WordNet

the abnormal development of male sexual characteristics in a female (usually as the result of hormone therapies or adrenal malfunction) (同)masculinisation, virilization, virilisation
the development of male secondary sexual characteristics in a female (or prematurely in a young boy)

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2016/04/07 18:58:59」(JST)

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Defeminization and masculinization are the processes that a fetus goes through to become a male.^{[citation needed]}

It has often been said by biologists that in sexual differentiation in mammals, the female is the "default" developmental pathway, in the sense that elimination of any of several gene actions necessary for formation of male genitalia leads to the development of external female genitalia (though development of functional ovaries requires effective action of several less understood sex-specific genes).^{[citation needed]} Two processes: defeminization, and masculinization, are involved in producing male typical morphology and behavior. Disruption of either of these processes in males produces female-typical development.^{[citation needed]} The opposite is not true, disruption of normal sexual development in females does not lead to male-typical endpoints.^{[citation needed]}

Defeminization involves the suppression of the development of female typical morphology (development of the Müllerian ducts into the fallopian tubes, uterus and vagina) and behavioural predispositions. Masculinization involves the production of male typical morphology (development of the Wolffian ducts into male reproductive structures) and behavioural predispositions. Both defeminization and masculinization are required for a mammalian zygote to become a fully reproductively functional male.

A brief version of the female default paradigm can be stated as follows:

A set of specific genetic instructions must be present and a series of differentiating events mediated by hormones must occur in order for a mammalian zygote to become a fully reproductively functional male.
1. The SRY, SOX9, and SF1 genes must be present and functional.
2. Functional Leydig cells must form in the gonads.
3. The Leydig cells must be able to produce testosterone.
4. The target cells must have the hormone receptors to respond to the testosterone. The target cells of the external genitalia must have functional 5-alpha-reductase enzyme to convert some of the testosterone to more active dihydrotestosterone.
5. There is some evidence that the brain must be exposed and respond to androgens either prenatally or early in life to produce characteristic mating behavior. This is well demonstrated in many animal species but remains mostly speculative with respect to humans.
To a large extent, each step builds on the previous. If anything goes wrong at any of the first four steps, the subsequent pathway of development results in female anatomy and behavior.
No ovarian organizing gene homologous to SRY has been discovered. Both sexes are exposed to maternal estrogen prenatally. No hormones have yet been discovered that are necessary early in life to produce female sexual development. Estrogen seems not to be necessary until puberty for purposes of differentiation.
1. The full development of male characteristics also includes personal experience throughout life, determining gender identity, gender roles and sexual orientation. However, there is much debate on the balance between nature and nurture in the determination.

History

This paradigm dates back to the 1950s. Even stronger versions were commonly stated in the 1960s and 1970s. One version, perhaps most associated with John Money, (who termed it the Adam principle), held that additional steps in the cascade to male identity were the recognition by parents and doctor that the external genitalia were male, which resulted in a male sex assignment, which in turn resulted in a male sex of rearing by parents and society, which in turn (coupled with the reinforcing appearance of male genitalia) resulted in a male gender identity. At least by implication, female gender identity simply required a female sex of rearing and lack of an obvious penis.

In Germany in the 1970s, Günter Dörner extrapolated the cascade to include direct testosterone effect on the brain as necessary for a male gender identity and sexual orientation, proposing that transsexualism and or homosexuality in biological males could result from deficiency of prenatal or early postnatal testosterone effect on the brain.

Notes and references

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1. 女性におけるアンドロゲン欠乏症および治療の概要 overview of androgen deficiency and therapy in women
2. アスリートにおけるアンドロゲンおよびその他のホルモンの使用 use of androgens and other hormones by athletes
3. アンドロゲン受容体障害の病因および臨床症状 pathogenesis and clinical manifestations of disorders of androgen action
4. 副腎アンドロゲンの測定 measurement of adrenal androgens
5. 性腺機能低下を呈する男性に対するテストステロン治療 testosterone treatment of male hypogonadism

English Journal

Effect of risedronate in osteoporotic HIV males, according to gonadal status: a pilot study.

