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Testosterone secretion

Molecular studies explained this apparent paradox when the temperature-sensitive G a Ala366Ser mutation of the G a protein was identified. At 32°C, the G a 366Ser mutation results in the constitutive cAMP accumulation that causes the testosterone secretion that is the hallmark of the testotoxicosis phenotype. At 37°C, however, the G a 366Ser mutation results in loss of adenylyl cyclase signaling, causing PHP-Ia. As a result, a single mutation that performs differently in different tissues causes precocious puberty and abnormalities of PTH and TSH (91). [Pg.123]

Ethanol oxidation, via alcohol dehydrogenase, reduces testosterone secretion, due to a high NADH/NAD ratio is the Leydig cells in the testes. [Pg.328]

The explanation for this phenomenon is that in the prepubertal phase the amount of testosterone that is secreted is not sufficient to cause development of the male genitalia, which is normally stimulated by dihydrotestosterone. However, at puberty the secretion of testosterone increases. The increase is large in this syndrome, because lack of dihydrotestosterone decreases the extent of the feedback inhibition of the hormone secretions by the pituitary so that more gonadotrophins are released which stimulate, markedly, the rate of testosterone secretion and hence its concentration in the blood. At these high levels, testosterone has sufficient androgenic effects to stimulate development of the external genitalia. [Pg.439]

Luteinizing hormone (LH) Glycoprotein, MW 28,500 very similar to TSH Gonadotropin-releasing hormone (GuRH) pyro-Glu-His-Trp- Ser-Tyr-Gly-Leu-Arg-Pro-Gly-NH2b Unknown Causes ovulation in female and testosterone secretion in male... [Pg.395]

The 17-KSs are metabolites of precursors secreted by the adrenal glands, the testes, and to some extent the ovaries. In men, approximately one third of the total urinary 17-KSs represent metabolites of testosterone secreted by the testes, whereas most of the remaining two thirds are derived from the steroids produced by the adrenal glands. In women, who normally excrete smaller quantities than men, the total 17-KS concentrations are derived almost exclusively from the adrenal glands. [Pg.2134]

Synthetic GnRH Agonists Synthetic derivatives of GnRH with more biological activity than the native hormone have been used for the suppression of spermatogenesis after 2 or more weeks of treatment that downregu-lated GnRH receptors in the anterior pituitary. However, in most trials there was no uniform induction of azoospermia, probably because the reduction of LH and testosterone secretion was incomplete. [Pg.790]

GnRH antagonist directly competes with GnRH receptors in pituitary, suppressing LH and FSH production, and reducing testosterone secretion by testes... [Pg.2314]

Gestation is the period during which each individual s sexuality is first expressed and shaped. But impact on the organization of fetal sexuality seems to be most effective during certain sensitive gestational periods, windows of vulnerability. The exact periods for human behavioral effects of sex hormones remain unknown. The period 8—24 weeks of gestation may be most critical because that s when testosterone secretion surges in male fetuses, but there may be multiple sensitive... [Pg.152]


See other pages where Testosterone secretion is mentioned: [Pg.1361]    [Pg.1367]    [Pg.469]    [Pg.490]    [Pg.845]    [Pg.854]    [Pg.438]    [Pg.252]    [Pg.650]    [Pg.872]    [Pg.35]    [Pg.99]    [Pg.313]    [Pg.161]    [Pg.171]    [Pg.177]    [Pg.185]    [Pg.425]    [Pg.425]    [Pg.344]    [Pg.345]    [Pg.248]    [Pg.119]    [Pg.182]    [Pg.185]    [Pg.312]    [Pg.307]    [Pg.2097]    [Pg.564]    [Pg.2424]    [Pg.2432]    [Pg.75]    [Pg.282]    [Pg.2]    [Pg.399]    [Pg.156]    [Pg.35]    [Pg.1012]    [Pg.1012]    [Pg.1016]    [Pg.1016]   
See also in sourсe #XX -- [ Pg.2015 ]

See also in sourсe #XX -- [ Pg.1012 , Pg.1013 ]

See also in sourсe #XX -- [ Pg.158 ]




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