Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of aging on serum LH and testosterone (T) pulse frequency and gonadotroph sensitivity to androgen and estrogen feedback was studied in young (less than 55 yr old) and elderly (greater than 65 yr) Trappist monks. LH pulse frequency (sampling interval, 20 min) was significantly lower [0.25 +/- 0.03 (+/- SEM) vs. 0.38 +/- 0.02 pulses/h; P less than 0.01] in elderly (n = 21) than in young monks (n = 27); the pulse amplitudes were similar. Similarly, T pulse frequency was lower in the elderly than in the young monks (0.13 +/- 0.04 vs. 0.23 +/- 0.02 pulses/h; P less than 0.01). In elderly men, the hypothalamo-pituitary complex was more sensitive to 5 alpha-androstan-17 beta-ol-3-one feedback, as determined by the decrease in serum LH and T levels. Moreover, during 5 alpha-androstan-17 beta-ol-3-one (125 mg/day, percutaneously, for 10 days) administration, the LH response to LHRH (100 micrograms, iv) was significantly higher in the elderly men compared to the pretreatment response. During estradiol (1.5 mg/day, percutaneously for 10 days) administration, the LH response to LHRH was decreased in the elderly men, but unchanged in the young men, suggesting greater responsiveness to estradiol in the elderly men. We conclude that in aged men, decreased testicular androgen secretion is not exclusively the consequence of a primary testicular alteration, but that important changes occur in hypothalamo-pituitary function, specifically decreased LH pulse frequency and increased LH responsiveness to sex hormone feedback.
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PMID:Influence of age on pulsatile luteinizing hormone release and responsiveness of the gonadotrophs to sex hormone feedback in men. 353 84

Cycling standardbred mares were infused with saline or 20 micrograms gonadotropin-releasing hormone (GnRH) in a pulsatile pattern (one 5-sec pulse/h, 2 h or 4 h) beginning on Day 16 of the estrous cycle. Although serum concentrations of luteinizing hormone (LH) increased significantly earlier in all three GnRH-treated groups (within one day of the initiation of infusion) compared to saline-infused controls, there were no differences in peak periovulatory LH concentrations among treatments (overall mean +/- SEM, 8.98 +/- 0.55 ng/ml). The number of days from the start of treatment to ovulation was significantly less in mares infused with 20 micrograms GnRH/h (mean +/- SEM, 2.9 +/- 0.6 days after the initiation of treatment, or 18.9 days from the previous ovulation; N = 7) compared to mares treated with saline (5.9 +/- 0.3 days, or 21.9 days from previous ovulation; N = 7) or 20 micrograms GnRH per 4 h (5.4 +/- 0.9 days or 21.4 days from previous ovulation; N = 5). Although mares infused with 20 micrograms GnRH/2 h ovulated after 4.3 +/- 0.7 days of treatment (Day 20.3; N = 7), this was not significantly different from either the control or 20 micrograms GnRH/h treatment groups. Neither the duration of the resulting luteal phase nor the length of the estrous cycle was different between any of the treatment groups (combined means, 14.7 +/- 0.2 days and 21.3 +/- 0.4 days, respectively). We conclude that pulsatile infusion of GnRH is effective in advancing the time of ovulation in cycling mares, but that the frequency of pulse infusion is a critical variable.
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PMID:Pulsatile administration of gonadotropin-releasing hormone advances ovulation in cycling mares. 354 34

