Ontogeny of Gonadal Luteinizing Hormone and Follicle-Stimulating Hormone Receptors in the Fetal Pig and Related Changes in Gonadotropin and Testosterone Secretion1

Goxe, Béatrice; Prunier, Armelle; Rémy, Jean-Serge; Salesse, Roland

doi:10.1095/biolreprod49.3.609

Cited by 23 publications

(21 citation statements)

References 43 publications

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“…In contrast to observations of the current study relative to FSH, Goxe et al (1993) reported no difference in serum FSH concentration and FSH receptor levels between MS and a White breed of pigs. However, these investigators also observed no difference in gonadal weights between the two breeds.…”

Section: Discussioncontrasting

confidence: 99%

“…Littermates to each of these boars were castrated on 7, 14 and 25 dpp. These age groups represent early gonadotropin secretion in the porcine fetus (Liwska 1975, Goxe et al 1993) and the neonatal peak in gonadotropin secretion (Lunstra et al 1997). Procedures for handling all animals in this study complied with those specified in the Guide for the Care and Use of Agricultural Animals in Agricultural Research and Teaching (FASS 1999).…”

Section: Sample Collection and Histological Methodsmentioning

confidence: 99%

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Stereological evaluation of Sertoli cell ontogeny during fetal and neonatal life in two diverse breeds of swine

McCoard¹,

Wise²,

Lunstra³

et al. 2003

Journal of Endocrinology

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Chinese Meishan (MS) boars have smaller testes due to fewer Sertoli cells compared with White Composite (WC) boars. The objective was to describe Sertoli cell development relative to circulating FSH concentrations in fetal and neonatal MS and WC boars. Testes and blood samples were collected on days 60, 75, 90 and 105 postcoitum (dpc) and 1, 7, 14 and 25 postpartum (dpp). One testis was immunostained for GATA4 or Ki67 antigen to evaluate total and proliferating Sertoli cell numbers respectively. Testicular size was greater (P,0·01) in WC than MS boars at all ages, associated with a greater mass of interstitial tissue. Tubular mass (P,0·01) was greater in prenatal WC boars, but postnatally increased more rapidly (P,0·001) in MS boars, exceeding WC boars by 25 dpp. Sertoli cell numbers increased with age, was greater (P,0·001) in WC than MS boars during prenatal development but increased rapidly (P,0·01) by 1 dpp in MS and thereafter was similar in both breeds. The proportion of Ki67-positive Sertoli cells was maximal at 90 dpc, declining thereafter, did not differ between breeds through 7 dpp, but was greater (P,0·05) in WC than MS boars at 14 and 25 dpp. Plasma FSH concentrations were greater (P,0·05) in WC than MS boars at 75 dpc. FSH concentrations were elevated at 105 dpc (MS) and 1 dpp (WC) but declined thereafter with advancing postnatal age in both breeds. This study illustrates that late gestation represents the period of maximal Sertoli cell proliferation. Despite asynchronous Sertoli cell population growth between breeds during early postnatal life, differential mature Sertoli cell numbers and testicular size are probably due to differences in duration of the proliferative period after 25 dpp, potentially regulated by Sertoli cell maturation and blood-testis barrier formation. These events were not associated with fetal or early postnatal changes in FSH secretion.

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Section: Discussioncontrasting

confidence: 99%

Section: Sample Collection and Histological Methodsmentioning

confidence: 99%

Stereological evaluation of Sertoli cell ontogeny during fetal and neonatal life in two diverse breeds of swine

McCoard¹,

Wise²,

Lunstra³

et al. 2003

Journal of Endocrinology

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“…Additionally, the roles of FSH and LH in fetal ovarian maturation are currently under investigation (12,13). In fetal pigs, lower levels of FSH and LH receptor concentrations have been demonstrated in the ovaries compared to those in the fetal testes (13).…”

Section: Discussionmentioning

confidence: 99%

“…In fetal pigs, lower levels of FSH and LH receptor concentrations have been demonstrated in the ovaries compared to those in the fetal testes (13). It has been suggested that this dichotomous finding is responsible for the relative lack of fetal ovarian growth compared to fetal testicular growth.…”

Section: Discussionmentioning

confidence: 99%

Menstrual Bleeding in a Female Infant with Congenital Adrenal Hyperplasia: Altered Maturation of the Hypothalamic-Pituitary-Ovarian Axis

