta-hydroxysteroid dehydrogenase. (medicine-opera.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)
- In vitro experiments showed the endogenous high expression of 11β-HSD1 lead to osteoclast formation and maturation. (ijbs.com)
- Glucocorticoids are actively generated within osteoblasts by the 11beta-HSD1 enzyme and this generation increases with proinflammatory cytokines, glucocorticoids, and probably with age. (nih.gov)
- Rhythm of Fetoplacental 11β-Hydroxysteroid Dehydrogenase Type 2 - Fetal Protection From Morning Maternal Glucocorticoids. (nih.gov)
- 2. Glucocorticoids and 11beta-hydroxysteroid dehydrogenase type 1 in obesity and the metabolic syndrome. (nih.gov)
- 6. Glucocorticoids and 11beta-hydroxysteroid dehydrogenase in adipose tissue. (nih.gov)
- 7. Extra-adrenal regeneration of glucocorticoids by 11beta-hydroxysteroid dehydrogenase type 1: physiological regulator and pharmacological target for energy partitioning. (nih.gov)
- Glucocorticoids inhibit interconversion of 7-hydroxy and 7-oxo metabolites of dehydroepiandrosterone: a role for 11β-hydroxysteroid dehydrogenases? (scholaris.sk)
- This review summarises the data relating to 11beta-HSD expression and activity in human bone and describes how this has implications for age-related, inflammation-associated, and glucocorticoid-induced osteoporosis. (nih.gov)
- Osteoblastic 11beta-hydroxysteroid dehydrogenase type 1 activity increases with age and glucocorticoid exposure. (nih.gov)
- Modulation of 11beta-hydroxysteroid dehydrogenase isozymes by proinflammatory cytokines in osteoblasts: an autocrine switch from glucocorticoid inactivation to activation. (nih.gov)
- The enzyme 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) catalyzes the conversion of the hormonally inactive cortisone to active cortisol, thus facilitating glucocorticoid receptor activation in target tissues. (nih.gov)
- 2] The type 1 form of familial primary aldosteronism is due to an aberrantly formed chimeric gene product that combines the glucocorticoid-responsive (inhibitable) promoter of the 11beta-hydroxylase gene (CYP11B1) with the coding region of the aldosterone synthetase gene (CYP11B2). (medscape.com)
- 3. Tissue-specific glucocorticoid reactivating enzyme, 11 beta-hydroxysteroid dehydrogenase type 1 (11 beta-HSD1)--a promising drug target for the treatment of metabolic syndrome. (nih.gov)
- Mice lacking the intracellular glucocorticoid-amplifying enzyme 11β-hydroxysteroid dehydrogenase type 1 (11βHSD1(-/-)) have "healthier" adipose tissue distribution and resist metabolic disease with diet-induced obesity. (ox.ac.uk)
- Elevated pancreatic islet activity of the intracellular glucocorticoid amplifying enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) was hypothesized to drive this process in genetically obese rodents. (endocrine-abstracts.org)
- 11β-Hydroxysteroid dehydrogenase type 1 (11β-HSD1) is a key modulator of glucocorticoid effect within target tissues and high adipose or liver levels of this enzyme may contribute to obesity and/or metabolic disease. (endocrine-abstracts.org)
- There are at least two isozymes of the corticosteroid 11-beta-dehydrogenase, a microsomal enzyme complex responsible for the interconversion of cortisol and cortisone. (nih.gov)
- Increased expression of 11beta-HSD1 in adipose tissue has been associated with obesity and insulin resistance. (nih.gov)
- Moreover, augmented 11βHSD1(-/-) adipose tissue angiogenesis is associated with enhanced peroxisome proliferator-activated receptor γ (PPARγ)-inducible expression of the potent angiogenic factors VEGF-A, apelin, and angiopoietin-like protein 4. (ox.ac.uk)
- The type II isozyme, encoded by this gene, has only 11-beta-dehydrogenase activity. (nih.gov)
- In this study, we investigated the association of two 11beta-HSD1 gene (HSD11B1) polymorphisms with the metabolic syndrome (MetS) and its characteristics in the Bosnian population. (nih.gov)
- A new compound heterozygous mutation in the 11 beta-hydroxysteroid dehydrogenase type 2 gene in a case of apparent mineralocorticoid excess. (expasy.org)