To explore further the relationship of gonadal sex steroids to the rise in somatomedin-C (Sm-C) during puberty, we studied a group of children with true precocious puberty before and after treatment which suppressed sex steroid output. Plasma estradiol and testosterone and serum acid-ethanol-extractable Sm-C were determined by specific RIAs in 7 boys and 12 girls with true precocious puberty before and at regular intervals during treatment with a potent LHRH-agonist (LHRH-A), D-Trp6-Pro9-NEt-LHRH. For comparison, Sm-C and sex steroid concentrations were determined in 266 normal adolescents and 37 normal prepubertal children, 1-9 yr of age. The mean +/- SEM Sm-C levels in normal male individuals peaked at 15 yr (2.46 +/- 0.23 U/ml) and at pubertal (genital) stage III (2.29 +/- 0.19 U/ml), and those in normal females reached their highest concentration at 12-15 yr of age and at pubertal (breast) stage III (2.47 +/- 0.15 U/ml). Sm-C concentrations correlated better with pubertal (genital or breast) stage than with chronological age for both sexes and better with testosterone levels in males than with estradiol levels in females. The mean +/- SEM Sm-C concentrations in both males and females with true precocious puberty were 2.07 +/- 0.16 U/ml before therapy and decreased significantly to 1.52 +/- 0.13 U/ml after 6 months of therapy. The mean Sm-C level of the patients remained significantly elevated for chronological age, but decreased into the normal range for bone age after 6-12 months of therapy. Sm-C correlated significantly with testosterone and estradiol levels, but not with growth rate. Mean nighttime GH secretion decreased significantly after 6 months of LHRH-A therapy. In summary, children with true precocious puberty have Sm-C elevations typical of normal puberty. The decrease in Sm-C levels after suppression of gonadal sex steroid output with LHRH-A is evidence that sex steroids are necessary to induce this elevation in Sm-C concentration. The decrease in GH secretion during LHRH-A therapy suggests that the effect of sex steroids on Sm-C levels during normal puberty is mediated, at least in part, through stimulation of GH secretion.
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PMID:Somatomedin-C in normal puberty and in true precocious puberty before and after treatment with a potent luteinizing hormone-releasing hormone agonist. 388 35

This experiment determined whether pulsatile administration of gonadotropin-releasing hormone (GnRH) would induce estrus and ovulation in seasonally anestrous primiparous sows and compared endocrine responses of GnRH-induced sows with those of primiparous sows that exhibited spontaneous estrus after weaning. Seventeen primiparous Landrace X Large White sows farrowed in August 1982, lactated 23.8 +/- 0.4 days (mean +/- SEM), and weaned 9.0 +/- 0.3 pigs per litter. Blood for determination of progesterone, luteinizing hormone (LH), and estradiol-17 beta (E) was collected every 6 h from 1 day before to 12 days after weaning. Twelve sows exhibited spontaneous estrus 135 +/- 9 h after weaning, and these sows were considered to be normal. Five sows were anestrous for at least 23 days postweaning and failed to ovulate, as indicated by concentrations of progesterone that were less than 1.0 ng/ml in blood samples collected daily during this period. From Day 0 to Day 30 postweaning, levels of estradiol in anestrous sows varied between 3 and 30 pg/ml, concentrations of LH were low, and preovulatory-like LH surges did not occur. Beginning on Day 30 postweaning, four anestrous sows were given 1.5 micrograms GnRH (i.v.) hourly until onset of estrus and blood was collected every 6 h during GnRH treatment. The average interval from beginning of GnRH treatment to onset of estrus was 84 +/- 5 h (range 72 to 96 h). Patterns of estradiol and LH secretion around estrus were similar in normal sows and those treated with GnRH.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pulsatile administration of gonadotropin-releasing hormone to anestrous sows: endocrine changes associated with GnRH-induced and spontaneous estrus. 389 3

