デヒドロエピアンドロステロン dehydroepiandrosterone
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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2013/08/06 21:40:19」(JST)
wiki ja
| IUPAC命名法による物質名 | |
|---|---|
| 3-hydroxy-10,13-dimethyl -1,2,3,4,7,8,9,11,12,14,15,16 |
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| 臨床データ | |
| 胎児危険度分類 | ? |
| 法的規制 | 商業利用可能 (US), Rx Only (CA) |
| 投与方法 | 経口 |
| 薬物動態的データ | |
| 代謝 | 肝臓 |
| 半減期 | 12 時間 |
| 排泄 | 尿:?% |
| 識別 | |
| CAS登録番号 | 53-43-0 |
| ATCコード | A14AA07 |
| PubChem | CID 76 |
| 化学的データ | |
| 化学式 | C19H28O2 |
| 分子量 | 288.43 |
| 物理的データ | |
| 融点 | 148.5 °C (299 °F) |
デヒドロエピアンドロステロン（Dehydroepiandrosterone、略称 DHEA）とは、副腎や性腺で産生される男性ホルモンの一種である。 アンドロゲン（男性ホルモン）活性としてはテストステロンの約5%である。 成人女性においては、アンドロステンジオンとともに主要なアンドロゲンとして重要である。
昭和の時代、前立腺癌増殖は男性ホルモンの中で最も生理活性が高いテストステロンによって促進されると考えられていた。1993年頃になると前立腺細胞内においては、男性ホルモンの15％程度が DHEA と言われていたが、前立腺癌診療ガイドライン（2006年版、日本泌尿器科学会編）にはその40％を占めると述べられている。泌尿器科医師による前立腺癌の存在を否定されていない壮年男子が DHEAサプリメントを服用した場合、もし前立腺癌が存在すれば増殖を促進させてしまうことが危惧されている。
DHEAはテストステロンやエストラジオールと同様に性ステロイドホルモンであり、生体内でコレステロールを原料として生合成される。
作用[編集]
DHEAを経口投与などで増加させることにより、老化プロセスを遅らせたり止めたり、あるいは若返らせる「若返りホルモン」としてサプリメントが輸入代行されている。ほかに以下の症状に効果があるとされている。
- 循環器病
- 糖尿病
- 高コレステロール症
- 肥満
- 合併性硬化症
- パーキンソン病
- アルツハイマー症
- 免疫不全症
- うつ病
- 骨粗鬆症
関連項目[編集]
- 副腎皮質ホルモン
外部リンク[編集]
- デヒドロエピアンドロステロン、プラステロン - 「健康食品」の安全性・有効性情報 （国立健康・栄養研究所）
- N Engl J Med, 355: 1647-59, 2006
- Aging and Fountain-of-Youth Hormones
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| この項目は、医学に関連した書きかけの項目です。この項目を加筆・訂正などしてくださる協力者を求めています（プロジェクト:医学／Portal:医学と医療）。 |
wiki en
| Systematic (IUPAC) name | |
|---|---|
| (3S,8R,9S,10R,13S,14S)-3-hydroxy-10,13-dimethyl-1,2,3,4,7,8,9,11,12,14,15,16-dodecahydrocyclopenta[a]phenanthren-17-one | |
| Clinical data | |
| Pregnancy cat. | ? |
| Legal status | Prescription Only (S4) (AU) Rx Only (CA) OTC (US) |
| Routes | Oral |
| Pharmacokinetic data | |
| Metabolism | Hepatic |
| Half-life | 12 hours |
| Excretion | Urinary:?% |
| Identifiers | |
| CAS number | 53-43-0 Y |
| ATC code | A14AA07 G03EA03 (combination with estrogen) |
| PubChem | CID 5881 |
| IUPHAR ligand | 2370 |
| DrugBank | DB01708 |
| ChemSpider | 5670 Y |
| UNII | 459AG36T1B Y |
| ChEBI | CHEBI:28689 Y |
| ChEMBL | CHEMBL90593 Y |
| Synonyms | (3β)-3-Hydroxyandrost-5-en-17-one |
| Chemical data | |
| Formula | C19H28O2 |
| Mol. mass | 288.424 g/mol |
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InChI
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| Physical data | |
| Melt. point | 148.5 °C (299 °F) |
| Y (what is this?) (verify) |
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Dehydroepiandrosterone (DHEA; brand name Fidelin, Ovomax), also known as androstenolone or prasterone (INN), as well as 3β-hydroxyandrost-5-en-17-one or 5-androsten-3β-ol-17-one, is an important endogenous steroid hormone.[1] It is the most abundant circulating steroid in humans,[2] in whom it is produced in the adrenal glands,[3] the gonads, and the brain,[4] where it functions predominantly as a metabolic intermediate in the biosynthesis of the androgen and estrogen sex steroids.[1][5] However, DHEA also has a variety of potential biological effects in its own right, binding to an array of nuclear and cell surface receptors,[6] and acting as a neurosteroid.[7]
Contents
- 1 Effects and uses
- 1.1 Strength
- 1.2 Memory
- 1.3 Female reproductive health
- 1.4 Cardiovascular disease and risk of death
- 1.5 Lupus
- 2 Safety
- 3 Dehydroepiandrosterone sulfate
- 4 Production
- 5 Mechanism of action
