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PubMed1979

Effects of a systematic application of human chorionic gonadotropin, gonadotropin-releasing hormone analog and bovine anterior pituitary gonadotropin in cows with cystic ovarian disease.

Fourty-one cows with ovarian follicular cysts (cysts) diagnosed by rectal palpation and observation of estrus behavior were injected intramuscularly (i.m.) with 20,000 IU of human chorionic gonadotropin (HCG). Ten days after this treatment all the cows were examined per rectum for changes in the ovaries with special regard to luteinization of cysts. Cows not responding to HCG were administered 500(10)mug of an analog of gonadotropin-releasing hormone (Gn-RH), Des-Gly-LH-RH-ethylamide, i.m.. If the cysts remained unchanged 10 days subsequent to the second treatment, a third treatment, 400 KE of bovine anterior pituitary gonadotropin (APG), was given i.m. HCG was clinically effective in only 8 cows (20 %). All of the 8 cows conceived. Of 33 cows not responding to HCG, 18 cows (55 %) responded to Gn-RH analog and 12 cows (36 %) conceived. Eleven (73 %) of 15 cows failing to respond to Gn-RH analog were successfully treated with APG and 6 cows (40 %) conceived. In 37 cases, treatment effects were also evaluated by determining serum levels of progesterone prior to and 10 days subsequent to each treatment. When effects of treatment were judged by 1.0 ng/ml or more increase of serum progesterone levels 10 days after treatment, HCG was effective in 13 of 37 cows (35 %), retreatment with Gn-RH analog was successful in 8 of 16 cows (50 %) and APG was ineffective in 3 cows not responding to both HCG and Gn-RH analog. It may be concluded that the therapeutic effect of HCG is disappointing and about half of the cases not responding to HCG were successfully treated with Gn-RH analog. If the cows did not respond to both HCG and Gn-RH analog, they may not respond to APG either.

Journal Article↗
PubMed2006

Immunization of pigs against chicken gonadotropin-releasing hormone-II and lamprey gonadotropin-releasing hormone-III: effects on gonadotropin secretion and testicular function.

The objective of this experiment was to evaluate the effects of active immunization against 2 GnRH isoforms on gonadotropin secretion and testicular function in pigs. Synthetic chicken (c) GnRH-II and lamprey (l) GnRH-III peptides, with the common pGlu-His-Trp-Ser sequence at the N-terminal omitted, were conjugated to BSA. Forty-eight male piglets were randomly assigned to 1 of 4 treatments. Pigs on treatment 1 were actively immunized against cGnRH-II, whereas pigs on treatment 2 were actively immunized against lGnRH-III. Control pigs on treatment 3 were actively immunized against the carrier protein (BSA), and pigs on treatment 4 were castrated and actively immunized against BSA. The BSA conjugate was emulsified in Freund's Incomplete Adjuvant and diethylaminoethyldextran. Primary immunization was given at 13 wk of age (WOA) with booster immunizations given at 16 and 19 WOA. Body weight and plasma samples were collected weekly beginning at 11 WOA. Treatments did not affect BW during the experimental period. Antibody titers were increased in animals immunized against cGnRH-II and lGnRH-III (P < 0.001). Cross-reactivity of the antibodies to mammalian GnRH or between cGnRH-II and lGnRH-III was minimal. Concentrations of testosterone were maximal in control boars (treatment 3) and minimal in control barrows (treatment 4) and immunized pigs (treatment x week; P < 0.01). Immunized animals had concentrations of LH (P < 0.001) and FSH (treatment x week; P < 0.03) that were less than control barrows and similar to control boars. At the end of the experiment, intact (noncastrated) pigs were exsanguinated. Testes were removed immediately; Leydig cells were isolated and treated with 0, 1, or 10 ng/mL of LH. There was an LH x GnRH treatment effect on testosterone concentrations (P < 0.03), indicating that Leydig cells were sensitive to the immunization protocol and doses of LH. Taken together, these data suggest that immunization against GnRH isoforms decreased gonadotropin secretion compared with control barrows. Additionally, immunization against cGnRH-II and lGnRH-III reduced the ability of Leydig cells to respond to LH challenges.

