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PubMed1987

Inappropriate growth hormone response to luteinizing hormone-releasing hormone in diabetes mellitus.

We randomly administered luteinizing hormone-releasing hormone (LHRH) or thyrotropin releasing hormone (TRH) (25 micrograms and 200 micrograms, respectively, as a bolus), to 16 diabetic male subjects (9 type I, 7 type II) and to 9 healthy male controls in two different mornings. While GH in the basal state was similar in type I, type II, and normal subjects, LHRH administration surprisingly evoked a significant GH release in 7 (5 type 1, 2 type II) diabetic patients. GH-responders had higher glycated hemoglobin than non-responders (11 +/- 1 nu 8.3 +/- 0.5%) but superimposable fasting and intratest average glucose levels. Only one patient among the GH-responders to LHRH showed a GH release also after TRH. These data support the hypothesis that GH secretion in diabetes, especially when poorly controlled, is abnormal.

Blood Glucose↗
PubMed1990

Very-low-calorie diet-induced weight reduction reverses impaired growth hormone secretion response to growth hormone-releasing hormone, arginine, and L-dopa in obesity.

To determine whether impaired growth hormone (GH) secretion in obese subjects is a consequence of obesity or a pre-existing pituitary-hypothalamic disorder, we measured (1) plasma GH response to growth hormone-releasing hormone (GRH; 1 microgram/kg body weight [BW]), arginine (0.5 g/kg BW), and L-dopa (500 mg); and (2) plasma glucose, insulin, and free fatty acids (FFA) in obese subjects before and after weight reduction due to very-low-calorie diet therapy using Optifast (240 kcal/d for 8 to 12 weeks). Body weight and body mass index (BMI) values before and after weight reduction were 87.2 +/- 4.1 kg and 34.5 +/- 0.9 kg/m2, and 67.8 +/- 2.7 kg and 27.0 +/- 0.4 kg/m2, respectively. GH response to GRH, arginine, and L-dopa in obese subjects was markedly impaired before weight reduction, whereas significantly increased responses were noted after weight reduction (P less than .01). Impaired integrated GH response to GRH, arginine, and L-dopa in obese subjects was significantly restored after weight reduction (P less than .01). Plasma glucose levels did not change, while plasma insulin and FFA levels decreased significantly after weight reduction (P less than .01, P less than .05). There was no significant correlation between integrated GH response to these three stimuli and plasma levels of glucose, insulin, and FFA, respectively. The reversibility of GH response to all three stimuli after weight reduction suggests that impaired GH secretion is a consequence of obesity rather than a pre-existing pituitary-hypothalamic disorder.

Adolescent↗
PubMed1991

Age-related decrease in plasma growth hormone: response to growth hormone-releasing hormone, arginine, and L-dopa in obesity.

Aging is associated with a reduction in plasma growth hormone (GH) secretion in non-obese subjects. To determine whether or not age-related changes in plasma GH secretion exist in obese subjects, we measured (a) plasma GH response to growth hormone-releasing hormone (GRH; 1 microgram/kg body wt), arginine (0.5 g/kg body wt), L-dopa (500 mg), and (b) plasma glucose, insulin, and free fatty acids (FFAs) in 26 fasted obese subjects of various ages ranging from 16 to 71 years. Only subjects with a body mass index (BMI; kg/m2) between 30.0 and 39.0 were studied. Six subjects were adolescents, 9 were in their 20s, and 11 were 30 years or older. The mean peak levels of plasma GH in response to GRH, arginine, and L-dopa in obese subjects were 11.3 +/- 2.1, 21.9 +/- 4.4, and 5.2 +/- 0.3 ng/mL in adolescents, 8.2 +/- 1.6, 9.1 +/- 1.5, and 3.1 +/- 0.6 ng/mL in those in their 20s, and 4.5 +/- 0.4, 7.3 +/- 1.4, and 2.8 +/- 0.3 ng/mL in those 30 years or older, respectively, showing a significant decrease in peak GH level with advancing age (P less than .05 to P less than .01).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1992

Arginine abolishes the inhibitory effect of glucose on the growth hormone response to growth hormone-releasing hormone in man.

