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Testosterone

About: Testosterone is a research topic. Over the lifetime, 23258 publications have been published within this topic receiving 808079 citations. The topic is also known as: 4-androsten-17beta-ol-3-one & 4-Androsten-3-one-17b-ol.


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Journal ArticleDOI
TL;DR: The results strongly suggest that the sex differences that have been observed in morphine-induced analgesia are due to the organizational effects of sex steroids in the developing rat brain, rather than their acute activational effects in adulthood.
Abstract: The purpose of the present studies was to determine the role of either the organizational or activational sex steroids in mediating the sex differences observed in morphine-induced antinociception in the rat. To examine the organizational aspects, male pups were castrated at postnatal days 1 and 2; females were masculinized by large doses of testosterone on postnatal days 1 and 2. Adult male and female rats were also castrated over a period of 2 months to examine the role of the acute activational effects of the opiates in the already sexually differentiated adult rat brain. The results of these studies demonstrate that there were no alterations in the sex differences in opiate analgesia in castrated adult male and female rats; thus, male- and female-specific responses to opiate-induced antinociception were maintained even in the absence of the acute membrane-mediated effects of sex steroids. On the other hand, in male rats, castrated at postnatal days 1 and 2, the morphine dose-response curve shifted markedly to the right and, in fact, was almost identical to that observed in untreated females. Conversely, in female rats, masculinized by large doses of testosterone early in prenatal life, the morphine dose-response curve shifted to the left, yielding a dose-response curve that resembled that in normal males. These results strongly suggest that the sex differences that have been observed in morphine-induced analgesia are due to the organizational effects of sex steroids in the developing rat brain, rather than their acute activational effects in adulthood.

143 citations

Journal ArticleDOI
TL;DR: It is postulate that endogenous estrogens play a facilitatory role in neuroendocrine control of the somatotropic axis during puberty in boys and that any stimulatory role of androgens on GH secretion is exerted primarily through the estrogen receptor after aromatization.
Abstract: The increase in GH production during the male adolescent growth spurt has been attributed to both androgen and estrogen receptor-mediated processes. To evaluate the role of endogenous estrogens in the control of GH secretion, we administered the estrogen receptor antagonist tamoxifen to 10 late pubertal males. Blood samples were obtained for GH determination at 10-min intervals on 2 occasions during the last 24 h of a 4-day course of either tamoxifen or placebo. Waveform-specific, multiple parameter deconvolution analysis was employed to assess GH secretory and elimination dynamics. Estrogen receptor blockade resulted in a significant (P < 0.05) diminution in mean 24-h serum GH concentrations, from 3.9 +/- 1.0 (placebo; mean +/- SEM) to 2.7 +/- 0.6 micrograms/L (tamoxifen). This was associated with a significant (P < 0.01) decline in the GH production rate [237 +/- 55 vs. 155 +/- 33 micrograms/L GH distribution volume (Lv).24 h]. Furthermore, this reduction in GH secretion was the result of significant de...

143 citations

Journal ArticleDOI
TL;DR: It is demonstrated that sex steroid hormone levels are correlated with diversity and gut microbial composition, and provide fundamental information helpful for developing communication networks between human and microbial communities.

143 citations

Journal ArticleDOI
TL;DR: Gossypol acetic acid administered orally at 30 mg/kg body weight/day for five weeks inhibited the fertility of male rats without an apparent loss of libido, and degeneration in the tail region of epididymal spermatozoa revealed.
Abstract: Gossypol acetic acid administered orally at 30 mg/kg body weight/day for five weeks inhibited the fertility of male rats without an apparent loss of libido. Sperm in the ejaculate were rendered immotile and were reduced in number. Serum testosterone and LH were reduced significantly from pretreatment values, whereas FSH values were not altered. Leydig cells from treated animals produced less testosterone than did control Leydig cells when incubated with LH. Furthermore, testosterone production by normal Leydig cells that were incubated with LH and gossypol was inversely related to gossypol concentration. Ultrastructural examination of epididymal spermatozoa revealed degeneration in the tail region, particularly in the mitochondrial sheath of the middle piece. Within the seminiferous epithelium, late spermatids displayed a similar degeneration, although not as severe. After a six-week recovery period, normal fertility was re-established and normal litters were produced. Sperm motility and number, serum testosterone and LH levels, and sperm structure all returned to normal.

143 citations

Journal ArticleDOI
TL;DR: It is shown that the absence of androgen receptor expression in Sertoli cells underlies a physiological stage of androgens insensitivity within the male gonad in the fetal and early postnatal periods.
Abstract: From fetal life to adulthood, the testis evolves through maturational phases showing specific morphologic and functional features in its different compartments. The seminiferous cords contain Sertoli and germ cells, surrounded by peritubular cells, and the interstitial tissue contains Leydig cells and connective tissue. Sertoli cells secrete anti-Mullerian hormone (AMH), whereas Leydig cells secrete androgens. In the fetal and early postnatal testis, Leydig cells actively secrete androgens. Sertoli cells are morphologically and functionally immature--e.g., they secrete high levels of AMH--and germ cells proliferate by mitosis but do not enter meiosis. During infancy and childhood, Leydig cells regress and testosterone secretion declines dramatically. Sertoli cells remain immature and spermatogenesis is arrested at the premeiotic stage. At puberty, Leydig cells differentiate again, and testosterone concentration increases and provokes Sertoli cell maturation--e.g., down-regulation of AMH expression--and germ cells undergo meiosis, the hallmark of adult spermatogenesis driving to sperm production. An intriguing feature of testicular development is that, although testosterone production is as active in the fetal and early postnatal periods as in puberty, Sertoli cells and spermatogenesis remain immature until pubertal onset. Here, we review the ontogeny of the androgen receptor expression in the testis and its impact on Sertoli cell maturation and the onset of pubertal spermatogenesis. We show that the absence of androgen receptor expression in Sertoli cells underlies a physiological stage of androgen insensitivity within the male gonad in the fetal and early postnatal periods.

143 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
20224
2021509
2020435
2019438
2018456
2017505