Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “testosterone secretion”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,531 records · Page 85Linked to original sources
PubMed1992

Steroid hormones and gonadotropins in a case of ovarian endometriosis associated with virilization.

The clinical course, the hormone secretion, the testosterone receptors and the enzymatic activities related to androgen metabolism in a 56-year-old postmenopausal woman with a history of virilization and ovarian endometrioma are reported. Unexpectedly, at the time of examination, no evidence of biochemical hyperandrogenism was obtained. The uncommon association of virilization and ovarian endometrioma simulating a functioning tumor of the ovary is discussed.

Endometriosis↗
PubMed1983

Endocrine changes associated with onset of spermatogenesis in Holstein bulls.

After birth, a bull enters a period of infancy during which the reproductive organs are relatively quiescent. This is followed by the prepubertal period, which starts at 10 to 12 wk in well-fed Holstein bulls, characterized by profound changes of hypothalamic, pituitary, and gonadal function that culminate in puberty. The prepubertal sequence of events probably is: a) initiation of spontaneous discharge of luteinizing hormone; b) hormone induced differentiation of Leydig cells with increased secretion of androstenedione in response to luteinizing hormone stimulation; c) further differentiation of Leydig cells resulting in luteinizing hormone-stimulated secretion of testosterone; d) testosterone-induced differentiation of indifferent supporting cells to Sertoli cells concomitant with testosterone-induced differentiation of gonocytes to prespermatogonia and A-spermatogonia; e) increased sensitivity of the hypothalamus-anterior pituitary to negative feedback of gonadal steroids; f) diminished frequency and amplitude of luteinizing hormone discharge; g) formation of junctional complexes between Sertoli cells and establishment of the blood-testis barrier; h) formation of primary spermatocytes and ultimately spermatids and spermatozoa; and i) continued increase of efficiency of spermatogenesis until sufficient sperm are produced to provide the first ejaculum around 37 to 38 wk. Following puberty, the reproductive capacity of a bull increases for several years until the male is sexually mature.

Animals↗
PubMed1995

The effect of epitestosterone on spermatogenesis in rats.

The effect of 3-week treatment with increasing doses of endogenous steroid with antiandrogenic properties, epitestosterone (ET), on the spermatogenesis was studied in adult male rats by flow cytometry and correlated with the effect on gonadotropin gene expression and secretion, on testosterone and dihydrotestosterone plasma levels and on the weight of testes and prostates. Epitestosterone was administered to the rats by means of silastic capsules of different lengths filled with the steroid. A decrease of the number of total spermatides in the epitestosterone treated animals was observed. In the group with the lowest dose of ET the number of elongated spermatides was significantly reduced. The number of germ cell types and their relative proportions were correlated with the endocrine parameters reported previously. Significant negative correlation between the pituitary content of LH and total number of germ cells per 1 g of testicular tissue and of the number of spermatides/g and between testosterone level in serum and the number of diploid cells in the animals treated with higher doses of ET was found. In the group with highest ET dose a negative correlation of diploid cells and serum dihydrotestosterone was observed, too. The naturally occurring antiandrogen epitestosterone can be considered as one of the endogenous factors influencing spermatogenesis.

Journal Article↗
PubMed2001

[Proliferation and differentiation of regenerating Leydig cells following ethylene dimethane sulfonate exposure in rats].

Cell type of mammalian testis which is involved in the synthesis and secretion of testosterone and the maintenance of spermatogenesis are the fully differentiated interstitial Leydig cells (LC). Their ultrastructure possesses the typical characteristics of steroid-producing cells. It has been generally accepted that two waves of proliferation and differentiation can be discerned during the development of the Leydig cell population in the rodent and human testis. Treatment with ethane dimethane sulphonate (EDS) destroys selectively LC. A new LC population develops in the following weeks and this model has been used by us to study the proliferation and differentiation of new LC. Our results support the suggestion that the regeneration of a new LC population following EDS administration shows many similarities with the formation of the adult type LC in the prepubertal mammalian testis.