Acute hyperglycemia inhibits the growth hormone (GH) response to several stimuli including growth hormone-releasing hormone (GHRH), likely acting by stimulation of endogenous somatostatin release. The aim of our study was to verify whether arginine ([Arg] 30 g intravenously [IV] in 30 minutes), a well-known GH secretagogue likely acting via inhibition of hypothalamic somatostatin release, counteracts the inhibitory effect of oral glucose (OG) administration (100 mg orally) on the GH response to GHRH (1 micrograms/kg IV bolus) in seven normal subjects (aged 20 to 30 years). The GH response to GHRH (peak, 11.6 +/- 1.8 micrograms/L) was inhibited by previous OG load (peak, 7.4 +/- 0.8 micrograms/L; P less than .02 v GHRH alone) and potentiated by Arg coadministration (peak, 36.2 +/- 8.8 micrograms/L; P less than .03 v GHRH alone). The potentiating effect of Arg on the GHRH-induced GH increase was unaffected by previous OG load (peak, 30.4 +/- 6.9 micrograms/L). In conclusion, our results show that Arg abolishes the inhibitory effect of OG administration on the GHRH-induced GH response in man. These data, although indirect, suggest that both acute hyperglycemia and Arg act at the hypothalamic level, stimulating and inhibiting, respectively, the release of somatostatin.

Administration, Oral↗
PubMed1992

Arginine potentiates but does not restore the blunted growth hormone response to growth hormone-releasing hormone in obesity.

A blunted growth hormone (GH) response to several stimuli, including growth hormone-releasing hormone (GHRH), has been shown in obesity. Arginine (ARG) has been demonstrated to potentiate the GHRH-induced GH increase in normal subjects, likely acting via inhibition of hypothalamic somatostatin release. To shed further light onto the mechanisms underlying the blunted GH secretion in obesity, we studied the effect of ARG (0.5 g/kg infused intravenously [IV] over 30 minutes) on both basal and GHRH (1 micron/kg IV)-stimulated GH secretion. Eight obese subjects (aged 26.4 +/- 3.9 years; body mass index, 39.0 +/- 1.9 kg/m2) and eight normal control volunteers (aged 27.0 +/- 1.7 years; body mass index, 22.3 +/- 0.5 kg/m2) were studied. In obese subjects, the GH response to both GHRH and ARG was lower (P less than .01 and P less than .002, respectively) than in controls. ARG potentiated the GH response to GHRH in obese patients (P less than .0003). However, in these patients, the GH secretion elicited by GHRH, even when coadministered with ARG, persisted at reduced levels (P less than .005) when compared with controls. Basal insulin-like growth factor-1 (IGF-1) levels did not significantly differ in obese subjects and in normal subjects (161.1 +/- 37.0 v 181.0 +/- 12.8 micrograms/L). In conclusion, ARG enhances the blunted GHRH-induced GH increase in obese patients, but the GH responses to ARG alone and to ARG + GHRH persist at lower levels than in normals. Thus, our results suggest the existence of a reduced pituitary GH pool in obesity.

Adolescent↗
PubMed1994

Opioid dysregulation in anorexia nervosa: naloxone effects on preprandial and postprandial growth hormone response to growth hormone-releasing hormone.