Animals↗
PubMed1985

Active immunization of gilts against gonadotropin-releasing hormone: effects on secretion of gonadotropins, reproductive function, and responses to agonists of gonadotropin-releasing hormone.

Sexually mature gilts were actively immunized against gonadotropin-releasing hormone (GnRH) by conjugating GnRH to bovine serum albumin, emulsifying the conjugate in Freund's adjuvant, and giving the emulsion as a primary immunization at Week 0 and as booster immunizations at Weeks 10 and 14. Antibody titers were evident by 2 wk after primary immunization and increased markedly in response to booster immunizations. Active immunization against GnRH caused gonadotropins to decline to nondetectable levels, gonadal steroids to decline to basal levels, and the gilts to become acyclic. Prolactin concentrations in peripheral circulation were unaffected by immunization against GnRH. The endocrine status of the hypothalamic-pituitary-ovarian axis was examined by giving GnRH and two agonists to GnRH and by ovariectomy. An i.v. injection of 100 micrograms GnRH caused release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) in control animals, but not in gilts immunized against GnRH. In contrast, administration of 5 micrograms D-(Ala6, des-Gly-NH2(10] ethylamide or 5 micrograms D-(Ser-t-But6, des-Gly-NH2(10] ethylamide resulted in immediate release of LH and FSH in both control and GnRH-immunized gilts. Circulating concentrations of LH and FSH increased after ovariectomy in the controls, but remained at nondetectable levels in gilts immunized against GnRH. Prolactin concentrations did not change in response to ovariectomy. We conclude that cyclic gilts can be actively immunized against GnRH and that this causes cessation of estrous cycles and inhibits secretion of LH, FSH, and gonadal steroids.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Effects of decreasing the frequency of gonadotropin-releasing hormone stimulation on gonadotropin secretion in gonadotropin-releasing hormone-deficient men and perifused rat pituitary cells.

The effects of decreasing the frequency of pulsatile gonadotropin-releasing hormone (GnRH) stimulation on pituitary responsiveness were studied in (a) men with isolated GnRH deficiency who had achieved normal sex steroid levels during prior long-term pulsatile GnRH replacement and (b) perifused dispersed pituitary cells from male rats in the absence of sex steroids. In three groups of four GnRH-deficient men, the frequency of GnRH stimulation was decreased at weekly intervals from (a) every 2-3-4 h (group I), (b) every 2-8 h without testosterone replacement (group II), or (c) every 2-8 h with testosterone replacement (group III). In three groups of three columns of perifused dispersed pituitary cells, pulses of GnRH were administered every 2, 4, or 8 h. In groups I and II, mean area under the luteinizing hormone (LH) curve increased (P less than 0.025) and serum testosterone levels fell (P less than 0.035) as the frequency of GnRH stimulation was decreased. In group III, the area under the LH curve also increased (P less than 0.01) although serum testosterone levels were constant, thereby demonstrating that the increase in pituitary responsiveness to slow frequencies of GnRH stimulation occurs independently of changes in the sex steroid hormonal milieu. The area under the LH curve also increased in the perifused dispersed rat pituitary cells when the frequency of GnRH administration was decreased to every 8 h (P less than 0.05), thus demonstrating that the enhanced pituitary responsiveness to slow frequencies of GnRH stimulation is maintained even in the complete absence of gonadal steroids. Nadir LH levels fell in all three groups (P less than 0.01) as the frequency of GnRH stimulation was decreased. In contrast, mean peak LH levels, the rate of LH rise, and the rate of endogenous LH decay were constant as the frequency of GnRH stimulation was decreased. Finally, as the GnRH interpulse interval increased, mean LH levels fell, and mean follicle-stimulating hormone levels were stable or fell. These results indicate that (a) pituitary responsiveness to GnRH increases at slower frequencies of GnRH stimulation in models both in vivo and in vitro, (b) these changes in pituitary responsiveness occur independently of changes in gonadal steroid secretion, and (c) the increases in LH pulse amplitude and area under the curve at slow frequencies of GnRH stimulation are due to decreases in nadir, but not peak, LH levels. Slowing of the frequency of GnRH secretion may be an important independent variable in the control of pituitary gonadotropin secretion.

Adult↗
PubMed1991

Gonadotropins and combined gonadotropin-releasing hormone agonist--gonadotropins protocols in a randomized prospective study.