Animals↗
PubMed2001

Immunohistochemical observation on luteinizing hormone in rat testes before and after testicular capsulotomy.

AIM: In the testicular capsulotomized rats, although there was a significant increase in the luteinizing hormone (LH) levels, the secretion of testosterone remained low. In order to clarify the mechanisms of this phenomenon, the binding of endogenous LH to the testes were observed before and after testicular capsulotomy. METHODS: Peroxidase-antiperoxidase (PAP) method was used to detect the binding of LH to the testes in rats. RESULTS: An intense positive staining of LH was found in the Leydig cells of both the normal and sham-operated control testes. However, at 40 d after operation, the LH immunoreactivity was decreased in the Leydig cells of the capsulotomized testis. By d 60, only very weak positive staining could be observed in these cells. CONCLUSION: A progressive reduction of endogenous LH binding to the testis cccurred in the capsulotomized rat.

Animals↗
PubMed2002

[Inactivating and activating mutations of the human LH/hCG receptor leading to male pseudohermaphroditism and familial male-limited precocious puberty].

The human luteinizing hormone/chorionic gonadotropin receptor(LHR) plays an important role in normal reproductive function in humans. Binding of LH to the LHR triggers production of intracellular c-AMP resulting in transcriptional activation of LH responsive genes. Mutations of the human LHR receptor lead to the development of three clinical conditions, namely, Leydig cell hypoplasia, hypergonadotropic hypogonadism and primary amenorrhea, and familial male-limited precocious puberty(FMPP). These mutations cause the receptor to lose its signal transduction activity in the first two conditions and to gain constitutive activity in the third condition. Leydig cell hypoplasia is an autosomal recessive disorder leading to male under-virilization. FMPP is an autosomal dominant disorder, characterized by excessive secretion of testosterone by Leydig cells and pubertal development at a very young age. Sporadic cases are also reported.

Disorders of Sex Development↗
PubMed2006

Establishing sexual dimorphism in humans.

Sexual dimorphism, i.e. the distinct recognition of only two sexes per species, is the phenotypic expression of a multi-stage procedure at chromosomal, gonadal, hormonal and behavioral level. Chromosomal--genetic sexual dimorphism refers to the presence of two identical (XX) or two different (XY) gonosomes in females and males, respectively. This is due to the distinct content of the X and Y-chromosomes in both genes and regulatory sequences, SRY being the key regulator Hormones (AMH, testosterone, Insl3) secreted by the foetal testis (gonadal sexual dimorphism), impede Müller duct development, masculinize Wolff duct derivatives and are involved in testicular descent (hormonal sexual dimorphism). Steroid hormone receptors detected in the nervous system, link androgens with behavioral sexual dimorphism. Furthermore, sex chromosome genes directly affect brain sexual dimorphism and this may precede gonadal differentiation.

Animals↗
PubMed2006

[Male hormonal contraception].

Human reproduction is a complex phenomenon remaining at the center of interest of many medical and extra-medical disciplines and the search for new contraceptive methods is an important part of research effort. The development of effective forms of male hormonal contraception (MHC) is one of the priorities of the World Health Organization (WHO Task Force on Methods of Regulation of Male Fertility). The principle of MHC consists in the suppression of spermatogenesis while preserving all other functional aspects of the male glands (especially the sexual functions, bone metabolism and lean muscle mass). It is possible to stop spermatogenesis by blocking gonadotrophin (FSH and LH) secretion by testosterone administration (isolated or in combination with other hormones). The currently existing variants of MHC are based on testosterone application (which has in the same time the role of substitutive treatment--the so-called androgen "add-back") either in monotherapy (oral, intramuscular, transdermal and subcutaneous form) or in combination with various progestins (levonorgestrel, norethisterone, desogestrel, eronogestrel, medroxyprogesterone), antiandrogens or GnRH analogues. The most promising, at present, seem to be the methods which use a combination of depot testosterone preparations with long-acting progestins. To what extent will the role of MHC be important in the future--this can only be judged after establishing their effectiveness, full reversibility, safe application, acceptability, and financial accessibility in clinical practice.

