Spermatic and Peripheral Plasma Concentrations of Testosterone and Androstenedione in Prepubertal Boys

In normal men a single dose of hCG induces an increase in plasma testosterone (T) and 17 alpha-hydroxyprogesterone (17 alpha-OHP) 2-4 h after the injection; after 24-36 h a maximum increase in plasma 17 beta-estradiol (E2) and 17 alpha-OHP occurs followed by a second surge in T after 48-96 h. The present investigation focuses on the effect of a single dose of hCG (3500 IU/m2 body surface) on testicular steroid production in 12 boys aged 13 months to 12 yr. Plasma hCG, 17 alpha-OHP, androstenedione (A), T, dihydrotestosterone, and E2 were measured basally and 2, 4, 24, 48, 72, and 96 h after hCG administration. Plasma hCG was measured using a double antibody RIA technique and steroids by RIA after celite chromatography. The results show that hCG peaked 2 h after administration of the hormone and high levels persisted for up until 72 h. Plasma T and dihydrotestosterone increased after 48 h and remained significantly high for another 48 h; 17 alpha-OHP, A, and E2 did not change. These findings show that hCG stimulation in prepubertal boys induces significant production of T without affecting the precursors or aromatization product, in contrast to observation in the adult man, where 17 alpha-OHP, A, and E2 increase significantly. A response comparable to that observed in children has been recorded in adult males with hypogonadotropic hypogonadism.

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“…In our subjects plasma A remained unchanged, in agreement with Forti et al (25), who found an inconstant…”

Section: Discussionsupporting

confidence: 93%

Response to a Single Dose of Human Chorionic Gonadotropin in Prepubertal Boys*

Toscano

Balducci

Adamo

et al. 1983

The Journal of Clinical Endocrinology & Metabolism

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“…In this regard, the male rhesus monkey appears to be at least quantitative¬ ly different from man, since prepubertal children remain responsive to GnRH administration, at least in terms of FSH release, and one can usually observe values of serum FSH above the normal prepubertal range in children with congenital or traumatic anorchia (Winter & Faiman 1972). Fur¬ thermore, in boys there is evidence for continued low-level secretion of sex steroids throughout the juvenile period (Forti et al 1981). Therefore, it seems likely, in the human male, that central inhibition of gonadotropin release before puberty may be supplemented by some degree of steroidmediated feedback inhibition.…”

Section: Discussionmentioning

confidence: 99%

The role of gonadal steroids in feedback regulation of gonadotropin secretion at different stages of primate development

Winter¹,

Ellsworth²,

Fuller³

et al. 1987

Acta Endocrinologica

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The serum gonadotropin response to castration was assessed in 8 foetal, 2 neonatal, 30 juvenile, and 2 adult rhesus monkeys (M. mulatta). In the 30 castrated juvenile monkeys and 8 sham-operated controls, concentrations of oestrone, oestradiol, androstenedione, dihydrotestosterone, testosterone and 17OH-progesterone were measured in 10 ml serum pools before, one month after, and one year after the surgical procedure. Castration during foetal life (83\p=n-\ 137 days gestation) was followed within 48\p=n-\72h by a significant rise in serum FSH levels in males, but had no effect on the already high levels in females. Similarly, castration of males during the first post-natal month raised serum FSH and LH into the adult castrate range; however, after 3 months of age serum gonadotropin levels again declined to the normal juvenile range in spite of the open feedback loop. Orchiectomy of pre\ x=req-\ pubertal juvenile monkeys (age 3 months\p=n-\2\m=8/12\years) had no immediate effect on serum gonadotropins, but was followed by a delayed rise in FSH (at age 2\m=3/12\\p=n-\4\m=3/12\ years) and LH (at age 2\m=7/12\\p=n-\4\m=4/12\ years) to adult castrate levels. Orchiectomy of older prepubertal (by serum testosterone) or adult males resulted within a few days in a progressive and sustained rise in serum FSH and a more gradual rise in LH. Prepubertal gonadotropin regulation appeared to be sexually dimorphic, since ovariectomy in juvenile females (age 3 months\p=n-\1\m=5/12\ years) was followed by generally elevated, if somewhat erratic, serum FSH values, with a secondary rise in both FSH and LH levels at 2\p=n-\2\m=1/12\ years. In both sexes, prepubertal castration caused a significant and sustained decline in serum concentrations of oestradiol; castrated males also showed a decline in serum testosterone levels. Although prepubertal castration also caused in both sexes a slight decline in serum oestrone, and ovariectomy a decline in serum androstenedione and dihydrotestosterone, these effects were not sustained one year later, and values were not significantly different from sham-operated controls. Taken together, these data lend support to a model of primate sexual maturation in which the primary regulator of gonadotropin secretion in both sexes during the prolonged juvenile phase is central inhibition of the hypothalamic GnRH regulator. However, during foetal and neonatal life, and again following the onset of puberty, the major modulator of gonadotropin secretion becomes sex steroid-mediated feedback inhibition.During primate sexual maturation, a character¬ istic triphasic and sexually dimorphic temporal pattern in circulating gonadotropin concentra¬ tions occurs, which is imposed by the interaction of two regulatory mechanisms: central inhibition of hypothalamic gonadotropin releasing hormone (GnRH) neurosecretion, and the feedback effects of sex steroids in the circulation (Winter et al.