Pepe J1, Isidori AM, Falciano M, Iaiani G, Salotti A, Diacinti D, Del Fiacco R, Sbardella E, Cipriani C, Piemonte S, Raimo O, Biondi P, Biamonte F, Lenzi A, Minisola S.
Endocrine.Endocrine.2014 Nov;47(2):456-62. doi: 10.1007/s12020-014-0349-0. Epub 2014 Aug 8.
The aim of the study was to evaluate the effect of risedronate on bone mineral density (BMD) and bone turnover markers in HIV-infected osteoporotic males, according to their gonadal status. HIV patients were followed up for 24 months and divided into two groups: patients with osteoporosis or osteop
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European survey of diagnosis and management of the polycystic ovary syndrome: results of the ESE PCOS Special Interest Group's Questionnaire.

Conway G1, Dewailly D1, Diamanti-Kandarakis E1, Escobar-Morreale HF1, Franks S1, Gambineri A1, Kelestimur F1, Macut D1, Micic D1, Pasquali R2, Pfeifer M1, Pignatelli D1, Pugeat M1, Yildiz B1; ESE PCOS Special Interest Group.
European journal of endocrinology / European Federation of Endocrine Societies.Eur J Endocrinol.2014 Oct;171(4):489-98. doi: 10.1530/EJE-14-0252. Epub 2014 Jul 21.
BACKGROUND: There is evidence for differences between endocrinologists and other specialists in their approach to diagnosis and management of the polycystic ovary syndrome (PCOS).OBJECTIVE: A mailed survey consisting of a simple questionnaire aiming to understand current practice for diagnosis and m
PMID 25049203

Reproductive neuroendocrine dysfunction in polycystic ovary syndrome: insight from animal models.

Roland AV1, Moenter SM2.
Frontiers in neuroendocrinology.Front Neuroendocrinol.2014 Oct;35(4):494-511. doi: 10.1016/j.yfrne.2014.04.002. Epub 2014 Apr 18.
Polycystic ovary syndrome (PCOS) is a common endocrinopathy with elusive origins. A clinically heterogeneous disorder, PCOS is likely to have multiple etiologies comprised of both genetic and environmental factors. Reproductive neuroendocrine dysfunction involving increased frequency and amplitude o
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Japanese Journal

子宮内膜癌発生ならびにNatural Killer細胞活性に及ぼすNeonatal Androgenizationの効果

森川真一,内藤正文,高見沢裕吉
日本産科婦人科學會雜誌 38(11), 1957-1963, 1986-11-01
概要新生仔期にアンドロゲンを投与(neonatal androgemzation)し、子宮内膜癌発生の実験モデルの無排卵不妊ラット(以下ASR)を作製し、子宮内膜癌発生ならびにnatural killer (以下NK)細胞活性に及ぼす影響を検討し以下の結果を得た。 1)ASRは生後500日齢以後61例中3例に異型腺増殖、4例に癌(腺癌3例、扁平上皮癌1例)が発生した。一方、正常対象廸以下NR)1 …
NAID 110002114834

Danazol療法時のandrogen動態

浅井光興,大沢政巳,市川弥生,呉明超,正橋鉄夫,成田牧,松井信夫,柏俣重夫
日本産科婦人科學會雜誌 37(6), 1001-1006, 1985-06-01
Danazol投与中のandrogen動態について検討するために,% free testosterone (%freeT)や,Sex-hormone binding globulin (SHBG)などの測定,およびdanazolのSHBGやandrogen receptorに対する作用について研究を行なった.% free Tはdanazol投与中約3倍にまで増加するが,SHBGはこれとは逆に,有意 …
NAID 110002232464

7,12-dimethylbenz[a]anthracene誘発ラット子宮内膜腫瘍発生に及ぼすneonatal androgenizationの効果

森川真一,内藤正文,岩沢博司,高見沢裕吉
日本産科婦人科學會雜誌 37(3), 365-369, 1985-03-01
… neonatal androgenizationが7,12-dimethylbenz[a]anthracene(DMBA)誘発ラット子宮腫瘍の発生にいかなる効果を及ぼすかを検討した.1.Vehicle(密ロウ)投与群:正常ラット(以下NR)122例およびneonatal androgenization施行ラット(androgen sterilized rat以下ASR)98例はVehicle投与後16週,40週で,子宮腫瘍の発生は認められなかった.2.0.2mgDMBA投与群:DMBA投与16週後にはNR80例,ASR72例は子宮腫瘍が発生しなかった.40週後では悪性子宮腫瘍が30例のASRには …
NAID 110002218880