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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The secretory response of the primate corpus luteum (CL) to CG after implantation suggests that gonadotropin receptors are not depleted despite increasing CG production and continuous elevated tropic stimulation. Such continuous stimulation is known to cause down-regulation of receptors in other tissues. To determine if CG secretion is intermittent during the initial stages of CL rescue, we assessed the secretory pattern of CG during the periimplantation period by collecting frequent (4/h) blood samples in two studies (for 4 h on 3 separate days between days 8-13, or for 2 separate 13-h sequences between days 10-15 postovulation) in 13 chair-adapted females. Day 0 of gestation was defined as the day of ovulation, as estimated by peak urinary estrone conjugate excretion in females mated on days 9, 11, and 13 of the menstrual cycle. Hormone concentrations were measured by either RIA [irFSH; estradiol and progesterone (P)] or Leydig cell bioassay (bioLH or bioCG). In the first study, 4 of 6 females conceived, and the mean for bioLH was not significantly elevated until days 12-13. In the second study, 5 of 7 females conceived, and the episodic secretory pattern of circulating pituitary bioLH typically observed in cycling females (2.7 +/- 0.3 peaks/13 h) was replaced by a relatively nonpulsatile, but steadily increasing profile during days 12-15 of gestation (1.5 +/- 0.4 peaks/13 h). Although occasional large fluctuations in bioLH/CG and P were noted, the bioLH/P peaks were less congruent than those in nonfertile cycles, and there was no diurnal pattern in the secretion of either hormone. In contrast, irFSH concentrations did not fluctuate and were similar in the two groups of females [2.93 +/- 0.28 vs. 2.34 +/- 1.7 ng/ml (mean +/- SEM)]. These data demonstrate that 1) a steady, gradually increasing secretory pattern of CG is associated with rescue of the CL; 2) the circulating profile of CG during the periimplantation interval is not consistently episodic and does not support the hypothesis that intermittent CG release prevents LH/CG receptor down-regulation in the CL during early pregnancy; 3) increased bioLH/CG levels during conceptive cycles in rhesus monkeys are not detected until days 12-13 after the midcycle bioLH peak; 4) irFSH patterns on pooled aliquots appear to be uninformative with regard to gonadotropin dynamics in early pregnancy; and 5) urinary estrone conjugate measurements provide a practical method for the precise timing of infrequent events, such as implantation, in the laboratory macaque.
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PMID:Absence of regular pulsatile gonadotropin secretion during implantation in the rhesus macaque. 279 65

The physiological significance of locally produced prostaglandins (PGs) in the regulation of the functional lifespan of the primate corpus luteum is unknown. In the current study, the PG synthesis inhibitor sodium meclofenamate was administered to adult female rhesus monkeys beginning in the midluteal phase of the menstrual cycle. Meclofenamate was infused continuously for 7 days into the corpus luteum (100 micrograms/h, n = 6) or the jugular vein (100 micrograms/h, n = 3; 1000 micrograms/h, n = 3) via osmotic minipump. As controls, PBS was infused into the corpus luteum (n = 7) or jugular vein (n = 5). In some of the monkeys receiving intraluteal infusions, chronic aortic and utero-ovarian venous catheters were implanted, and blood samples were collected on alternate days for the measurement of PGE and PGF2 alpha by RIA. Saphenous venous blood was collected daily, and progesterone and cortisol levels were determined by RIA. LH levels were determined by the mouse Leydig cell bioassay. Progesterone levels over 5 days preceding treatment were not different among groups. A decline in progesterone levels on day 1 after surgery was observed in all treatment groups and was accompanied by a 1-day elevation in cortisol levels. Thereafter, five of seven monkeys who received intraluteal infusions of PBS displayed normal progesterone patterns during treatment and normal luteal phase lengths of 15.4 +/- 1.2 days (mean +/- SEM). In six monkeys that received intraluteal infusions of meclofenamate, progesterone levels typically fell to less than 1 ng/ml within 72 h after initiation of infusion; progesterone levels during 7 days of intraluteal infusion were significantly lower (P less than 0.01) in meclofenamate- vs. PBS-treated monkeys. Meclofenamate infusion into the corpus luteum significantly shortened (P less than 0.01) the luteal phase to 10.5 +/- 1.0 days. In contrast, progesterone levels during 7 days of meclofenamate infusion into the jugular vein did not differ from those in PBS-treated monkeys, and the length of the luteal phase was unaltered. LH levels, measured daily, did not differ among groups either before or during treatment. Although an venous/arterial gradient in PGE was detected at the time of surgery, we were unable to detect a significant gradient across the ovary in PGE or PGF2 alpha at any time after surgery in monkeys treated with either PBS or meclofenamate. The present data suggest an obligatory luteotropic role for locally produced metabolites of arachidonic acid, but a physiological role for either PGE or PGF2 alpha in regulating the primate corpus luteum remains equivocal.
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PMID:Intraluteal infusion of a prostaglandin synthesis inhibitor, sodium meclofenamate, causes premature luteolysis in rhesus monkeys. 316 22

