Effect of prenatal administration of testosterone on ovarian function in rats

Fels, E; Bosch, L.R.

doi:10.1016/0002-9378(71)90954-9

Cited by 36 publications

(19 citation statements)

References 4 publications

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“…This would be reflected in statistical analyses as a common environmental effect in males. In other mammals, testosterone diffuses between fetuses through the amniotic membranes (Fels and Bosch, 1971)' or via the maternal circulation (Meisel and Ward, 1981). Indirect evidence for hormonal exchange between human twins arises from a preliminary study of opposite-sexed twins, in which we noted a trend toward larger teeth in females with twin brothers, than in females with twin sisters (Dempsey dill., 1994), indicating a possible masculinizing effect on females.…”

Section: Multivariate Analysesmentioning

confidence: 90%

Genetic Covariance Structure of Incisor Crown Size in Twins

et al. 1995

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Abstract. Previous studies of tooth size in twins and their families have suggested a high degree of genetic control, although there have been difficulties separating the various genetic and environmental effects. A genetic analysis of variation in crown size of the permanent incisors of South Australian twins was carried out, with structural equation modeling used to determine the relative contributions of genetic and environmental factors. Maximum mesiodistal crown dimensions of maxillary and mandibular permanent incisors were recorded from dental models of 298 pairs of twins, including 149 monozygous (MZ) and 149 dizygous (DZ) pairs. The analysis revealed that: (i) an adequate fit required additive genetic and unique environmental components; (ii) augmenting the model with non-additive genetic variation did not lead to a Significant improvement in fit; (iii) there was evidence of shared environmental influences in the upper central incisors of males; (iv) the additive genetic component constituted a general factor loading on all eight teeth, with group factors loading on antimeric pairs of teeth; (v) unique environmental effects were mostly variable-specific; (vi) most factor loadings on antimeric tooth pairs could be constrained to be equal, indicating a symmetry of genetic and environmental influences between left and right sides; and (vii) estimated heritability of the incisor mesiodistal dimensions varied from 0.81 to 0.91.

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Section: Multivariate Analysesmentioning

confidence: 90%

Genetic Covariance Structure of Incisor Crown Size in Twins

et al. 1995

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“…On the other hand, in other studies, late gestational treatment of mice with testosterone (Keisler et al 1991) or rats with TP (Swanson & Werff ten Bosch 1964, Fels & Bosch 1971, Huffman & Hendricks 1981, Slob et al 1983, Tyndall et al 2012) had no effect on cyclicity or ovarian function, inferred by the presence of follicles at various stages and CL. Variations in the observed phenotypes induced by prenatal treatment with testosterone or TP may be due to the degree of transplacental transfer of the administered steroid into the foetus (Fels & Bosch 1971). The timing of the prenatal androgen exposure may also play a role, as a previous study has identified that androgen exposure on gestational days 16-19 increases the number of preantral and antral follicles observed, while testosterone treatment on day 20 of gestation only had no effect on follicle populations (Ramezani et al 2014).…”

Section: Testosteronementioning

confidence: 95%

“…Both prenatal aromatisable (testosterone) and non-aromatisable (DHT) androgen exposure abolished an E 2 benzoate-induced LH surge, implying that direct prenatal AR activation is involved in altering the GnRH/LH neurosecretory system (Foecking et al 2005). On the other hand, in other studies, late gestational treatment of mice with testosterone (Keisler et al 1991) or rats with TP (Swanson & Werff ten Bosch 1964, Fels & Bosch 1971, Huffman & Hendricks 1981, Slob et al 1983, Tyndall et al 2012) had no effect on cyclicity or ovarian function, inferred by the presence of follicles at various stages and CL. Variations in the observed phenotypes induced by prenatal treatment with testosterone or TP may be due to the degree of transplacental transfer of the administered steroid into the foetus (Fels & Bosch 1971).…”