To examine the hypothesis that the frequency of endogenous pulsatile LHRH stimulation controls the relative secretion of FSH and LH from the pituitary, we studied men with elevated FSH levels and normal LH levels to determine whether they have an altered frequency of pulsatile LHRH secretion compared to normal men. Because peripheral blood measurements of LHRH do not reflect the pulsatile characteristics of hypothalamic LHRH secretion, and it is generally accepted that the pulse frequency of LH secretion is an index of the frequency of endogenous LHRH pulsation, we used LH pulse frequency as the indicator of LHRH pulse frequency. Frequent blood sampling was performed to characterize LH pulse patterns in five men with selective elevations of FSH and seven age-matched normal men. Beginning at 0800-0930 h, blood samples were obtained every 10 min for 24 h through an indwelling iv catheter. Serum LH and FSH levels were measured by RIA in each sample, and the pattern of LH secretion was determined. Testosterone (T), estradiol, sex hormone-binding globulin, and free T were measured in a pooled serum sample from each man. Men with selective elevations of FSH had fewer LH pulses per 24 h (mean +/- SEM, 10.6 +/- 0.5) than the control group (12.9 +/- 0.6; P less than 0.01). There was no statistically significant difference in LH pulse amplitude (23 +/- 4 vs. 17 +/- 3 ng/ml). There were no statistically significant differences in T (4.9 +/- 0.5 vs. 6.1 +/- 0.5 ng/ml), estradiol (23 +/- 7 vs. 31 +/- 5 pg/ml), sex hormone-binding globulin (7.7 +/- 1.4 vs. 7.7 +/- 1.2 ng bound dihydrotestosterone/ml), or free T (0.16 +/- 0.02 vs. 0.23 +/- 0.04 ng/ml) in these men vs. normal subjects. We conclude that 1) compared to normal men, men with selectively elevated FSH levels have decreased LH pulse frequency, which suggests decreased LHRH pulse frequency; and 2) the relative secretion rates of LH and FSH by the pituitary may be regulated by the frequency of pulsatile LHRH secretion from the hypothalamus.
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PMID:Evidence for decreased luteinizing hormone-releasing hormone pulse frequency in men with selective elevations of follicle-stimulating hormone. 391 66

The effects of fetal exposure to spironolactone (SPL), an aldosterone antagonist with weak antiandrogen and gestagen properties, upon the pituitary-gonadal axis were studied in the offspring of rats that had been treated daily from gestation day 14 to day 20 with 10 or 20 mg SPL or the solvent vehicle (for controls). At 70-80 days of age, SPL-exposed rats showed no alterations in external genitalia or in body weight. However, males displayed a dose-dependent decrease in the weights of the ventral prostate and seminal vesicles. Whereas basal and gonadotropin-releasing hormone (GnRH)-induced plasma luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone, and 5 alpha-dihydrotestosterone levels were similar to controls, basal plasma and pituitary prolactin (Prl) levels were reduced (SPL-exposed 6.8 +/- 1.0 vs. controls 15.8 +/- 2.8 ng/ml and 6.1 +/- 1.2 vs. 11.6 +/- 1.8 microgram/anterior pituitary gland; mean +/- SEM). Cytosolic androgen receptors in ventral prostate were nonsignificantly decreased, but they increased after GnRH in contrast to controls. Nuclear androgen receptors were normal. Females displayed normal estrous cycles. Basal and GnRH-induced plasma FSH, Prl, estradiol, and progesterone concentrations were similar to controls, whereas plasma LH was elevated. Estrogen receptors in uterine cytosol were low and increased after GnRH. Ovaries and uteri were enlarged. The present study demonstrates that in utero exposure to SPL leads to endocrine dysfunctions that persist into adulthood. They are characterized in males by hypoprolactinemia, reduced weights of accessory sex organs, and a suggestion of functional modifications of androgen receptors. In females they are characterized by increased LH secretion, increased ovarian and uterine weights, and decreased uterine cytosol estrogen receptors, suggesting enhanced estrogenic action.
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PMID:Modifications of the gonadal function in the adult rat after fetal exposure to spironolactone. 392 11