- 6 Measurement
- 7 Increasing endogenous production
- 8 Isomers
- 9 Society and culture
- 9.1 Legality
- 9.1.1 United States
- 9.1.2 Canada
- 9.1.3 Australia
- 9.1.4 Sports and athletics
- 9.2 Marketing
- 9.1 Legality
- 10 Research
- 10.1 Cancer
- 11 References
- 12 External links
Effects and uses[edit source | edit]
In women with adrenal insufficiency and the healthy elderly there is insufficient evidence to support the use of DHEA.[8][9]
Strength[edit source | edit]
Evidence is inconclusive in regards to the effect of DHEA on strength in the elderly.[10]
In middle-aged men, no statistically significant effect of DHEA supplementation on lean body mass, strength, or testosterone levels was found in a randomized placebo-controlled trial.[11] However, there is new evidence DHEA increases free testosterone levels.[12]
In postmenopausal women, within a randomized placebo-controlled trial, no statistically significant effect of DHEA supplementation on muscle strength during a 12 week combined endurance and weight training program.[13][14]
Memory[edit source | edit]
DHEA supplementation has not been found to be useful for memory function in normal middle aged or older adults.[15] It has been studied as a treatment for Alzheimer's disease, but there is no evidence that it is effective.[16]
Female reproductive health[edit source | edit]
Since 2000, DHEA supplementation has been used in reproductive medicine in combination with gonadotropins as a way to treat female infertility.[17]
Cardiovascular disease and risk of death[edit source | edit]
A review in 2003 found the then-extant evidence sufficient to suggest that low serum levels of DHEAS may be associated with coronary heart disease in men, but insufficient to determine whether DHEA supplementation would have any cardiovascular benefit.[18]
A 1986 study found that a higher level of endogenous DHEA, as determined by a single measurement, correlated with a lower risk of death or cardiovascular disease.[19] However, a 2006 study found no correlation between DHEA levels and risk of cardiovascular disease or death in men.[20] A 2007 study found that DHEA restored oxidative balance in diabetic patients, reducing tissue levels of pentosidine—a biomarker for advanced glycation endproducts.[21]
Lupus[edit source | edit]
There is some evidence of short term benefit in those with systemic lupus erythematosus but little evidence of long term benefit or safety.[22]
Safety[edit source | edit]
DHEA is produced naturally in the human body, but the long term effects of its use are largely unknown.[23][24] In the short term, several studies have noted few adverse effects. In a study by Chang et al., DHEA was administered at a dose of 200 mg/day for 24 weeks with slight androgenic effects noted.[25] Another study utilized a dose up to 400 mg/day for 8 weeks with few adverse events reported.[26] A longer term study followed patients dosed with 50 mg of DHEA for 12 months with the number and severity of side effects reported to be small.[27] Another study delivered a dose of 50 mg of DHEA for 10 months with no serious adverse events reported.[28]
As a hormone precursor, there has been a smattering of reports of side effects possibly caused by the hormone metabolites of DHEA.[24][29]
