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)

In order to improve our knowledge on human placental hCG production, we studied the binding of an LHRH agonist (N-Ac-Pro1,D-Leu6)-LHRH to third trimester intact placental cells from normal and anencephalic fetuses. In normal pregnancies, specific and saturable binding was found for both LHRH and its analogs with two classes of binding sites. Association constants were 4.7 +/- 2.2 (mean +/- SEM) X 10(5) M-1 for the low affinity sites and 1.7 +/- 0.8 X 10(8) M-1 for the higher affinity sites (P less than 0.01), and the estimated number of sites was 1.71 +/- 0.52 nmol/mg of cell protein and 2.79 +/- 0.54 pmol/mg of cell protein, respectively. Preincubation with increasing concentrations of LHRH agonist induced a progressive decrease in specific binding sites and manifested by a reduction in hCG production which paralleled the concentration of the agonist in preincubation buffer. Studies with placental cells from three anencephalic fetuses showed a decreased binding capacity for LHRH and its agonist, when compared to normal trophoblastic cells, as well as a reduced capacity to produce hCG. Our results suggest that mechanisms dependent upon LHRH binding to its receptor are required for placental hCG production in normal pregnancies. Furthermore our investigation suggests a role for the endocrine feto-placental milieu in the manifestation of these placental LHRH binding sites.
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PMID:Dynamics of LHRH binding to human term placental cells from normal and anencephalic gestations. 303 Aug 51

The pulsatile IV administration of gonadotropin-releasing hormone (GnRH) was evaluated as a method to induce fertile estrus in 8 anestrous Beagle bitches. Bitches received 1.25 micrograms of GnRH every 90 minutes for 11 to 13 days. Gonadotropin-releasing hormone was delivered by use of an automatic pump. Reproductive history was known for all bitches, 4 of which, on the basis of 3 or 4 preceding cycles, had an interestrous interval of 219 +/- 14 days (mean +/- SEM). Estrus induction was attempted during early anestrus in 6 bitches (ie, 148 +/- 10 days since the preceding estrus) and late anestrus in 1 bitch (ie, 260 days since the preceding estrus); another bitch had not had an estrous cycle for nearly 2 years before GnRH administration. Signs of estrus were seen within 16 days after the start of GnRH administration in the bitches with regular estrous cycles (group 1, n = 7), and within 23 days in the bitch (group 2) with prolonged anestrus. All bitches were bred, and 7 of 8 (87.5%) became pregnant, with a mean litter size of 4.5 +/- 0.75. A normal hormonal response pattern was observed in group-1 bitches--a peak increase in plasma estrogen concentration of 22.3 +/- 2 pg/ml immediately before the onset of estrus. Peak plasma progesterone concentration (17.3 +/- 3 ng/ml) was observed 1 to 14 days after the onset of diestrus in the group-1 bitches that ovulated, and adequate plasma progesterone concentration was maintained throughout gestation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Use of pulsatile intravenous administration of gonadotropin-releasing hormone to induce fertile estrus in bitches. 307 80

The reproductive hormone response to severe caloric restriction (600 Cal day-1) was studied in six men 33-67% over ideal body weight who completed a 32-day protocol consisting of three periods in the following order: control (4 days), maintenance protein and energy; diet A (14 days), 50 g lean beef protein plus 50 g casein; and diet B (14 days), 50 g lean beef protein plus 50 g carbohydrate. Weight loss (8.7-12.5 kg) was associated with a decrease in mean blood glucose [4.52 +/- 0.60 (+/- SEM), 3.49 +/- 0.29, and 3.80 +/- 0.30 mM] and an increase in beta-hydroxybutyrate (less than 0.10, 2.09 +/- 0.44, and 1.06 +/- 0.34 mM), as determined on the final morning of each period. On the same days, mean serum FSH and LH responses to LHRH infusion of 0.2 micrograms min-1 for 4 h (expressed as milliinternational units per ml area under the concentration-time curve) were: FSH, 1558 +/- 359, 1336 +/- 545, and 1337 +/- 321 (P = NS); and LH, 1730 +/- 545, 1612 +/- 481, and 1782 +/- 556 (P = NS), respectively. Basal serum FSH, LH, free testosterone (T), and total T changed, while 24-h urinary LH and FSH excretion increased on diet A only. Unlike 10 days of total fasting, during which the same amount of weight was lost, basal serum FSH and LHRH-stimulated serum FSH responses were both significantly diminished by 25%, and serum T was diminished by 19% (1), these same parameters were little changed by either low energy diet. The increased urinary excretion of FSH and LH during diet A suggests that greater ketosis increases renal gonadotropin clearance.
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PMID:Effects of severe dietary restriction on male reproductive hormones. 307 71