- Transcriptional regulation of type 11 17β-hydroxysteroid dehydrogenase expression in prostate cancer cells. (nih.gov)
- 17beta-hydroxysteroid dehydrogenase type 11 (Pan1b) expression in human prostate cancer. (nih.gov)
- Identification and characterization of the ER/lipid droplet-targeting sequence in 17beta-hydroxysteroid dehydrogenase type 11. (nih.gov)
- 1. 11beta-hydroxysteroid dehydrogenase type 1 and obesity. (nih.gov)
- 5. 11β-Hydroxysteroid dehydrogenase type 1: relevance of its modulation in the pathophysiology of obesity, the metabolic syndrome and type 2 diabetes mellitus. (nih.gov)
- 9. Anti-diabetic and anti-adipogenic effects of a novel selective 11β-hydroxysteroid dehydrogenase type 1 inhibitor in the diet-induced obese mice. (nih.gov)
- 10. Inhibition of 11beta-hydroxysteroid dehydrogenase type 1 as a promising therapeutic target. (nih.gov)
- 11. Obesity and corticosteroids: 11beta-hydroxysteroid type 1 as a cause and therapeutic target in metabolic disease. (nih.gov)
- 13. Is 11beta-hydroxysteroid dehydrogenase type 1 a therapeutic target? (nih.gov)
- 14. Inhibitors of 11β-hydroxysteroid dehydrogenase type 1 in antidiabetic therapy. (nih.gov)
- 15. 11Beta-hydroxysteroid dehydrogenase type 1 in human disease: a novel therapeutic target. (nih.gov)
- 16. Dietary manipulation reveals an unexpected inverse relationship between fat mass and adipose 11β-hydroxysteroid dehydrogenase type 1. (nih.gov)
- 17. Liver-selective transgene rescue of hypothalamic-pituitary-adrenal axis dysfunction in 11beta-hydroxysteroid dehydrogenase type 1-deficient mice. (nih.gov)
- 19. 11Beta-hydroxysteroid dehydrogenase type 1 and its role in the hypothalamus-pituitary-adrenal axis, metabolic syndrome, and inflammation. (nih.gov)
- 20. The role and regulation of 11β-hydroxysteroid dehydrogenase type 1 in obesity and the metabolic syndrome. (nih.gov)
- 11β-Hydroxysteroid dehydrogenase type 1 within muscle protects against the adverse effects of local inflammation. (ox.ac.uk)
- Increased angiogenesis protects against adipose hypoxia and fibrosis in metabolic disease-resistant 11β-hydroxysteroid dehydrogenase type 1 (HSD1)-deficient mice. (ox.ac.uk)
- To determine the direct effects of elevated 11β-HSD1 on β-cell function in diabetes in vivo we created a transgenic model overexpressing 11β-HSD1. (endocrine-abstracts.org)
- 18. 11β-HSD1 contributes to age-related metabolic decline in male mice. (nih.gov)
- 4. 11-Dehydrocorticosterone causes metabolic syndrome, which is prevented when 11β-HSD1 is knocked out in livers of male mice. (nih.gov)
- Here we show that adipose tissues of 11βHSD1(-/-) mice exhibit attenuated hypoxia, induction of hypoxia-inducible factor (HIF-1α) activation of the TGF-β/Smad3/α-smooth muscle actin (α-SMA) signaling pathway, and fibrogenesis despite similar fat accretion with diet-induced obesity. (ox.ac.uk)
- Scintigram obtained by using iodine-131-beta-iodomethyl-norcholesterol (NP-59) in a 59-year-old man with hypertension shows fairly intense radionuclide uptake in the right adrenal tumor. (medscape.com)
- This appears to be the case in bone where the 11beta-hydroxysteroid dehydrogenase (11beta-HSD) enzymes are expressed. (nih.gov)
- Genetic expression differences of 11 beta-hydroxysteroid dehydrogenase in the bone microvascular endothelial cells derived from different regions of the human femoral head]. (nih.gov)
- Liver mRNA level for hydroxysteroid 11-beta dehydrogenase 1 (Hsd11b1), which exhibit age-dependent increases and promote insulin secretion, was also markedly increased. (elsevierpure.com)
- Estrogen signaling in mammalian cells is primarily mediated at the molecular level by two members of the nuclear receptor superfamily-estrogen receptors alpha (ER-α) and beta (ER-β). (nih.gov)
- Mutants of 11beta-hydroxysteroid dehydrogenase (11-HSD2) with partial activity: improved correlations between genotype and biochemical phenotype in apparent mineralocorticoid excess. (expasy.org)
- Human dehydrogenase/reductase (SDR family) member 8 (DHRS8): a description and evaluation of its biochemical properties. (nih.gov)
- 11 (high probability of substitution). (expasy.org)