It is not known whether DHEA is safe for long-term use. Some researchers believe DHEA supplements might actually raise the risk of breast cancer, prostate cancer, heart disease, diabetes,[24] and stroke. DHEA may stimulate tumor growth in types of cancer that are sensitive to hormones, such as some types of breast, uterine, and prostate cancer.[24] DHEA may increase prostate swelling in men with benign prostatic hyperplasia (BPH), an enlarged prostate gland.[23]
DHEA is a steroid hormone. High doses may cause aggressiveness, irritability, trouble sleeping, and the growth of body or facial hair on women.[23] It also may stop menstruation and lower the levels of HDL ("good" cholesterol), which could raise the risk of heart disease.[23] Other reported side effects include acne, heart rhythm problems, liver problems, hair loss (from the scalp), and oily skin. It may also alter the body's regulation of blood sugar.[23]
DHEA should not be used with tamoxifen, as it may promote tamoxifen resistance.[23] Patients on hormone replacement therapy may have more estrogen-related side effects when taking DHEA. This supplement may also interfere with other medicines, and potential interactions between it and drugs and herbs should be considered. Always tell your doctor and pharmacist about any supplements and herbs you are taking.[23]
DHEA is possibly unsafe for individuals experiencing the following conditions: pregnancy and breast-feeding, hormone sensitive conditions, liver problems, diabetes, depression or mood disorders, polycystic ovarian syndrome (PCOS), or cholesterol problems.[30] Individuals experiencing any of these conditions should consult with a doctor before taking.
Dehydroepiandrosterone sulfate[edit source | edit]
Main article: Dehydroepiandrosterone sulfate
Dehydroepiandrosterone sulfate (DHEAS) is the sulfate ester of DHEA. This conversion is reversibly catalyzed by sulfotransferase (SULT2A1) primarily in the adrenals, the liver, and small intestine. In the blood, most DHEA is found as DHEAS with levels that are about 300 times higher than those of free DHEA. Orally ingested DHEA is converted to its sulfate when passing through intestines and liver. Whereas DHEA levels naturally reach their peak in the early morning hours, DHEAS levels show no diurnal variation. From a practical point of view, measurement of DHEAS is preferable to DHEA, as levels are more stable.[citation needed]
Production[edit source | edit]
Comprehensive overview of steroidogenesis, showing DHEA at left among the androgens.
DHEA is produced from cholesterol through two cytochrome P450 enzymes. Cholesterol is converted to pregnenolone by the enzyme P450 scc (side chain cleavage); then another enzyme, CYP17A1, converts pregnenolone to 17α-hydroxypregnenolone and then to DHEA.[31]
Mechanism of action[edit source | edit]
Although it predominantly functions as an endogenous precursor to more potent androgens such as testosterone and DHT, DHEA has been found to possess some degree of androgenic activity in its own right, acting as a low affinity (Ki = 1 μM), weak partial agonist of the androgen receptor. However, its intrinsic activity at the receptor is almost completely negligible, and on account of that, due to competition for binding with full agonists like testosterone, it actually behaves much more like an antagonist there, and hence, like an antiandrogen. However, its affinity for the receptor is very low, and for that reason, is unlikely to be of any significance under normal circumstances.[32][33]