A prospective study was designed to compare cycles stimulated by human menopausal gonadotropin (hMG) (group A) with cycles pretreated with gonadotropin-releasing hormone agonist causing pituitary desensitization followed by hMG stimulation (group B). Three hundred two cycles were randomly allocated to each group. Cancellation rate was 27.2% in group A compared with only 3.3% in group B. Significantly less hMG ampules for a shorter period were needed in group A patients. Lower estradiol and higher luteinizing hormone levels were detected in the hMG group. Patients in group B yielded significantly more oocytes and more embryos per retrieval. A significantly higher pregnancy rate per cycle was obtained in group B (27%) as compared with that of group A (13%). Moderate and severe ovarian hyperstimulation syndrome was significantly more frequent in group B than in group A.

Adult↗
PubMed1997

Preovulatory changes in the levels of three gonadotropin-releasing hormone-encoding messenger ribonucleic acids (mRNAs), gonadotropin beta-subunit mRNAs, plasma gonadotropin, and steroids in the female gilthead seabream, Sparus aurata.

Gilthead seabream females undergo daily cycles of final oocyte maturation (FOM), ovulation, and spawning throughout their spawning season. FOM consists of lipid droplet and yolk granule coalescence, germinal vesicle (GV) migration, and GV breakdown. Plasma maturational gonadotropin (GtH-II) levels fluctuate throughout the day, reaching a peak at 8 h before spawning, when the GV is at the periphery of the oocyte. The preovulatory GtH-II surge is accompanied by an increase in the plasma levels of 17alpha,20beta-dihydroxy-4-pregnen-3-one and estradiol, while testosterone and 17alpha,20beta,21-trihydroxy-4-pregnen-3-one levels remain unchanged. Concurrent with the preovulatory GtH-II surge, there is an increase in pituitary GtH-II beta subunit mRNA levels followed by an increase in GtH-Ibeta mRNA levels. Gilthead seabream brain contains three different forms of GnRH: salmon (s)GnRH, seabream (sb)GnRH, and chicken (c)GnRH-II. All three GnRH-encoding mRNAs fluctuate throughout the day, reaching highest levels 8 h before spawning, concurrent with the preovulatory GtH-II surge. On the basis of these correlations and of the anatomical organization of the three GnRH systems, it is hypothesized that in the daily-spawning gilthead seabream females, preovulatory GtH-II secretion, and probably synthesis, are induced by a surge of sbGnRH secretion. The involvement of the other two GnRH forms, sGnRH and cGnRH-II, in the control of ovulation and spawning is presumed, on the basis of the elevation of their mRNA levels at the time of the preovulatory GtH-II secretion and spawning.

Animals↗
PubMed1990

Is deglycosylated human chorionic gonadotropin an antagonist to human chorionic gonadotropin? Characterization of deglycosylated human chorionic gonadotropin action in two testicular interstitial cell fractions.

In order to determine the significance of carbohydrate residues of human chorionic gonadotropin (hCG) in receptor interaction and signal transduction leading to steroidogenesis, the effect of deglycosylated hCG (DG-hCG) was studied in vitro with two different hCG-responsive purified testicular interstitial cell fractions. Fraction I light cells, previously found to bind 125I-labeled hCG with high affinity without producing testosterone, also bound 125I-labeled DG-hCG with high affinity (Kd 7.2.10(-10) M) without stimulating testosterone production. Fraction IV heavier cells, which produced testosterone in response to hCG without detectable high-affinity hCG-binding sites, neither bound DG-hCG nor sufficiently produced cAMP and testosterone in response. With the addition of intact hCG, DG-hCG inhibited cAMP levels, although not sufficiently to inhibit testosterone production. This observation was contrary to previous studies in which DG-hCG was shown to be an antagonist to hCG action. We conclude that: (a) DG-hCG retains its binding activity in light cells and this high-affinity binding is unrelated to steroidogenesis; (b) DG-hCG does not bind to heavier cells with high affinity and loses its biological activity as result of deglycosylation; (c) DG-hCG actions in this study strengthen the concept of two different hCG-responsive cells in the rat interstitium which, if not separated, will yield misleading data supporting the coexistence of hCG high-affinity binding and biological response in the same cell; and (d) DG-hCG partially antagonizes the activation of adenylate cyclase but does not block testosterone production, thus questioning the usefulness of this analogue in antagonizing the action of native hCG in rat testis.