Gynaecomastia caused by Leydig cell tumours (LCT) in adult men may appear a long time before clinical evidence of testicular swelling. To evaluate the diagnostic criteria for LCT, hormonal status was studied in 14 cases and compared with results of a control group (CG) and 10 men with idiopathic gynaecomastia (IG). The mean plasma T level was significantly (P less than 0.005) lower in LCT (16.7 +/- 1.7 SEM nmol/l) than in CG (23.0 +/- 1.3 nmol/l). However, individual plasma T levels were in the normal range in 9/14 LCT. The mean plasma E2 level was significantly (P less than 0.001) higher in LCT (204.9 +/- 27.6 pmol/l) than in CG (87.9 +/- 7.7 pmol/l). However, individual plasma E2 levels were in the normal range in 5/14 LCT. In LCT, neither means of basal gonadotrophin levels nor the gonadotrophin responses to LHRH were different from CG. The mean of the plasma T responses to hCG did not differ between LTC, CG and IG. However the mean of E2 peak responses appeared significantly (P less than 0.005) higher in LCT (735.3 +/- 103.4 pmol/l) than in CG (420.5 +/- 40.4 pmol/l). The mean of the E2 peak responses was significantly (P less than 0.001) lower in IG (196.5 +/- 33.4 pmol/l) than in CG. Likewise the mean of plasma E2 levels, measured on day three following hCG administration, remained significantly (P less than 0.001) higher in LCT (662 +/- 94 pmol/l) than either in CG (228 +/- 14 pmol/l) or in IG (158 +/- 25 pmol/l). On day 3 following hCG administration, there was no overlap in individual plasma E2 levels between either LCT and CG or LCT and IG. In all LCT, plasma beta-hCG levels were in the normal range. A testicular echogram, performed in 12 LCT, confirmed the presence of a palpable tumour in 10 and revealed an occult tumour in two cases. We conclude that normal plasma beta-hCG levels, a prolonged plasma E2 response to hCG and testicular echogram appear to be the best criteria for early diagnosis of LCT responsible for gynaecomastia in adult men.
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PMID:Evaluation of diagnostic criteria for Leydig cell tumours in adult men revealed by gynaecomastia. 330 89

Golden hamster testes regress after short day exposure. The present study asks: 1) are Leydig cell numbers depleted during short days, and 2) if so, how are they replenished during recrudescence. Control hamsters were shown 14 h of light and 10 h of dark (LD 14:10) for 10 weeks (n = 12). Testicular regression was induced by LD 6:18 for 10 weeks (n = 4), and recrudescence by switching regressed hamsters to LD 14:10 for 3 and 5 weeks (n = 8 for each group). All hamsters were injected with [3H]thymidine [3 microCi/gm body wt., intraperitoneally (i.p.)] 1 h or 2 weeks before sacrifice. Leydig cell number per testis was determined by stereological analysis of sections of perfusion-fixed testes, and labeling indices were determined by autoradiography. Leydig cell numbers were reduced significantly from 18.2 X 10(6) in control to 9.0 X 10(6) in regressed testes (p less than 0.05); then increased to 14.0 X 10(6) and 17.9 X 10(6) in 3- and 5-week recrudesced hamsters. The labeling index was nondetectable (n.d.) for regressed hamsters. In control and recrudescing hamsters the labeling index was measured at two times (t1 = 1 h vs. t2 = 2 weeks post-injection): in controls, t1 = 0.22 +/- 0.15% (mean +/- SEM) vs. t2 = 0.28 +/- 0.22%; in 1 week recrudesced, n.d. vs. 1.92 +/- 0.77% (p less than 0.05); at 3 wk, n.d. vs. 4.58 +/- 1.74% (p less than 0.05); at 5 weeks, 1.92 +/- 0.61% vs. 2.25 +/- 0.59%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Photoperiodic variation of Leydig cell numbers in the testis of the golden hamster: a possible mechanism for their renewal during recrudescence. 343 Jan 23