Contraceptive Agents, Male↗
PubMed1989

Physiology of puberty.

Adolescence represents the period of important somatic changes which lead to sexual maturation, pubertal growth and active functions of reproduction. Mean ages of onset of puberty are 10.9 and 11.2 in girls and boys respectively. Menarche occurs at a mean age of 13.4 yr and may be related to a critical weight. In boys, testicular growth above 4 cm2 or 4 ml is the first clinical sign of gonadal pubertal maturation. In girls, the first sign is the budding of the breast. At onset of puberty, the hypothalamus after a "quiescent" period resumes a marked pulsatile secretion of gonadotrophin-releasing hormone, leading to an increased secretion of pituitary gonadotropins which in turn stimulate the gonadal functions, i.e. the secretion of testosterone or estradiol and maturation of the spermatogenesis or the ovarian follicle. Neuroendocrine factors which probably control the onset of puberty are numerous: cerebral adrenergic and/or dopamine neurotransmitters, endogenous opioids, melatonin from the pineal gland. Gonadal maturation (gonadarche) is preceded in the infant by a post-natal surge of luteinizing hormone and at age 7 to 8 yr by an adrenal maturation (adrenarche).

Adolescent↗
PubMed1987

Influence of hormonal imprinting on hormone level. Permanent receptor damaging effect of pituitary hormones administered to newly-hatched cockerels.

The overlapping effect of TSH and FSH on the gonad and on the thyroid gland can be demonstrated in cockerels even at the age of five weeks. These hormones influence the secretion of testosterone in a similar way and to a similar extent, while on the thyroxine level the influence of the specific hormone is more pronounced. Neonatal FSH and TSH treatment considerably decreased the basal testosterone level measured at the age of five weeks. Neonatal FSH treatment increased the basal T4 level while TSH treatment decreased it. The effect of TSH treatment administered at the age of five weeks in increasing the testosterone level was weakened after neonatal pretreatment with any iodine hormone. The effect of TSH treatment could only be inhibited by neonatal FSH pretreatment. Neonatal pretreatment with any of the trophormones caused a diminution of the T4 level augmenting of FSH and TSH administered at the age of five weeks.

Animals↗
PubMed1987

Normal sexual maturation.

Puberty represents a period of important changes which lead to sexual maturation and active functions of reproduction. Sequences of the somatic and hormonal changes are presented both in boys and girls. Mean ages of onset of puberty are 10.9 and 11.2 in girls and boys, respectively. Menarche occurs at a mean age of 13.4 years and may be related to a critical weight. In boys, testicular growth above 4 cm2 or 4 ml is the first clinical sign of gonadal pubertal maturation. In girls, the first sign is the budding of the breast. At onset of puberty, the hypothalamus resumes a marked pulsatile secretion of gonadotropin-releasing hormone, leading to an increased secretion of pituitary gonadotropins which in turn stimulate the gonadal functions, i.e. the secretion of testosterone or estradiol and maturation of the spermatogenesis or the ovarian follicle. Neuroendocrine factors which probably control the onset of puberty are numerous: adrenergic or dopamine neurotransmitters, endogenous opioids, melatonin from the pineal gland. Gonadal maturation (gonadarche) is preceded in the infant by a postnatal surge of luteinizing hormone and at age 7-8 years by an adrenal maturation called adrenarche.

Adolescent↗
PubMedDate not supplied

[Male pseudohermaphroditism. State and present problems (author's transl)].

The authors describe the male phenotypic sexual development in the fetus: transformation of the undifferentiated gonad into testis under the HY antigen influence; testicular secretion of testosterone (which allows the development of the wolffian ducts derivatives) and of MIF (which inhibits the development of the mullerian duct; masculinization of the external genitalia under the influence of dihydrotestosterone. They outline the three abnormalities which may lead to a male pseudohermaphroditism: disorders of testicular differentiation, defects of testicular function and androgen insensitiveness at the target areas. They consider the diagnostic steps and the therapeutic management especially in relation to the choice of the sex and the risk of gonadoblastoma.

Androgens↗