In addition to its affinity for the androgen receptor, DHEA has also been found to bind to and activate the ERα and ERβ estrogen receptors with Ki values of 1.1 μM and 0.5 μM, respectively, and EC50 values of >1 μM and 200 nM, respectively. Though it was found to be a partial agonist of the ERα with a maximal efficacy of 30-70%, the concentrations required for this degree of activation make it unlikely that the activity of DHEA at this receptor is physiologically meaningful. Remarkably however, DHEA acts as a full agonist of the ERβ with a maximal response similar to or actually slightly greater than that of estradiol, and its levels in circulation and local tissues in the human body are high enough to activate the receptor to the same degree as that seen with circulating estradiol levels at somewhat higher than their maximal, non-ovulatory concentrations; indeed, when combined with estradiol with both at levels equivalent to those of their physiological concentrations, overall activation of the ERβ was doubled. As such, it has been proposed that DHEA may be an important and potentially major endogenous estrogen in the body.[6][32]
Unlike the case of the androgen and estrogen receptors, DHEA does not bind to or activate the progesterone, glucocorticoid, or mineralocorticoid receptors.[32][34]
Other nuclear receptor targets of DHEA include the PPARα, PXR, and CAR. In addition, it has been found to directly act on several membrane receptors, including the NMDA receptor as a positive allosteric modulator, the GABAA receptor as a negative allosteric modulator, and the σ1 receptor as an agonist. It is these actions that have conferred the label of a "neurosteroid" upon DHEA. Finally, DHEA is thought to regulate a handful of other proteins via indirect, genomic mechanisms, including the enzymes P4502C11 and 11β-HSD1—the latter of which is essential for the biosynthesis of the glucocorticoids such as cortisol and has been suggested to be involved in the antiglucocorticoid effects of DHEA—and the carrier IGFBP1.[32][35]
Measurement[edit source | edit]
As almost all DHEA is derived from the adrenal glands, blood measurements of DHEAS/DHEA are useful to detect excess adrenal activity as seen in adrenal cancer or hyperplasia, including certain forms of congenital adrenal hyperplasia. Women with polycystic ovary syndrome tend to have elevated levels of DHEAS.[36]
Increasing endogenous production[edit source | edit]
Regular exercise is known to increase DHEA production in the body.[37][38] Calorie restriction has also been shown to increase DHEA in primates.[39] Some theorize that the increase in endogenous DHEA brought about by calorie restriction is partially responsible for the longer life expectancy known to be associated with calorie restriction.[40]
Isomers[edit source | edit]
The term "dehydroepiandrosterone" is ambiguous chemically because it does not include the specific positions within epiandrosterone at which hydrogen atoms are missing. DHEA has a number of naturally occurring isomers that may have similar pharmacological effects. Some isomers of DHEA are 1-dehydroepiandrosterone and 4-dehydroepiandrosterone. These isomers are also technically DHEA, since they are dehydroepiandrosterones in which hydrogens are removed from the epiandrosterone skeleton.
Society and culture[edit source | edit]
Legality[edit source | edit]
United States[edit source | edit]
DHEA is legal to sell in the United States as a dietary supplement. It is currently grandfathered in as an "Old Dietary Ingredient" being on sale prior to 1994. DHEA is specifically exempted from the Anabolic Steroid Control Act of 1990 and 2004[41] It is banned from use in athletic competition.