Animals↗
PubMed1995

Luteinizing hormone/chorionic gonadotropin bioactivity in the common marmoset (Callithrix jacchus) is due to a chorionic gonadotropin molecule with a structure intermediate between human chorionic gonadotropin and human luteinizing hormone.

Chorionic gonadotropin (CG), a pregnancy-specific heterodimeric hormone found in primates, is responsible for CL rescue with pregnancy maintenance. Of the primates, the human and baboon gene sequences are the only structures so far determined. In order to study the structure and function of CG in other primates, we have isolated and sequenced the coding regions for the two subunits of marmoset CG (mCG) by the reverse transcription/polymerase chain reaction method. Study of multiple clones confirmed a high degree of homology with the human sequences (88% and 80% for the alpha and beta nucleotide sequences, respectively). Marmoset CG alpha has an extra four amino acids compared to hCG alpha, whereas the mCG beta sequence has a 3-bp deletion that maintains the reading frame and C-terminal amino acid sequence. Most of the differences between hCG beta and mCG beta peptides occur in the C-terminal region, which includes the loss of two of the O-linked glycosylation consensus sequences and the presence of an N-linked glycosylation consensus sequence. When mCG alpha and beta were co-expressed in CHO cells, assembly of biologically active hormone was confirmed by induced steroid secretion by MA10 cells. Partially purified mCG beta was used to raise anti-mCG antibodies. To date, an antibody has been obtained that is capable of detecting recombinant mCG beta, recombinant mCG dimer, and mCG dimer secreted by cultured marmoset trophoblast. Marmoset CG alpha and beta were also detectable at the transcriptional level in cultured trophoblast by in situ hybridization. This suggests that the LH/CG bioactivity reported from marmoset placentae and embryos is due to a molecule with structural features common to hLH (glycosylation pattern) and hCG (CG beta C-terminal structure).

Amino Acid Sequence↗
PubMed1976

Plasma gonadotropin and gonadotropin-releasing hormone levels after intranasal administration of gonadotropin releasing hormone.

Intranasal administration of gonadotropin hormone (GnRH) in doses ranging from 2-4 mg produced a consistently prolonged LH response in patients with secondary amenorrhea. In 4 cases, a delayed secondary rise occurred. A similarly prolonged FSH response was observed in the majority of patients. Six hours after intranasal GnRH, FSH and LH values were well above basal levels and were higher than those observed at a similar interval after intravenous GnRH. Plasma GnRH levels after intranasal administration failed to achieve the high peaks found after the intravenous route but maintained elevated levels for at least an hour and often longer. Despite the much lower plasma GnRH levels, intranasal GnRH produced a sustained effect on LH and FSH secretion, greater than GnRH given by the intravenous route.

Administration, Intranasal↗
PubMed1984

Chorionic gonadotropin receptors and immunoreactive chorionic gonadotropin in implantation of the rabbit blastocyst.

To determine the temporal relationship between immunoreactive chorionic gonadotropin, chorionic gonadotropin receptors, and implantation of the rabbit blastocyst, (1) immunoreactive chorionic gonadotropin in plasma, uterine flushings and blastocysts; (2) chorionic gonadotropin receptors on blastocysts (day 5 and 6) and embryonic and interembryonic segments of the uterus (day 7); and (3) chorionic gonadotropin receptors on the endometrium and myometrium (day 1 through 6) were measured. Binding of I125-labeled beta-subunit of human chorionic gonadotropin (hCG) by cell membranes from blastocysts increased significantly from 6.0 +/- 1.1 fmol/mg of protein (mean +/- SE) on day 5 (N = 6) to 16.1 +/- 1.3 fmol/mg of protein on day 6 (n = 6) (P less than 0.001). Immunoreactive chorionic gonadotropin levels in blastocyst fluid increased from 0.3 ng/ml of day 5 to 0.65 ng/ml on day 6. Specific binding of I125-labeled hCG was absent in endometrial and myometrial cell membranes before implantation (days 1 to 6) but was found in decidual cells from embryonic segments on day 7. Plasma immunoreactive chorionic gonadotropin or chorionic gonadotropin--like material increased from 6 ng/ml of day 1 to 52 ng/ml on day 7. Uterine flushings had chorionic gonadotropin levels of 0.4 ng/ml of day 2, which increased slowly to 1.0 ng/ml on day 7. Intrauterine instillation of hCG into nonpregnant uterine horns demonstrated transuterine absorption of hCG with plasma hCG levels showing a dose-related response. Our findings demonstrate that (1) immunoreactive chorionic gonadotropin or chorionic gonadotropin--like material is detectable in plasma, uterine flushings, and blastocyst fluid before implantation, (2) chorionic gonadotropin receptors are present on the blastocyst cells before implantation, and (3) the uterus can absorb chorionic gonadotropin from its lumen.