The long-acting analogue of luteinizing hormone releasing hormone, D-Trp6-Pro9-NEt-LHRH (LHRHa), is effective in the short-term treatment of central precocious puberty. We report the results of two to four years of LHRHa therapy in 27 children with this disorder. Secondary sex characteristics regressed in most patients. Sex steroid levels and basal and LHRH-stimulated gonadotropin levels remained suppressed compared with pretreatment values. Linear growth rates decreased from 11.0 +/- 0.8 (SEM) cm/yr before treatment to 5.7 +/- 0.4 cm/yr at two years of treatment and 3.7 +/- 0.7 cm/yr at four years of treatment. Predicted heights by the Bayley-Pinneau method increased from 156.4 +/- 2.0 cm before treatment to 162.3 +/- 2.3 cm at two years and 163.4 +/- 2.4 cm at three years. Five patients treated for four years had a mean increase in predicted height of 5.5 cm. To date no adverse effects have been observed. However, the ultimate safety of this analogue is not known. We conclude that LHRHa appears to be an effective long-term therapy for central precocious puberty.
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PMID:Luteinizing hormone releasing hormone analogue therapy for central precocious puberty. Long-term effect on somatic growth, bone maturation, and predicted height. 308 11

In order to investigate whether isolated elevated FSH levels in men with idiopathic oligospermia can be lowered by pulsatile LHRH therapy, six patients were treated for 6 weeks with 5 micrograms LHRH pulses every 2 h. The pulses were delivered from a portable minipump (Zyklomat) through a subcutaneously inserted needle. At the end of treatment prepulse serum LH levels were no different from the levels before treatment while serum FSH was significantly reduced in all patients (16.9 +/- 2.5 U/l vs 11.3 +/- 1.9 U/l, mean +/- SEM; P less than 0.01). The normal FSH range was reached in one of the six patients. The areas under the LH curves following the first and the last (i.e. 504th) pulse were no different, while the areas under the FSH curves were significantly smaller (2870 +/- 434 vs 1776 +/- 237 U/l X min; P less than 0.01). Serum testosterone and oestradiol were significantly higher at the end of treatment (11.0 +/- 1.2 vs 15.2 +/- 1.9 nmol/l 146 +/- 18 vs 214 +/- 25 pmol, respectively). Thus increased FSH levels in men with idiopathic oligospermia can be selectively reduced by pulsatile LHRH treatment. If the increased FSH levels are not the result but rather a factor contributing to the pathogenesis of certain types of oligospermia these findings may have implications for the treatment of this condition.
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PMID:Selective reduction of elevated FSH levels in infertile men by pulsatile LHRH treatment. 308 94