Canada[edit source | edit]
In Canada, a prescription is required to buy DHEA.[42]Template:Coglin
Australia[edit source | edit]
In Australia, a prescription is required to buy DHEA, where it is also comparatively expensive compared to off-the-shelf purchases in US supplement shops. Australian customs classify DHEA as an "anabolic steroid[s] or precursor[s]" and, as such, it is only possible to carry DHEA into the country through customs if one possesses an import permit (which may be obtained if one has a valid prescription for the hormone). For details on its current import status, consult the Australia government's Therapeutic Goods Administration site[43]
Sports and athletics[edit source | edit]
DHEA is a prohibited substance under the World Anti-Doping Code of the World Anti-Doping Agency,[44] which manages drug testing for Olympics and other sports. In January 2011, NBA player O.J. Mayo was given a 10-game suspension after testing positive for DHEA. Mayo termed his use of DHEA as "an honest mistake".[45] Mayo is the seventh player to test positive for performance-enhancing drugs since the league began testing in 1999. Rashard Lewis, then with the Orlando Magic, tested positive for DHEA and was suspended 10 games before the start of the 2009-10 season.[46] 2008 Olympic 400 meter champion Lashawn Merritt has also tested positive for DHEA and was banned from the sport for 21 months.[47]
Marketing[edit source | edit]
In the United States, DHEA or DHEAS have been advertised with exaggerated claims that they may be beneficial for a wide variety of ailments. DHEA and DHEAS are readily available in the United States, where they are marketed as over-the-counter dietary supplements.[48] A 2004 review in the American Journal of Sports Medicine concluded that "The marketing of this supplement's effectiveness far exceeds its science."[49]
Research[edit source | edit]
Cancer[edit source | edit]
Some in vitro studies have found DHEA to have both antiproliferative and apoptotic effect on cancer cell lines.[50][51][52] The clinical significance of these findings, if any, is unknown. Higher levels of DHEA and other endogenous sex hormones are strongly associated with an increased risk of developing breast cancer in both pre- and postmenopausal women.[53][54]
References[edit source | edit]
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- ^ Memphis Grizzlies' O.J. Mayo gets 10-game drug suspension, ESPN, January 27, 2011
- ^ Memphis Grizzlies' O.J. Mayo suspended 10 games for violating NBA anti-drug program
- ^ "US 400m star LaShawn Merritt fails drug test". BBC Sport. 22 April 2010.
- ^ Calfee, R.; Fadale, P. (March 2006). "Popular ergogenic drugs and supplements in young athletes". Pediatrics 117 (3): e577–89. doi:10.1542/peds.2005-1429. PMID 16510635. "In 2004, a new Steroid Control Act that placed androstenedione under Schedule III of controlled substances effective January 2005 was signed. DHEA was not included in this act and remains an over-the-counter nutritional supplement."
- ^ Tokish, J. M.; Kocher, M. S.; Hawkins, R. J. (2004). "Ergogenic aids: a review of basic science, performance, side effects, and status in sports". The American Journal of Sports Medicine 32 (6): 1543–53. doi:10.1177/0363546504268041. PMID 15310585.
- ^ Yang, N. C.; Jeng, K. C.; Ho, W. M.; Hu, M. L. (2002). "ATP depletion is an important factor in DHEA-induced growth inhibition and apoptosis in BV-2 cells". Life Sci. 70 (17): 1979–88. doi:10.1016/S0024-3205(01)01542-9. PMID 12148690.
- ^ Schulz, S.; Klann, R. C.; Schönfeld, S.; Nyce, J. W. (1992). "Mechanisms of cell growth inhibition and cell cycle arrest in human colonic adenocarcinoma cells by dehydroepiandrosterone: role of isoprenoid biosynthesis". Cancer Res. 52 (5): 1372–6. PMID 1531325.
- ^ Loria, R. M. (2002). "Immune up-regulation and tumor apoptosis by androstene steroids". Steroids 67 (12): 953–66. doi:10.1016/S0039-128X(02)00043-0. PMID 12398992.
- ^ Tworoger, S. S.; Missmer, S. A.; Eliassen, A. H. et al. (2006). "The association of plasma DHEA and DHEA sulfate with breast cancer risk in predominantly premenopausal women". Cancer Epidemiol. Biomarkers Prev. 15 (5): 967–71. doi:10.1158/1055-9965.EPI-05-0976. PMID 16702378.
- ^ Key, T.; Appleby, P.; Barnes, I.; Reeves, G. (2002). "Endogenous sex hormones and breast cancer in postmenopausal women: reanalysis of nine prospective studies". J. Natl. Cancer Inst. 94 (8): 606–16. doi:10.1093/jnci/94.8.606. PMID 11959894.
External links[edit source | edit]
- Information on DHEA from the Mayo Clinic
- DHEA in elderly women and DHEA or testosterone in elderly men, published in the New England Journal of Medicine in 2006. "Neither DHEA nor low-dose testosterone replacement in elderly people has physiologically relevant beneficial effects on body composition, physical performance, insulin sensitivity, or quality of life."