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“…This is because of the early activation of Leydig cell precursors which are capable of responding to luteinizing hormone (LH) stimulation with testosterone secretion ( Chemes et al ., 198 5, 1992; Cigorraga et al ., 1994 ; Chemes, 1996). These precursors are responsible for testosterone production during infancy when differentiated Leydig cells are absent from the intertubular spaces ( Forti et al ., 1981 , Chemes, 1996). Leydig cell precursors can be defined on the basis of their ability to produce discrete amounts of testosterone and/or to exhibit typical Leydig cell markers such as 3β hydrosysteroid dehydrogenase ( Pelliniemi et al ., 1981 ; Chemes et al ., 1992 ; Cigorraga et al ., 1994 ).…”

Section: Leydig Cell Changes In Infancymentioning

confidence: 99%

Infancy is not a quiescent period of testicular development

Chemes¹

2001

Int J of Andrology

152

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Postnatal evolution of the testis in most laboratory animals is characterized by the close continuity between neonatal activation and pubertal development. In higher primates, infancy, a long period of variable duration, separates birth from the beginning of puberty. This period has been classically considered as a quiescent phase of testicular development, but is actually characterized by intense, yet inapparent activity. Testicular volume increases vigorously shortly after birth and in early infancy due to the growth in length of seminiferous cords. This longitudinal growth results from active proliferation of infantile Sertoli cells which otherwise display a unique array of functional capabilities (oestrogen and anti-müllerian hormone secretion, increase of FSH receptors and maximal response to FSH). Leydig cells also show recrudescence after birth, possibly determined by an active gonadotrophic-testicular axis which results in increased testosterone secretion of uncertain functional role. This postnatal activation slowly subsides during late infancy when periodic phases of activation of the hypothalamo-pituitary-testicular axis are paralleled by incomplete spermatogenic spurts. The beginning of puberty is marked by the simultaneous reawakening of Leydig cell function and succeeding phases of germ cell differentiation/degeneration which ultimately lead to final spermatogenic maturation. The marked testicular growth in this stage is due to progressive increase at seminiferous tubule diameter. Sertoli cells, which have reached mitotic arrest, develop and differentiate, establishing the seminiferous tubule barrier, fluid secretion and lumen formation, and acquiring cyclic morphological and metabolic variations characteristic of the mature stage. All of these modifications indicate that, far from being quiescent, the testis in primates experiences numerous changes during infancy, and that the potential for pubertal development and normal adult fertility depends on the successful completion of these changes.

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Spermatic and Peripheral Plasma Concentrations of Testosterone and Androstenedione in Prepubertal Boys

Cited by 25 publications

References 10 publications

Response to a Single Dose of Human Chorionic Gonadotropin in Prepubertal Boys*

Response to a Single Dose of Human Chorionic Gonadotropin in Prepubertal Boys*

The role of gonadal steroids in feedback regulation of gonadotropin secretion at different stages of primate development

Infancy is not a quiescent period of testicular development

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