Absorption↗
PubMed1990

Effects of gonadotropin-releasing hormone and human chorionic gonadotropin on pregnancy rate in dairy cattle.

This study was to determine if gonadotropin-releasing hormone, human chorionic gonadotropin, or their interaction would affect pregnancy rate or milk progesterone profiles in dairy cattle. Cows and heifers eligible for first, second, and third services were assigned to four treatments: 1) saline i.m. within 5 min after AI (d 0) and saline 15 d after AI (n = 222 AI); 2) gonadotropin-releasing hormone (100 micrograms) i.m. within 5 min after AI and saline on d 15 (n = 223); 3) saline after AI and human chorionic gonadotropin (3500 IU) i.m. on d 15 (n = 196); 4) gonadotropin-releasing hormone at AI and human chorionic gonadotropin on d 15 (n = 195). Progesterone was quantified in milk samples collected twice weekly for 5 wk from all cows. Neither gonadotropin-releasing hormone, human chorionic gonadotropin, gonadotropin-releasing hormone x human chorionic gonadotropin interaction, age, nor service number affected pregnancy rate, which averaged 46.2%. Pregnancy and human chorionic gonadotropin affected milk progesterone profiles. Pregnancy maintained progesterone concentrations and human chorionic gonadotropin on d 15 increased them. This study does not support the general use of gonadotropin-releasing hormone at AI or human chorionic gonadotropin 15 d after AI as methods for enhancing pregnancy rates of dairy cattle.

Animals↗
PubMed1993

Comparison of exogenous gonadotropins and pulsatile gonadotropin-releasing hormone for induction of ovulation in hypogonadotropic amenorrhea.

To compare the efficacy and safety of ovulation induction with exogenous gonadotropins vs. pulsatile GnRH in patients with hypogonadotropic amenorrhea, results from 30 patients in 111 cycles of gonadotropins and 41 patients in 118 cycles of pulsatile GnRH were analyzed retrospectively. Exogenous gonadotropins were administered using an individually adjusted protocol, using a starting dose of 150 IU. Pulsatile GnRH was delivered iv at a physiological frequency based upon our normative data. The doses administered ranged from 75-250 ng/kg. Preovulatory serum estradiol (E2) and luteal phase progesterone (P) levels were compared to those in normal cycling women (n = 87). The mean body mass index, age, and baseline gonadotropin levels were similar in the two groups. Overall ovulatory rates and conception rates per cycle and per patient were not significantly different between the two groups. However, the cumulative chance of conception after six cycles of treatment by life table analysis appeared to be higher with pulsatile GnRH treatment (96%) than with exogenous gonadotropins (72%). The risk of multiple gestation was also higher with exogenous gonadotropins (14.8% vs. 8.3%), although this was not statistically significant. All higher order multiple gestations (triplets or more) occurred in the gonadotropin-treated group. More than two dominant follicles were seen on ultrasound in 47.6% of gonadotropin-treated cycles compared to 18.9% of cycles with pulsatile GnRH treatment (P < 0.01). Three or more follicles were seen in 16.6% of the gonadotropin cycles compared to 5.4% with pulsatile GnRH (P < 0.05). No case of severe ovarian hyperstimulation was observed in either group, although the mean luteal phase ovarian size was significantly higher in the gonadotropin group (P < 0.05). Mean peak preovulatory E2 levels were significantly higher in the gonadotropin group (1684.5 +/- 124.4 vs. 1315.3 +/- 74.9 pmol/L; P < 0.05). The mean luteal phase P level 1 week after ovulation was significantly higher than normal in the gonadotropin group (84.9 +/- 10.8 vs. 61.1 +/- 3.2 nmol/L; P < 0.05), but was not significantly different from that in the pulsatile GnRH group (70.3 +/- 6.0 nmol/L). We conclude that pulsatile GnRH, when compared to exogenous gonadotropins, results in high rates of ovulation and conception, but a decreased risk of multiple folliculogenesis, higher order multiple gestations, and ovarian enlargement.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1984