- DHEA, from the Skeptic's Dictionary
- ChemSub Online: Dehydroepiandrosterone - DHEA
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UpToDate Contents
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- 1. デヒドロエピアンドロステロンおよびその硫酸塩 dehydroepiandrosterone and its sulfate
- 2. 副腎アンドロゲンの測定 measurement of adrenal androgens
- 3. 男性型多毛症を有する閉経期女性の評価 evaluation of premenopausal women with hirsutism
- 4. 副腎アンドロゲン過剰症 adrenal hyperandrogenism
- 5. 加齢に伴う内分泌の変化 endocrine changes with aging
English Journal
- Identification and characterization of zebrafish SULT1 ST9, SULT3 ST4, and SULT3 ST5.
- Mohammed YI, Kurogi K, Shaban AA, Xu Z, Liu MY, Williams FE, Sakakibara Y, Suiko M, Bhuiyan S, Liu MC.SourceDepartment of Pharmacology, College of Pharmacy, The University of Toledo, Toledo, OH 43614, USA.
- Aquatic toxicology (Amsterdam, Netherlands).Aquat Toxicol.2012 May 15;112-113:11-8. Epub 2012 Jan 30.
- By searching the GenBank database, we identified sequences encoding three new zebrafish cytosolic sulfotransferases (SULTs). These three new zebrafish SULTs, designated SULT1 ST9, SULT3 ST4, and SULT3 ST5, were cloned, expressed, purified, and characterized. SULT1 ST9 appeared to be mostly involved
- PMID 22360938
- Low serum sex hormone-binding globulin: Marker of inflammation?
- Liao CH, Li HY, Yu HJ, Chiang HS, Lin MS, Hua CH, Ma WY.SourceDivision of Urology, Department of Surgery, College of Medicine, Ph.D. Program in Nutrition and Food Sciences, and Graduate Institute of Basic Medicine, School of Medicine, Fu Jen Catholic University, Taipei, Taiwan.
- Clinica chimica acta; international journal of clinical chemistry.Clin Chim Acta.2012 Apr 11;413(7-8):803-7. Epub 2012 Jan 24.
- BACKGROUND: Low sex hormone-binding globulin (SHBG) is associated with metabolic syndrome (MetS), but its relationship with inflammation is unclear.METHODS: This cross-sectional study included 696 subjects (255 men, 235 pre-menopausal women, and 206 postmenopausal women). Body mass index, waist circ
- PMID 22293276
Japanese Journal
- 海外留学報告 DHEAはPTSDのレジリエンスと関連する因子か? : チューリヒ大学病院精神科精神療法科 研究報告
- 大江 美佐里
- 久留米医学会雑誌 75(10・11), 中付11-14, 2012-11-00
- NAID 40019559570
- Enhanced expression of organic anion transporting polypeptides (OATPs) in androgen receptor-positive prostate cancer cells: Possible role of OATP1A2 in adaptive cell growth under androgen-depleted conditions
- Arakawa Hiroshi,Nakanishi Takeo,Yanagihara Chihiro,Nishimoto Tomohiro,Wakayama Tomohiko,Mizokami Atsushi,Kawai Keiichi,Tamai Ikumi
- Biochemical Pharmacology 84(8), 1070-1077, 2012-10-15
- … Growth of both cell lines was stimulated by DHEAS and the effect was attenuated by STX64, an inhibitor of steroid sulfatase which can covert DHEAS to DHEA. …
- NAID 120004997008
- 運動負荷による骨代謝の変化に性ホルモンが及ぼす影響
- 朴 鍾薫,秋本 崇之,麻見 直美
- 日本運動生理学雑誌 19(2), 59-63, 2012-07-20
- … On the other hand, the exercise also increases circulating sex steroid hormones such as dehydroepiandrosterone (DHEA) and estradiol (E_2). …
- NAID 110009479352
Related Links
- デヒドロエピアンドロステロン（Dehydroepiandrosterone、略称 DHEA）とは、副腎や 性腺で産生される男性ホルモンの一種である。 アンドロゲン（男性ホルモン）活性として はテストステロンの約5%である。 成人女性においては、アンドロステンジオンとともに 主要 ...