Hypogonadotropic hypogonadism due to a deficiency in hypothalamic gonadotropin-releasing hormone is common in female athletes ("hypothalamic amenorrhea"). It is not known, however, whether a similar phenomenon occurs in male athletes. We investigated the integrity of the hypothalamic-pituitary-gonadal axis in six highly trained male marathon runners (who were running 125 to 200 km per week). The mean (+/- SEM) frequency of spontaneous luteinizing hormone pulses was diminished in the runners, as compared with healthy controls (2.2 +/- 0.48 vs. 3.6 +/- 0.24 pulses per eight hours, P less than 0.05). The amplitude of the pulses was also low in the runners (0.9 +/- 0.24 vs. 1.6 +/- 0.15 mlU per milliliter; P less than 0.05), and the responses of luteinizing hormone to gradually increasing doses of exogenous gonadotropin-releasing hormone were decreased. Plasma testosterone levels were similar in the two groups and increased equally in response to an intramuscular injection of 2000 units of human chorionic gonadotropin. During short-term intense physical exercise (a treadmill run at 72 percent of maximal oxygen consumption for two hours), the plasma gonadotropin levels in the athletes remained stable, but significant elevations in plasma levels of cortisol, prolactin, and testosterone occurred. We conclude that highly trained male athletes, like their female counterparts, may have a deficiency of hypothalamic gonadotropin-releasing hormone. This condition may be caused by the prolonged, repetitive elevations of gonadal steroids and other hormones known to suppress gonadotropin-releasing hormone secretion that are elicited by their daily exercise.
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PMID:Decreased hypothalamic gonadotropin-releasing hormone secretion in male marathon runners. 309 Apr 37

The antifungal drug ketoconazole is known to inhibit testosterone biosynthesis and decrease serum testosterone concentrations. To assess whether the ketoconazole-induced reduction in serum testosterone might stimulate LH and FSH output in a manner suitable as a test of pituitary gonadotropin reserve, we gave normal men ketoconazole every 8 h for 1 week in dosages of 300-1200 mg/day. Ketoconazole administration caused a dose-dependent reduction in serum testosterone which correlated inversely with serum ketoconazole (r = -0.82; P less than 0.001). This fall in serum testosterone stimulated increases in serum LH and FSH which were maximal at a ketoconazole dose of 900 mg/day [LH increase, 127 +/- 27% (+/- SEM); FSH increase, 63 +/- 15%]. Ketoconazole tended to blunt the LH and FSH responses to LHRH. Ketoconazole increased serum 17-hydroxyprogesterone, reflecting blockade of 17,20-desmolase by the drug, while having inconsistent effects on serum estradiol. I conclude that ketoconazole administration for 1 week to normal men stimulates LH and FSH output in a fashion that makes it potentially suitable, after additional verification in subjects with normal and abnormal pituitary-testicular function, as a test of pituitary gonadotropin reserve.
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PMID:Ketoconazole-induced stimulation of gonadotropin output in men: basis for a potential test of gonadotropin reserve. 309 21

To investigate whether food deprivation affects hormone release from pituitary gonadotrophs, luteinizing hormone (LH) and follicle-stimulating hormone (FSH) responses to intravenous (IV) administration of 50 micrograms gonadotropin-releasing hormone (GnRH) were determined in 12 healthy subjects (six women and six men) after an overnight fast and after a fasting period of 56 hours. In the female participants, these GnRH tests were performed early in the follicular phase of the menstrual cycle. Blood glucose declined during the fast from 4.4 +/- 0.1 (mean +/- SEM) to 3.3 +/- 0.1 mmol/L (P less than .001). LH and FSH responsiveness to GnRH--as reflected by hormone incremental areas--increased from 1973 +/- 256 to 3267 +/- 450 (IU/L X min) for LH (P less than .001), and from 376 +/- 44 to 705 +/- 112 (IU/L X min) for FSH (P less than .01). When control studies were carried out in nonfasted subjects in exactly the same way as in the fasted participants, the gonadotropin responsiveness to GnRH did not change significantly between the tests. To explore possible mechanisms behind the increased gonadotropin responsiveness in fasted subjects, six of the above mentioned healthy women were given nine small oral doses of glucose (each dose 0.5 g/kg) during an additional 56-hour fast to prevent blood glucose from falling significantly during the period of food deprivation. This did not change the hormone response pattern at all, since both the LH and the FSH responses to GnRH increased significantly during the glucose-supplemented fasting period.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increased gonadotropin responsiveness to gonadotropin-releasing hormone during fasting in normal subjects. 309 23