Priming with gonadotropin-releasing hormone restores gonadotropin secretion during first but not second trimester of pregnancy.

This study was designed to determine whether the lack of secretion of endogenous gonadotropin-releasing hormone is the etiology of the hypogonadotropic state of pregnancy. For this purpose, five pregnant women in their first trimester received a single intravenous dose of 150 micrograms of gonadotropin-releasing hormone. Another five women in the first trimester and five women in the second trimester of pregnancy received daily intramuscular injections of 500 micrograms of gonadotropin-releasing hormone for 10 consecutive days. This was followed by a single 150 micrograms gonadotropin-releasing hormone test and then a 24-hour pulsatile infusion of gonadotropin-releasing hormone of 10 micrograms/min/6 min given every hour. Baseline plasma beta-luteinizing hormone and follicle-stimulating hormone were undetectable in all women. Mean +/- SEM plasma beta-human chorionic gonadotropin was significantly higher (p less than 0.001) in the first trimester than in the second trimester, and mean plasma estradiol and prolactin were significantly increased (p less than 0.001 and 0.05, respectively) during the second trimester of pregnancy. After the 10-day treatment with gonadotropin-releasing hormone there was a significant increase (p less than 0.05) in baseline beta-luteinizing hormone and follicle-stimulating hormone only in the first-trimester pregnant women. The single as well as the pulsatile administration of gonadotropin-releasing hormone resulted in a further significant increase in both beta-luteinizing hormone and follicle-stimulating hormone. In contradistinction, women in the second trimester of pregnancy showed a blunted response to the daily and pulsatile administration of gonadotropin-releasing hormone. Since the pituitary secretion of gonadotropin was functionally restored by the administration of exogenous gonadotropin-releasing hormone, possibly there is a lack of secretion of endogenous gonadotropin-releasing hormone during the first trimester of pregnancy. An increased negative feedback produced by increasing levels of plasma estradiol might be the cause of pituitary refractoriness to gonadotropin-releasing hormone during the second trimester of pregnancy.

Female↗
PubMed1988

Dynamics of gonadotropin release following ovariectomy and injection of gonadotropin-releasing hormone in early postpartum dairy cows.

The influence of the ovary and of injection of low doses of gonadotropin-releasing hormone on secretion and gonadotropin-releasing hormone-induced release of gonadotropins in early postpartum cows was examined in a 2 x 2 factorial design (6 cows/group). Twelve cows were ovariectomized 2 d postpartum (calving = d 0; groups 1 and 2) and 12 cows were left intact (groups 3 and 4). Groups 1 and 3 received gonadotropin-releasing hormone (5 micrograms) every 120 min for 70 h from d 6 to d 9; groups 2 and 4 received saline by the same regimen. All animals received 50 micrograms gonadotropin-releasing hormone on d 9. Mean concentrations of FSH were higher following ovariectomy compared with those of intact cows 6 to 8 d postpartum, whereas no differences in FSH were observed between cows receiving gonadotropin-releasing hormone or saline during this period. Concentrations of LH were similar in intact and ovariectomized cows on d 6 to 8 but were increased in cows receiving gonadotropin-releasing hormone compared with cows receiving saline. Ovariectomy did not alter the gonadotropin-releasing hormone-induced release of gonadotropins on d 9. Injection of gonadotropin-releasing hormone on d 6 to 8 resulted in a decreased gonadotropin-releasing hormone-induced release of gonadotropins on d 9. It was concluded that removal of ovarian influence resulted in increased secretion of FSH but did not affect gonadotropin-releasing hormone-induced release of LH and FSH during the early postpartum period.