- ＤＨＥＡ,不妊・妊娠・出産・育児-女性の為の健康生活ガイド『ジネコ』。ジネコは、不妊・・ 妊娠・出産・育児の悩みの口コミ情報、先生の専門的な意見が満載。月間50万人以上 のユーザーと300人以上の先生のQ＆Aコミュニティです。
Related Pictures
★リンクテーブル★
| リンク元 | 「副腎皮質ホルモン」「アンドロゲン」「6-アミノニコチンアミド」「デヒドロエピアンドロステロン」「dehydroepiandrosterone」 |
| 拡張検索 | 「DHEAS」「DHEA-S」 |
| 関連記事 | 「DH」「DHE」 |
「副腎皮質ホルモン」
- 英
- adrenocortical hormone
- 同
- 副腎皮質ステロイド adrenocorticoids
- 関
- 副腎皮質刺激ホルモン放出ホルモン、副腎皮質刺激ホルモン
- ステロイド
- 関
- 副腎、副腎皮質、ステロイド、コルチコステロイド、ステロイドホルモン、コルチコイド。副腎皮質ホルモン剤
種類(主要なもののみ)
- 網状層から分泌される。アンドロステンジオン
臨床関連
- 21-hydroxylaseが正常に機能しないことにより生じる (L.320)
薬理学
副腎皮質から分泌されるホルモン (SP.895)
| 名称 | 血漿濃度 (ng/ml) |
1日分泌量 (mg/day) | |
| 糖質コルチコイド | コルチゾール | 40～180 | 15～20 |
| コルチコステロン | 2～6 | 2～5 | |
| 鉱質コルチコイド | アルドステロン | 0.05～0.20 | 0.05～0.15 |
| 11-DOC | 0.05～0.30 | 0.10～0.20 | |
| 副腎アンドロジェン | DHEA | 2～8 | 7～15 |
| DHEA-S | 1～4 | ||
| アンドロステンジオン | 1～2 | 2～3 | |
「アンドロゲン」
概念
- 構造：C19ステロイド
- 副腎性：アンドロステンジオン androstenedione
- 精巣性：テストステロン testosterone
アンドロゲン
- アンドロゲンは肝臓で不活化されるため、経口投与ではほとんど効果がない。
(http://ja.wikipedia.org/wiki/%E3%82%A2%E3%83%B3%E3%83%89%E3%83%AD%E3%82%B2%E3%83%B3)
種類
分類
性状
- ステロイド
産生組織
- 卵胞内の卵胞上皮細胞で芳香環化されてエストロゲンに変換される。
- 両性：副腎皮質
標的組織
受容体
作用
- アンドロゲンとは雄の副生殖器の発育および機能を促進し、二次性徴を発現させる作用をもつ物質の総称であり、数種類のホルモンからなる。
分泌の調整
- 男性：テストステロン、ジヒドロテストステロンの濃度上昇によりLHの分泌が抑制される。
分子機構
生合成
臨床関連
「6-アミノニコチンアミド」
- 英
- 6-aminonicotinamide, 6-AN
- ペントースリン酸経路の最初の反応を規定する律速酵素である、グルコース6-リン酸デヒドロゲナーゼ G6PDを阻害することが知られている。
- G6PD阻害物質の1つ：ヒドロエピアンドロステロン(DHEA)と6-アミノニコチンアミド(6AN)がしられている。
「デヒドロエピアンドロステロン」
- C19ステロイド。アンドロゲン
産生組織
「dehydroepiandrosterone」
「DHEAS」
- 同
- DHEAS
- 関
- Dehydroepiandrosterone sulfate
- 同
- 硫酸デヒドロエピアンドロステロン
「DHEA-S」
「DH」
[★] ドイツ水平線 Deutsche Horizontale