Uli

Chin²,

David³

et al. 1997

The Journal of Clinical Endocrinology & Metabolism

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Vaginal bleeding during the neonatal period is commonly related to the withdrawal of maternal estrogens. Vaginal bleeding has also been reported in female infants with congenital adrenal hyperplasia and has been proposed to be due to a treatment-induced activation of the hypothalamic-pituitary-ovarian axis.We report a female infant with the salt-losing form of congenital adrenal hyperplasia due to 21-hydroxylase deficiency, who had the onset of vaginal bleeding at 3 months of life. Adrenal steroid suppression had been achieved by 2.5 weeks of age. At the time of bleeding, imaging studies revealed an enlarged right ovary with a dominant 3-cm cyst and additional small cysts that had not been seen on the newborn sonogram. The uterus was enlarged and stimulated. Three weeks later (1 week after the cessation of bleeding), repeat ultrasound demonstrated a marked decrease in the size of the right ovary, and the dominant cyst was no longer seen. The patient had a heightened FSH response to GnRH and elevated levels of estradiol for age. At 5 months of age, no further episodes of sustained vaginal bleeding were observed. Repeat hormonal levels were prepubertal, and pelvic sonogram demonstrated no evidence of stimulation.The findings in our patient suggest that a decline in adrenal androgens after glucocorticoid treatment resulted in an increase in gonadotropin levels, which then triggered a transient and augmented end-organ response (menses). Further, we suggest that our infant's hormonal findings may reflect a delay in the timely development of the negative restraint by sex steroids on gonadotropins that is normally observed in infancy. (J Clin Endocrinol Metab 82: 3298 -3302, 1997)

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“…However, although FSHR has been detected in the fetal ovary of the pig [19] and cow [20], our understanding of the ontogeny and developmental expression of the FSHR in primates is incomplete [21,22]. The current study was designed in part to determine whether fetal ovarian folliculogenesis is associated with expression of FSHR.…”

Section: Introductionmentioning

confidence: 99%

Developmental Regulation of Follicle-Stimulating Hormone Receptor Messenger RNA Expression in the Baboon Fetal Ovary1

Zachos

Billiar

Albrecht

et al. 2003

Biology of Reproduction

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In the adult ovary, pituitary FSH via interaction with its receptor (FSHR) is required for follicular maturation and granulosa cell development. In humans and nonhuman primates, the pool of follicles available for adult ovarian function is established in utero. However, our understanding of the ontogeny and developmental regulation of FSHR in the ovary of the primate fetus is incomplete. Our goal was to determine whether the baboon fetal ovary expresses the full-length FSHR mRNA transcript and whether levels are developmentally regulated. Fetal ovaries were obtained at mid (Day 100) and late (Day 165) gestation (term = Day 184) from untreated baboons and on Day 165 from baboons in which fetal estrogen levels were either decreased by >95% by treatment with the aromatase inhibitor CGS 20267 or restored to 30% of normal by treatment with CGS 20267 plus estradiol benzoate administered s.c. to the mother on Days 100-164. The full-length 2088-base pair FSHR mRNA transcript was expressed in ovaries of adult and fetal baboons untreated or treated with CGS 20267 or CGS 20267 and estrogen. Mean (+/-SEM) FSHR mRNA levels (ratio of FSHR mRNA:18S rRNA), quantified by reverse transcription polymerase chain reaction, were increased (P < 0.05) 2-fold between mid (0.34 +/- 0.06) and late gestation (0.76 +/- 0.07), an increase prevented (P < 0.05) in estrogen-depleted baboons (0.44 +/- 0.10) and partially restored by treatment with CGS 20267 and estrogen (0.58 +/- 0.16). We previously showed that the number of follicles/0.33 mm2 in fetal ovaries of untreated baboons in late gestation was reduced 50% by treatment with CGS 20267 and restored to normal in baboons treated with CGS 20267 and estrogen. Thus, when corrected for the number of follicles/0.33 mm2, FSHR mRNA levels were similar in baboon fetal ovaries untreated (0.010 +/- 0.001) or treated with CGS 20267 (0.009 +/- 0.002) or CGS 20267 and estrogen (0.007 +/- 0.003). We conclude that estrogen plays a major role in regulating ovarian FSHR mRNA expression in the primate fetus, and that the developmental increase in FSHR mRNA levels reflects the estrogen-dependent increase in folliculogenesis (i.e., increased number of granulosa cells and oocytes).

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Ontogeny of Gonadal Luteinizing Hormone and Follicle-Stimulating Hormone Receptors in the Fetal Pig and Related Changes in Gonadotropin and Testosterone Secretion1

Cited by 23 publications

References 43 publications

Stereological evaluation of Sertoli cell ontogeny during fetal and neonatal life in two diverse breeds of swine

Stereological evaluation of Sertoli cell ontogeny during fetal and neonatal life in two diverse breeds of swine

Menstrual Bleeding in a Female Infant with Congenital Adrenal Hyperplasia: Altered Maturation of the Hypothalamic-Pituitary-Ovarian Axis

Developmental Regulation of Follicle-Stimulating Hormone Receptor Messenger RNA Expression in the Baboon Fetal Ovary1

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