Animals↗
PubMed1991

Comparison of gonadotropin-releasing hormone and gonadotropin therapy in male patients with idiopathic hypothalamic hypogonadism.

OBJECTIVE: To compare pulsatile gonadotropin-releasing hormone (GnRH) therapy with gonadotropin therapy in male patients with idiopathic hypothalamic hypogonadism. DESIGN: Prospective study. Patients had free choice between the two forms of therapy. SETTING: Patients were treated on an outpatient basis in our department. PATIENTS: Eighteen patients of matched age (mean [+/- SD] age: 21.1 +/- 3.0 years and 23.6 +/- 7.3 years) and similar testicular volume were treated in each group. INTERVENTIONS: Pulsatile GnRH therapy was started with 4 micrograms GnRH subcutaneously every 2 hours using a portable pump and gonadotropin therapy with 3 x 2,500 IU human chorionic gonadotropin (hCG) weekly injected intramuscularly. After 8 to 12 weeks of hCG treatment, 150 IU human menopausal gonadotropin two to four times weekly were added. RESULTS: Testosterone (T) and estradiol (E2) levels increased significantly higher (T: P less than 0.03; E2; P less than 0.001) in the gonadotropin group than in the GnRH group (T: 22.5 +/- 8.1 versus 16.8 +/- 5.5 nmol/L; E2: 150 +/- 70 versus 88. +/- 59 pmol/L). Five patients developed gynecomastia during gonadotropin therapy. The rise of testicular volume was significantly more pronounced (P less than 0.001) in the GnRH group (delta testicular volume = 8.1 +/- 2.0 mL) than in the gonadotropin group (delta testicular volume = 4.8 +/- 1.8 mL). Ten patients of the GnRH and 8 of the gonadotropin group had positive sperm counts, ranging from 1.5 to 26 x 10(6) spermatozoa/mL. The latter was achieved more rapidly in the GnRH group (12 +/- 1.6 versus 20 +/- 2.3 months: P less than 0.02). CONCLUSIONS: Endocrine and exocrine testicular function can be normalized by both forms of therapy. Gonadotropin therapy has more side effects. Gonadotropin-releasing hormone leads to a higher testicular volume and a more rapid initiation of spermatogenesis compared with gonadotropin therapy.

Adult↗
PubMed1985

Effects of gonadotropin-releasing hormone receptor blockade on rat testicular gonadotropin and lactogen receptors, steroidogenesis, and responses to human chorionic gonadotropin stimulation.

Testicular endocrine regulation was studied in adult male rats after treatment with a potent GnRH antagonist analog [N-Ac-D-p-Cl-Phe1,2, D-Trp3, D-Lys6, D-Ala10-GnRH (Ant.)] given in doses of 1 mg/kg at 0, 12, and 24 h. One group of animals also received an injection of human CG (hCG) (600 IU/kg) at 12 h, and all animals were killed at 36 h for hormone and receptor (R) measurements. Treatment with Ant. blocked greater than 95% of the pituitary and testicular GnRH-R, and decreased serum LH concentration by greater than 90%. Testicular lactogen-R content was decreased by 60% (P less than 0.01), but there was no change in LH-R and FSH-R concentrations. Ant. decreased serum and testicular testosterone levels by 90%, and testicular capacity to produce testosterone in vitro by 50% (P less than 0.01). No decrease was observed in production rates of cAMP and progesterone. hCG alone abolished testicular LH-R, decreased lactogen-R by 55% (P less than 0.01), and GnRH-R by 65% (P less than 0.01). Desensitization of cAMP and testosterone production, and an increase in progesterone-testosterone ratio, were seen after hCG. hCG + Ant. treatment resulted in R, cAMP, and steroid responses that were indistinguishable from those seen after hCG alone. These findings indicate that: 1) Ant.-induced hypogonadotropism decreases testicular lactogen-R concentration and testosterone production; 2) testicular GnRH-R and lactogen-R are subject to heterologous down-regulation by hCG; and 3) inhibition of the putative GnRH-mediated regulation of testis by Ant. blockade of the GnRH-R does not change testicular response to hCG-treatment in vivo. Hence, the present observations still leave the physiological role of testicular GnRH-R open.

Animals↗