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.

Mood, sexuality, hormones, and the menstrual cycle. II. Hormone levels and their relationship to the premenstrual syndrome.

Abstract: In women with premenstrual syndrome, negative changes start soon after ovulation gradually increasing as the corpus luteum develops, and reach a maximum during the last 5 days of the luteal phase. They decline rapidly once menstruation starts, disappearing within one or two days of ovarian steroids reaching baseline levels. Positive moods are at maximum when preovulatory estradiol reaches its peak. A comparison of hormone levels in women with high and low degrees of cyclical mood change showed no difference in progesterone, estradiol, testosterone, or androstenedione.

Concentrations of putrescine and polyamines and their enzymic synthesis during androgen-induced prostatic growth.

Abstract: 1 Castration of adult rats resulted in marked decreases in the amounts of putrescine, spermidine and spermine in the ventral prostate gland Spermidine concentrations decline rapidly over the first 11 days after androgen withdrawal, reaching a value of only 12% of normal controls Spermine concentrations diminish more slowly, reaching 24% of normal within 11 days The spermidine/spermine molar ratio falls from 09 to 046 under these conditions Putrescine concentrations decrease by 70% at 7 days after castration and then remain constant for some days 2 After daily injections of testosterone propionate to rats castrated 7 days previously, prostatic spermidine and putrescine concentrations increase significantly within 24h; normal or even greater values are observed within 8 and 4 days respectively In contrast, the spermine concentration does not increase until 5 days after commencement of androgen treatment 3 The activities of two enzymes involved in polyamine biosynthesis (ornithine decarboxylase and a putrescine-activated S-adenosyl-l-methionine decarboxylase system) were greatly decreased soon after castration: after 7 days the respective values were 15% of normal for ornithine decarboxylase and 7% of normal for putrescine-dependent decarboxylation of S-adenosyl-l-methionine Injection of testosterone propionate into animals castrated 7 days previously induced a rapid increase in both enzymic activities: ornithine decarboxylase was doubled in 6h, and increased three- to four-fold within 48h, whereas the putrescine-dependent decarboxylation of S-adenosyl-l-methionine doubled in 3h and increased tenfold within 48h of commencement of daily androgen treatments 4 The activity of these enzyme systems was very low in the ventral prostates of hypophysectomized rats and was increased by administration of testosterone in a manner similar to that found in castrated rats 5 Alterations in the activity of two ventral-prostate enzymes involved in ornithine production (arginase) and utilization (ornithine-2-oxoglutarate transaminase) that result from changes in the androgenic status of rats are described 6 The findings presented suggest that the activities of ornithine decarboxylase and the putrescine-dependent S-adenosyl-l-methionine decarboxylase system, rather than ornithine concentrations, are rate-limiting for the formation of putrescine and polyamines in rat ventral prostate 7 The relation of polyamines to androgen-induced prostatic growth is discussed with particular reference to the biosynthesis of proteins and nucleic acids

Sex Steroids and All-Cause and Cause-Specific Mortality in Men

Abstract: Background: Sex steroid levels are related to metabolic outcomes that could convey higher risk of premature death. Methods: We examined whether total or free testosterone, dihydrotestosterone, and sex hormone–binding globulin levels are related to all-cause or cause-specific mortality in men. Data were obtained from the Massachusetts Male Aging Study, a population-based cohort study of 1709 men aged 40 to 70 years. Men were followed up for all-cause and cause-specific mortality. Results: Complete data were available for 1686 men, with 395 deaths occurring during 15.3 years of follow-up. With age adjustment, dihydrotestosterone and sex hormone– binding globulin levels were associated with ischemic heart disease mortality, and free testosterone level was associated with respiratory mortality. In multivariateadjusted models, higher free testosterone (P=.02) and lower dihydrotestosterone (P=.04) levels were significantly associated with ischemic heart disease mortality, although the latter association was not robust to differences in model selection. The relative risk of death from ischemic heart disease per 1-SD lower free testosterone level was 0.80 (95% confidence interval, 0.64-0.99). Free testosterone level was significantly associated with respiratory mortality (P = .002), with a multivariateadjusted relative risk per 1-SD lower free testosterone level of 1.90 (95% confidence interval, 1.24-2.92). Total testosterone level was unrelated to mortality, and sex hormone–binding globulin was not significantly associated with mortality after multivariate adjustment. Conclusions: In men, endogenous sex steroid levels seem to have relatively weak associations with mortality. These data provide little support for the hypothesis that endogenous sex steroid levels are associated with risk of premature death but suggest that further investigation of the relationship between sex steroids and mortality from ischemic heart disease and respiratory disease may be warranted.