Stereological analysis of Leydig cell and macrophage volume density along the long axis of the guinea pig testis was assessed quantitatively by histometric point counting. Morphological identification of Leydig cells was accomplished by staining for 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD), whereas macrophages were identified by vital staining (trypan blue). The average percentage of Leydig cell density constitutes about 10.17 +/- 0.23% at the cranial level (level 1) and about 8.8 +/- 0.21% at the caudal level (level 4). Leydig cell density through four testicular levels showed no significant difference among levels 1, 2, and 3, whereas level 4 was significantly different. The percentage of macrophage density, on the other hand, was approximately 0.4% +/- SEM per cross-sectional profile. It may thus be concluded that the macrophage density within the guinea pig testis does not bias histometric studies of the Leydig cell population to any significant degree, but that regional differences in Leydig cell volume density could influence validity of sampling if tissue procurement is from different testicular levels in successive experiments.
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PMID:Stereological study of Leydig cell density in the guinea pig testis. 378 73

One daily dose of 0.05 mg ethinyl oestradiol was administered to 5 patients with Turner's syndrome (mean age +/- SEM = 16.4 +/- 0.7 years) for 10 days. The effects of acute stimulation with luteinizing hormone-releasing hormone (LRH) (0.1 mg iv) on biologically active and immunoreactive LH were analysed before therapy and at the end of oestrogen treatment. Bioactive LH (BIO-LH) was measured by a sensitive and specific in vitro bioassay based upon testosterone production by mechanically dispersed mouse Leydig cell preparations. Immunoreactive LH (RIA-LH) was evaluated by a double antibody RIA method. Prior to oestrogen treatment, LRH induced a prompt rise in BIO-LH and RIA-LH levels, which reached peak values at 30 and 45 min, respectively. After oestrogen treatment, a delayed response (with peak values at 120 min) was observed for both BIO-LH and RIA-LH. Before oestrogen treatment, the mean bioactivity to immunoreactivity (B/I) ratio of LRH-stimulated LH showed a significant decrease from basal values (P less than 0.05). In contrast, after ethinyl oestradiol administration the mean LH B/I ratio increased significantly from basal values in response to LRH (P less than 0.05). The mean relative maximum response (delta %) for BIO-LH was significantly higher (P less than 0.05) in oestrogen-treated than in untreated patients, whereas the mean BIO-LH delta area was significantly lower in the former group (P less than 0.01). Similarly, oestrogens decreased significantly the mean RIA-LH delta area (P less than 0.05), whereas they did not affect significantly the mean RIA-LH delta %. The results further emphasize that oestrogens may change the quality of circulating LH.
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PMID:Effects of luteinizing hormone-releasing hormone (LRH) upon bioactive and immunoreactive serum LH in patients with Turner's syndrome before and after oestrogen treatment. 389 99

In 90%-hepatectomized rats, the plasma testosterone level (0.34 +/- 0.07 ng.ml, mean +/- SEM) is significantly lower (P less than 0.001) than in sham operated male rats (1.7 +/- 0.26 ng.ml, mean +/- SEM). In dogs, after 90% hepatectomy, the mean plasma testosterone concentration fell to 1/10 of the plasma testosterone level measured in sham operated animals either 24 or 72 h after surgery. In hepatectomized men, plasma testosterone is markedly decreased in contrast to what is observed after duodeno-pancreatectomy performed under the same conditions of anesthesia. These results suggest that 90% hepatectomy severely alters the Leydig cell function.
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PMID:Testosterone secretion is severely impaired after hepatectomy in rat, dog and man. 402 88

The responses of biologically active LH (BIO-LH) and immunoreactive LH (RIA-LH) to acute stimulation with LRH (0.1 mg iv) were studied in 8 pubertal boys (9-15 years, 2nd-4th Tanner's stage), and in 10 healthy adult men (20-46 years). Serum levels of BIO-LH were assessed by an in vitro bioassay method based upon testosterone production by mechanically dispersed mouse Leydig cell preparations. In pubertal boys the mean BIO-LH/RIA-LH (B/I) ratio of basally secreted LH was significantly lower than in adult men (1.2 +/- 0.2 (SEM) and 2.2 +/- 0.2 respectively, P less than 0.01). After acute administration of LRH the mean B/I ratio of circulating LH showed a significant increase from the basal value in pubertal boys (2.6 +/- 0.2, P less than 0.01 vs basal values), whereas no significant difference in LH B/I ratios were demonstrated throughout the study period in adult men (2.1 +/- 0.1, P = NS vs basal values). In agreement with this finding, the mean relative maximum response for BIO-LH (BIO-LH delta %) was higher in pubertal boys than in adult men (1702.7 +/- 500.3 and 499.6 +/- 65.4% respectively, P less than 0.05), whereas the mean RIA-LH delta % was similar in both groups (609.1 +/- 85.1 and 534.1 +/- 75.5% respectively, P = NS).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of acute stimulation with luteinizing hormone-releasing hormone (LRH) on biologically active and immunoreactive serum luteinizing hormone (LH) in pubertal boys. 639 Oct 56