Section: Testosteronementioning

confidence: 99%

Role of androgens in normal and pathological ovarian function

Walters

2015

Reproduction

138

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Androgens mediate their actions via the androgen receptor (AR), a member of the nuclear receptor superfamily. AR-mediated androgen action is essential in male reproductive development and function; however, only in the last decade has the suspected but unproven role for AR-mediated actions in female reproduction been firmly established. Deciphering the specific roles and precise pathways by which AR-mediated actions regulate ovarian function has been hindered by confusion on how to interpret results from pharmacological studies using androgens that can be converted into oestrogens, which exert actions via the oestrogen receptors. The generation and analysis of global and cell-specific female Ar knockout mouse models have deduced a role for AR-mediated actions in regulating ovarian function, maintaining female fertility, and have begun to unravel the mechanisms by which AR-mediated androgen actions regulate follicle health, development and ovulation. Furthermore, observational findings from human studies and animal models provide substantial evidence to support a role for AR-mediated effects not only in normal ovarian function but also in the development of the frequent ovarian pathological disorder, polycystic ovarian syndrome (PCOS). This review focuses on combining the findings from observational studies in humans, pharmacological studies and animal models to reveal the roles of AR-mediated actions in normal and pathological ovarian function. Together these findings will enable us to begin understanding the important roles of AR actions in the regulation of female fertility and ovarian ageing, as well as providing insights into the role of AR actions in the androgen-associated reproductive disorder PCOS.Reproduction (2015) 149 R193-R218

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“…Although 1 study reported that exposure of rodent fetuses to testosterone propionate (TP) by intra-amniotic administration induced anovulation in 64% of rats [21], in most studies, prenatal treatment of mice with T [22] or rats with TP [21,[23][24][25][26][27] had no effect on cyclicity or ovarian function, inferred by the presence of follicles at various stages and corpora lutea. A detailed study by Wu et al [28] showed that prenatal treatment of rats with T on Days 16 and 19 of gestation resulted in irregular estrous cycles and an ovarian phenotype of increased numbers of preantral and antral follicles but a decrease in preovulatory follicle and corpus lutea populations.…”

Section: Androgensmentioning

confidence: 96%

Rodent Models for Human Polycystic Ovary Syndrome1

Walters

Allan

Handelsman

2012

Biology of Reproduction

261

213

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Polycystic ovary syndrome (PCOS) is the most frequent female endocrine disorder, affecting 5%-10% of women, causing infertility due to dysfunctional follicular maturation and ovulation, distinctive multicystic ovaries and hyperandrogenism, together with metabolic abnormalities including obesity, hyperinsulinism, an increased risk of type 2 diabetes, and cardiovascular disease. The etiology of PCOS is unclear, and decisive clinical studies are limited by ethical and logistic constraints. Consequently treatment is palliative rather than curative and focuses on symptomatic approaches. Hence, a suitable animal model could provide a valuable means with which to study the pathogenesis of the characteristic reproductive and metabolic abnormalities and thereby identify novel and more effective treatments. So far there is no consensus on the best experimental animal model, which should ideally reproduce the key features associated with human PCOS. The prenatally androgenized rhesus monkey displays many characteristics of the human condition, including hyperandrogenism, anovulation, polycystic ovaries, increased adiposity, and insulin insensitivity. However, the high cost of nonhuman primate studies limits the practical utility of these large-animal models. Rodent models, on the other hand, are inexpensive, provide well-characterized and stable genetic backgrounds readily accessible for targeted genetic manipulation, and shorter reproductive life spans and generation times. Recent rodent models display both reproductive and metabolic disturbances associated with human PCOS. This review aimed to evaluate the rodent models reported to identify the advantages and disadvantages of the distinct rodent models used to investigate this complex endocrine disorder.

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Effect of prenatal administration of testosterone on ovarian function in rats

Cited by 36 publications

References 4 publications

Genetic Covariance Structure of Incisor Crown Size in Twins

Genetic Covariance Structure of Incisor Crown Size in Twins

Role of androgens in normal and pathological ovarian function

Rodent Models for Human Polycystic Ovary Syndrome1

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