To test the hypothesis that the frequency of pulsatile LHRH stimulation can differentially control LH and FSH secretion in man, we administered low doses of LHRH in pulsatile fashion in several different regimens to men with idiopathic hypogonadotropic hypogonadism (IHH) and presumed endogenous LHRH deficiency. In study 1, four men with IHH received a constant amount of LHRH per day in three different frequencies. After an initial 7-day period of LHRH (5.0 micrograms every 2 h), the men received 2.5 micrograms every 1 h and 7.5 micrograms every 3 h, each for 4 days, in varying order. Frequent blood samples were obtained before LHRH administration and at the end of each regimen. Before LHRH administration, mean serum FSH and LH levels were low [28 +/- 3 (+/- SEM) and 6 +/- 2 ng/mL, respectively], and they increased into the normal adult male range during LHRH treatment. As the frequency of LHRH administration decreased from every 1 to 2 to 3 h, serum FSH levels progressively increased from 99 +/- 33 to 133 +/- 34 to 181 +/- 58 ng/mL (P less than 0.05). Serum LH levels (34 +/- 6, 33 +/- 6, and 34 +/- 5 ng/mL) were significantly higher than those before LHRH administration and did not differ significantly among the three regimens. Total serum testosterone (T), estradiol, and free T levels were increased by LHRH, but were not significantly different during the three regions of LHRH administration. In study 2, three men with IHH received the same amount of LHRH per dose, given in two different pulse frequencies; 2.5 micrograms LHRH were administered in frequencies of every 0.5 h and every 1.5 h, each for 4 days, in varying order. During the 0.5 h frequency, the mean serum FSH level was 42 +/- 13 ng/mL, and it rose to 80 +/- 19 ng/mL during the 1.5 h frequency (P less than 0.05). Corresponding mean serum LH levels were 25 +/- 5 and 27 +/- 4 ng/mL. Serum T and estradiol levels were not significantly different during the two LHRH regimens. We conclude that the frequency of LHRH stimulation can differentially control FSH and LH secretion by the human pituitary gland, and the pattern of hormonal stimulation may be a determinant of target organ response.
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PMID:Differential control of luteinizing hormone and follicle-stimulating hormone secretion by luteinizing hormone-releasing hormone pulse frequency in man. 310 45

There is evidence that endogenous estrogens have a positive effect on plasma high density lipoprotein (HDL) concentration, whereas the relation between HDL and male sex hormones is unclear, since both positive and negative effects have been reported. This study examined the effects of LHRH agonist in combination with an antiandrogen on plasma lipids and lipoproteins in 17 elderly men with prostatic carcinoma. Subjects were examined prior to and after therapy at 4-week intervals up to 16 weeks. Prior to therapy, their lipid and lipoprotein profiles were not significantly different from a control group composed of individuals of similar age and living in the same community area. Following therapy plasma levels of testosterone and dihydrotestosterone were markedly decreased (above 90%) and their residual activity neutralized through effective use of an antiandrogen. Plasma estradiol decreased between 65% and 85% and the concentration of cortisol was unaffected. The very low density lipoprotein (VLDL) apo-B decreased and low density lipoprotein (LDL) apo-B increased; thus, no change was observed in the total plasma apo-B levels. Total plasma cholesterol increased by 6% (baseline v peak values, mg/dL, mean +/- SEM; 219 +/- 9 v 233 +/- 9, P less than 0.05) due to a significant rise in HDL cholesterol concentration (45.5 +/- 2.8 v 56.5 +/- 3.6, P less than 0.01). Both VLDL and LDL cholesterol levels remained unchanged. The mean elevation of 21% in HDL cholesterol was accompanied by a significant rise in HDL apo-A concentration (161 +/- 6 v 193 +/- 10, P less than 0.01), thus suggesting an increase in HDL mass and/or particle number.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increase in plasma high-density lipoprotein concentration following complete androgen blockage in men with prostatic carcinoma. 310 95


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