The relative roles of FSH and LH in the control of human spermatogenesis are not well established. We previously reported that supraphysiological doses of hCG can stimulate sperm production in gonadotropin-suppressed normal men despite prepubertal FSH levels. To determine whether more nearly physiological levels of human LH (hLH) also can stimulate spermatogenesis when FSH levels are suppressed, we administered hLH to normal men whose endogenous gonadotropin levels and sperm production were suppressed by exogenous testosterone enanthate (T). After a 3-month control period, 11 normal men received 200 mg T, im, weekly to suppress LH and FSH. T administration alone was continued for 3-4 months until 3 successive sperm concentrations (performed twice monthly) revealed azoospermia or severe oligospermia (sperm concentrations, less than 4 million/ml). Then, while continuing T, 4 of the 11 men (experimental subjects) simultaneously received 1100 IU hLH, sc, daily for 4-6 months to replace LH activity, leaving FSH activity suppressed. The effect on sperm production of the selective FSH deficiency produced by hLH plus T administration was determined. The remaining 7 men (control subjects) continued to receive T alone at the same dosage, without gonadotropin replacement, for an additional 6 months. In the four experimental subjects, sperm concentrations increased significantly from 0.7 +/- 0.7 million/ml (mean +/- SEM) during T treatment alone to 19 +/- 4 million/ml during hLH plus T administration (P less than 0.001). However, none of the men achieved sperm concentrations consistently in their own pretreatment range. Sperm motilities and morphologies were normal in all four subjects by the end of hLH plus T administration. In contrast, sperm concentrations in the seven control subjects remained suppressed (less than 3 million/ml) throughout the entire period of prolonged T administration alone. Serum LH bioactivity, determined monthly by in vitro mouse Leydig cell bioassay in all four experimental subjects, was markedly suppressed during T administration alone (120 +/- 10 ng/ml) compared to that during the control period (390 +/- 20 ng/ml; P less than 0.001). With the addition of hLH to T, LH bioactivity returned to control levels (400 +/- 40 ng/ml; P = NS compared to control value). Serum FSH levels determined monthly by RIA were reduced from 98 +/- 12 ng/ml during the control period to undetectable levels (less than 25 ng/ml) during the T alone and the hLH plus T periods (P less than 0.01).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Stimulation of sperm production by human luteinizing hormone in gonadotropin-suppressed normal men. 643 86

This study compared the effect of a single high dose of hCG (1500 IU) with that of the same dose administered in multiple small doses (300 IU, once daily for 5 days) on Leydig cell steroidogenesis. Administration of a single high dose of hCG to seven healthy men raised the mean plasma testosterone (T) level to peak levels 2.1 +/- 0.2 (SEM) X the baseline value at 48 h. Thereafter plasma T decreased to below normal (0.7 +/- 0.1 X baseline) 7 days after the injection. The mean 17-hydroxyprogesterone (17-OHP) level peaked at 24 h (2.5 +/- 0.2 X baseline) and then also fell to a nadir value of 0.6 +/- 0.2 X baseline on day 7. Reflecting the early accumulation of 17-OHP over T, the 17 OHP/T ratio reached its maximum (1.6 +/- 0.1 X baseline) at 24 h at the same time when plasma estradiol [(E2) 4.4 +/- 0.6 X baseline] and the ratio E2/T (2.7 +/- 0.3 X baseline) achieved their maximal values. Administration of 1500 IU hCG in five divided doses of 300 IU daily increased the mean plasma T levels to peak value of 2.1 +/- 0.2 X baseline at 5 days and the levels remained elevated thereafter. The response of T as reflected by the area under the curve was almost twice as great as in the single dose study (2844 +/- 360 vs. 1647 +/- 214). In contrast to the single high dose experiment, mean plasma 17-OHP levels in the divided dose protocol did not peak at 24 h but only gradually increased. As the increase of T exceeded the 17-OHP increase at almost all time intervals, no accumulation of 17-OHP over T occurred as in the single dose experiment. Instead the 17-OHP/T ratio fell to a nadir value of 0.6 +/- 0.1 X baseline on day 7. The initial E2 peak was absent in the divided dose protocol and the E2/T ratio only marginally increased. Considering both experiments together a close relation was found between the hCG-induced increases in E2 and 17-OHP (r = +0.88, P less than 0.001), as well as the ratio 17 OHP/T (r = +0.64, P less than 0.02).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Differential effect of single high dose and divided small dose administration of human chorionic gonadotropin on Leydig cell steroidogenic desensitization. 669 40


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