The basal plasma levels of cortisol, dehydroepiandrosterone (DHEA), DHEA sulfate (DHEA-S), and testosterone were studied in 20 patients with advanced prostatic cancer receiving combined treatment with an LHRH agonist and an antiandrogen [5,5-dimethyl-3-[4-nitro-3-(trifluoromethyl)-phenyl]-2 4-imidazolidinedione]. After 60 days of combined antihormonal therapy, plasma levels of testosterone decreased from 5.44 +/- 0.44 (SEM) to 0.136 +/- 0.052 ng/ml (2.5% of control). Somewhat unexpectedly, the plasma concentrations of the adrenal androgens DHEA and DHEA-S were reduced to 45 +/- 7 and 64 +/- 4% of control, respectively. The maximal reduction in plasma adrenal androgen levels occurred between 2 and 4 weeks of treatment. Whereas the increase in serum cortisol, 17-hydroxypregnenolone, and 17-hydroxyprogesterone concentrations 2 1/2 h after the injection of 0.25 mg human ACTH 1-24 was not affected by the combined treatment, the increment of DHEA and androstenedione after the same stimulus was reduced from 3.1 +/- 0.98 and 0.73 +/- 0.11 to 1.48 +/- 0.5 and 0.31 +/- 0.05 ng/ml, respectively. The reduced levels of serum DHEA and DHEA-S were not due to the LHRH agonist by itself, since similarly low levels of serum DHEA and DHEA-S were found in patients surgically castrated and receiving the same antiandrogen. These data suggest that treatment with an antiandrogen in castrated men inhibit the formation of adrenal androgens due to a blockade at the level of 17, 20-desmolase. The efficiency of the new combined antihormonal therapy (castration and antiandrogen) aimed at complete androgen neutralization in prostate cancer is thus further facilitated.
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PMID:Inhibition of basal and adrenocorticotropin-stimulated plasma levels of adrenal androgens after treatment with an antiandrogen in castrated patients with prostatic cancer. 608 97

Episodic secretion of LH, and the responses of serum LH, alpha-subunit, and testosterone concentrations to the acute administration of LHRH and the chronic administration of the LHRH agonist analog [D-Trp6-Pro9-NEt]LHRH (D-Trp6-Pro9) were evaluated in a 33-yr-old man previously reported to have an LH-secreting pituitary tumor unaccompanied by FSH hypersecretion. Basal serum LH and alpha-subunit concentrations were elevated [57 +/- 0.7 (SEM) mIU/ml (range, 45-71) and 26 ng/ml, respectively]. Frequent sampling revealed six LH secretory spikes over a 24-h period with increments above basal levels varying from 23-40% and interspike intervals ranging from 1.5-5 h. The concentrations of LH or alpha-subunit after iv administration of 150 micrograms LHRH did not increase above these intrinsic LH secretory increments (delta LH: 23%; delta alpha-subunit: 21%). The low basal serum FSH concentrations (3.5 mIU/ml) and elevated basal serum testosterone levels (1480 ng/dl) were unchanged after LHRH. Administration of clomiphene citrate produced no increase in serum LH, FSH, or testosterone concentrations. An attempt was made to decrease LH secretion in this patient using D-Trp6-Pro9. Administration of 200 micrograms daily sc of this LHRH analog for 21 days was associated with increases in serum LH and alpha-subunit concentrations. Mean serum LH and alpha-subunit levels for the 21 days of analog administration were 110 +/- 5.4 (SEM) mIU/ml (range, 70-170) and 64 +/- 3 (SEM) ng/ml (range, 32-84), respectively. During the 9-day period after discontinuance of the LHRH analog, levels of both serum LH and alpha-subunit declined precipitously and mean serum LH and alpha-subunit levels were 58 +/- 7 (SEM) mIU/ml (range, 18-90) and 22 +/- 3 (SEM) ng/ml (range, 12-44), respectively. We conclude that this patient's pituitary tumor has diminished responsiveness to acute LHRH administration and that the effect of chronic D-Trp6-Pro9 is stimulatory rather than inhibitory, as occurs after chronic administration of this analog to normal subjects. The blunted responsiveness to LHRH administration and the lack of response to clomiphene citrate suggest tumor autonomy. The presence of modest paradoxical responsiveness of serum LH and alpha-subunit concentrations during the course of daily D-Trp6-Pro9 administration suggests that central regulatory mechanisms, if present, are abnormal.
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PMID:The luteinizing hormone-releasing hormone (LHRH) agonist [D-Trp6-Pro9-NEt]LHRH increased rather than lowered LH and alpha-subunit levels in a patient with an LH-secreting pituitary tumor. 619 31

