Development of the gonad in normal and anencephalic human fetuses

Baker, T. G.; Scrimgeour, J.B.

doi:10.1530/jrf.0.0600193

Cited by 90 publications

(33 citation statements)

References 11 publications

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“…In hypophysectomized fetal sheep, the resulting reduction in testis size and tubule diameter (Liggins & Kennedy 1968) would also be consistent with reduced gonocyte numbers. Similarly, in anencephalic humans, it is reported that gonocyte/prespermatogonial numbers appear reduced (Baker & Scrimgeour 1980). Therefore, it is likely that gonocyte proliferation and survival during fetal development in most species are pituitary-dependent in the latter parts of gestation, although this effect is likely to be mediated through Sertoli cell number and activity.…”

Section: Germ Cellsmentioning

confidence: 99%

“…As hCG levels decline, however, towards the end of the second trimester, fetal LH may become more important in maintaining Leydig cell function (Fowler et al , 2009). Interestingly, in anencephalic human fetuses, studied in the late second and third trimesters, there is an apparent loss of fetal Leydig cells (Baker & Scrimgeour 1980), and the external genitalia are often small in newborns (Scott et al 2009). Similarly, hypophysectomy in the last third of gestation reduces the overall percentage of Leydig cells at term in the rhesus monkey (Gulyas et al 1977).…”

Section: Endocrinology Of the Fetal Testismentioning

confidence: 99%

“…Fetal hypophysectomy, for example, will reduce testis size and tubule diameter in the newborn sheep, while testis size is reduced in the hypophysectomized rhesus monkey fetus and anencephalic human (Liggins & Kennedy 1968, Gulyas et al 1977, Baker & Scrimgeour 1980. A reduced testis size in these species is consistent with reduced Sertoli cell number, but, in each case, the procedure used, or condition studied, will inevitably remove both FSH and LH and, thus, probably reduce testicular androgen levels.…”

Section: Endocrinology Of the Fetal Testismentioning

confidence: 99%

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Endocrinology of the mammalian fetal testis

O’Shaughnessy¹,

Fowler²

2011

Reproduction

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The testes are essential endocrine regulators of fetal masculinization and male development and are, themselves, subject to hormonal regulation during gestation. This review focuses, primarily, on this latter control of testicular function. Data available suggest that, in most mammalian species, the testis goes through a period of independent function before the fetal hypothalamic-pituitary-gonadal axis develops at around 50% of gestation. This pituitary-independent phase coincides with the most critical period of fetal masculinization. Thereafter, the fetal testes appear to become pituitary hormone-dependent, concurrent with declining Leydig cell function, but increasing Sertoli cell numbers. The two orders of mammals most commonly used for these types of studies (rodents and primates) appear to represent special cases within this general hypothesis. In terms of testicular function, rodents are born 'early' before the pituitary-dependent phase of fetal development, while the primate testis is dependent upon placental gonadotropin released during the pituitary-independent phase of development.

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Section: Germ Cellsmentioning

confidence: 99%

Section: Endocrinology Of the Fetal Testismentioning

confidence: 99%

Section: Endocrinology Of the Fetal Testismentioning

confidence: 99%

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Endocrinology of the mammalian fetal testis

O’Shaughnessy¹,

Fowler²

2011

Reproduction

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“…The role of pituitary gonadotrophins in ovarian development and function during foetal life is not well understood. In anencephalic female foetuses, normal follicular development up to 34 weeks of gestation is observed but, thereafter, large growing follicles that are common in healthy foetuses are not seen in anencephalic female foetuses [16]. This finding suggests that ovarian development up to the 7th month of pregnancy occurs independently of stimulation by the foetal hypothalamus, but pituitary gonadotrophins later have a role in follicular growth.…”

Section: Introductionmentioning

confidence: 99%

Activation of the Hypothalamic-Pituitary-Gonadal Axis in Infancy: Minipuberty

2014

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The hypothalamic-pituitary-gonadal (HPG) axis is active in the midgestational foetus but silenced towards term because of the negative feedback effects mediated by the placental hormones. This restraint is removed at birth, leading to reactivation of the axis and an increase in gonadotrophin levels. Gonadotrophin levels are high during the first 3 months of life but decrease towards the age of 6 months except for FSH levels in girls that remain elevated until 3-4 years of age. After this, the HPG axis remains quiescent until puberty. The postnatal gonadotrophin surge results in gonadal activation in both sexes. In boys, testosterone levels rise to a peak at 1-3 months of age and then decline following LH levels. Postnatal HPG axis activation is associated with penile and testicular growth and therefore considered important for the development of male genitalia. In girls, elevated gonadotrophin levels result in the maturation of ovarian follicles and in an increase in oestradiol levels. Biological significance and possible long-term consequences of this minipuberty remain elusive, as do the mechanisms that silence the HPG axis until puberty. However, the first months of life provide a ‘window of opportunity' for functional studies of the HPG axis prior to pubertal development.

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“…In the human [57] and rhesus monkey [58,59], fetal anencephaly, which results in a loss of pituitary gonadotropin secretion, is associated with a reduction in testes weight, germ cell numbers, and testosterone production. These findings, plus the observation that the human fetal testis expresses the receptors for FSH [60] and LH [61], support the suggestion that FSH and LH regulate fetal testis development [62].…”

Section: Discussionmentioning

confidence: 99%

Estrogen Promotes Germ Cell and Seminiferous Tubule Development in the Baboon Fetal Testis.

Albrecht

Lane²,

Marshall

et al. 2009

Biology of Reproduction

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The foundation for development of the male reproduction system occurs in utero, but relatively little is known about the regulation of primate fetal testis maturation. Our laboratories have shown that estrogen regulates key aspects of the physiology of pregnancy and fetal development. Therefore, in the present study, we characterized and quantified germ cells and Sertoli cells in the fetal baboon testis in late normal gestation (i.e., Day 165; term is 184 days) and in baboons administered the aromatase inhibitor letrozole throughout the second half of gestation to assess the impact of endogenous estrogen on fetal testis development. In untreated baboons, the seminiferous cords were comprised of undifferentiated (i.e., type A) spermatogonia classified by their morphology as dark (Ad) or pale (Ap), gonocytes (precursors of type A spermatogonia), unidentified cells (UI), and Sertoli cells. In letrozole-treated baboons, serum estradiol levels were decreased by 95% %. The number per milligram of fetal testis (310 4 ) of Ad spermatogonia (0.42 6 0.11) was 45% % lower (P ¼ 0.03), and that of gonocytes (0.58 6 0.06) and UI (0.45 6 0.12) was twofold greater (P , 0.01 and P ¼ 0.06, respectively), than in untreated baboons. Moreover, in the seminiferous cords of estrogen-deprived baboons, the basement membrane appeared fragmented, the germ cells and Sertoli cells appeared disorganized, and vacuoles were present. We conclude that endogenous estrogen promotes fetal testis development and that the changes in the germ cell population in the estrogen-deprived baboon fetus may impair spermatogenesis and fertility in adulthood.

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Development of the gonad in normal and anencephalic human fetuses

Abstract: Summary. The

Cited by 90 publications

References 11 publications

Endocrinology of the mammalian fetal testis

Endocrinology of the mammalian fetal testis

Activation of the Hypothalamic-Pituitary-Gonadal Axis in Infancy: Minipuberty

Estrogen Promotes Germ Cell and Seminiferous Tubule Development in the Baboon Fetal Testis.

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