Temporal changes of circulating serum hormones were measured to compare the reproductive endocrinology of laying and nonlaying mallards. In this study all sixteen control mallards left with their mates laid eggs, while only one of sixteen mallards stressed by daily movement into new pens, laid eggs. Serum levels of luteinizing hormone (LH), prolactin, estradiol, and progesterone were significantly lower (P less than 0.05) in stressed nonlaying mallards than in laying mallards over the 7-week period. Within 1 week of the rotation treatment, LH concentrations in stressed mallards averaged (means +/- SEM) 2.72 +/- 0.19 ng/ml and were significantly lower (P less than 0.05) than LH levels in the controls (3.62 +/- 0.18 ng/ml). After 7 weeks, injections of luteinizing hormone releasing hormone (LHRH) induced a greater change in circulating LH levels in stressed mallards (2.1 +/- 0.3 ng/ml) than in breeding control mallards (0.9 +/- 0.2 ng/ml). These data demonstrate that the lack of reproduction in stressed mallards was associated with LHRH-sensitive pituitary pools of LH, despite their low concentrations of serum LH. These data suggest that the block in reproduction is a failure of the hypothalamus to produce or release releasing hormones. The serum hormone levels of the control mallards varied temporally with stages in the nesting cycle. LH levels increased with the onset of nesting activity, and showed marked fluctuations during the laying period. LH levels fell at the onset of incubation but increased after loss of clutch. Estradiol levels were highest prior to the laying of the first egg and their peak coincided with the initial nest building behavior of the females. Progesterone levels increased sharply with the laying of the 2nd-4th eggs, decreased sharply with the laying of the 6th egg, and then increased slightly at the end of the nesting cycle. Prolactin levels were initially low but gradually increased with laying and incubation activity, declined with loss of clutch, and increased again with renesting activity. Prolactin levels in the stressed mallards also increased (P less than 0.01) over the 7-week period, but significantly less (P less than 0.05) than in layers.
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PMID:Serum levels of luteinizing hormone, prolactin, estradiol and progesterone in laying and nonlaying mallards (Anas platyrhynchos). 634 Jul 45

We have employed a perifusion technique to explore the time course and specificity of 17 beta-estradiol (E2) effects directly upon luteinizing hormone (LH) release from the isolated rat anterior pituitary under pulsatile luteinizing hormone releasing hormone (LHRH) stimulation. We first characterized the perifusion system and fitted the data to a simple dose-response model. Multiple perifusion studies were then performed with pulses of LHRH at approximately half-maximal response concentration (10(-8) M); LH responses to an initial LHRH pulse (#1) were compared with LH responses to a second LHRH pulse (#2) given at variable times after addition of E2, antiestrogen (LY 117018), and/or 17 alpha-estradiol (17 alpha-E2). Using this approach, we found that the direct inhibitory effect of E2 upon LH responsiveness to LHRH was rapid and specific. The ratio of LH secretion in response to LHRH pulse #2 to that in response to LHRH pulse #1 (LH secretion ratio) decreased steadily during 1 h of exposure to E2. This inhibition was significant (P less than 0.01) by 36 min of E2 exposure. It represented more than the removal of a LHRH self-priming effect because the LH secretion ratios were significantly less than 1.0 [0.80 +/- 0.05 (SEM), P less than 0.01] within 36 min of E2 exposure. The inhibitory effect was not seen when LY 117018 was added with E2, nor when 17 alpha-E2 replaced E2. The specificity of this rapid E2 inhibitory effect upon pituitary LH responsiveness to LHRH strongly suggests that it is receptor mediated. The rapidity of this apparent receptor-mediated estrogen effect suggests that it is a very rapid consequence of nuclear translocation of the E2-receptor complex.
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PMID:Direct inhibitory effect of estradiol on pituitary luteinizing hormone responsiveness to luteinizing hormone releasing hormone is specific and of rapid onset. 636 88


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