Previously, we have shown that in the opposite extremes of nutritional status, obesity and anorexia nervosa (AN), growth hormone (GH) response to growth hormone-releasing hormone (GH-RH) is not inhibited by the ingestion of a normal 800-cal meal consumed at lunch time (1 PM), which is at variance with results in normal subjects. However, in obese patients the postprandial increase in GH response to GH-RH is inhibited by an infusion of naloxone (NAL). In this study we have tested anorectic patients, performing the following tests at 1 PM: GH-RH test (50 micrograms IV) or, in a different day session, NAL (1.6 mg/h, starting 30 minutes before GH-RH) + GH-RH test (50 micrograms IV). The tests were performed in the following three different experimental conditions: (1) short-term fasting studies (lasting from breakfast), (2) long-term fasting studies (from midnight of the day before) and (3) postprandial studies (after a standard meal consumed 1 hour before the test). In AN, the GH response to GH-RH was not influenced by NAL infusion at 1 PM, in both short- and long-term fasting studies (short-term fasting: peak values after GH-RH alone, 26.5 +/- 6.5 ng/mL, during NAL, 28.0 +/- 3.3 ng/mL; long-term fasting: peak values after GH-RH alone, 32.2 +/- 6.8 ng/mL, during NAL, 30.6 +/- 4.0 ng/mL). A partial NAL-inhibitory effect was instead observed in postprandial studies, as evidenced by the calculation of areas under the curve ([AUCs] 1,662.1 +/- 90.0 after GH-RH alone v 1,090.5 +/- 245.4 ng/mL/h during NAL).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1990

Growth hormone response to growth hormone releasing hormone in depression and schizophrenia.

Growth hormone releasing hormone, a 44-amino acid peptide (GHRH-44), was administered (1 micrograms/kg i.v.) to 6 normal controls, 10 schizophrenic subjects, and 7 depressed subjects. A significantly lower growth hormone (GH) response was found in the schizophrenic and depressed groups. Two molecular forms of GH, 22K GH and 20K GH, were also measured but did not further differentiate the three groups of subjects.

Adult↗
PubMedDate not supplied

Growth hormone responses to growth hormone-releasing hormone (1-29)-NH2 and a D-Ala2 analog in normal men.

Synthetic analogs of growth hormone-releasing hormone, GHRH(1-29)-NH2 and D-Ala2 GHRH(1-29)-NH2 were administered as a bolus intravenous injection to five normal men in a dose range of 0.015 to 0.5 micrograms/kg body weight. Vehicle only was administered in a control study. Peak responses to GHRH analogs occurred at 15 or 30 min. An increase in the integrated plasma growth hormone (GH) response was observed at each dose. The dose-response curve of GHRH(1-29)-NH2 indicated that it has a similar molar potency to GHRH(1-40) and GHRH(1-44). The potency of D-Ala2 GHRH(1-29)-NH2 was approximately twice that of GHRH(1-29)-NH2. Neither analog affected blood levels of PRL, TSH, LH, FSH, ACTH, insulin, glucagon, glucose, cortisol, free thyroxine, and free triiodothyronine. No side effects were noted other than transient flushing with the highest dose administered. The findings demonstrate GHRH(1-29)-NH2 and its D-Ala2 analog are potent stimulators of GH release and have potential application in clinical medicine.

Adult↗
PubMed1996

Interaction of cyclic AMP- and calcium-dependent mechanisms in the regulation of growth hormone-releasing hormone-stimulated growth hormone release from ovine pituitary cells.

Growth hormone-releasing hormone (GHRH)-stimulated growth hormone (GH) release from the sheep pituitary is mediated through Ca(2+)-and cyclic AMP-dependent mechanisms. The initial Ca2+ influx is suggested to result from depolarization, whereas a secondary Ca2+ influx is thought to result from second messengers. This study sought to determine whether there was an interaction between these two signal transduction pathways. Sheep pituitary cells were placed in culture for 4 d and were then washed and incubated for 1 hr in serum-free medium before the application of specific antagonises and/or agonists. Both KCl and forskolin stimulated GH release (P < 0.05), but neither produced an effect similar to that of GHRH. The combination of both stimuli, however, mimicked GH release, as seen with a maximal dose of GHRH. Pretreatment with H89 (protein kinase A [PKA] inhibitor) inhibited GHRH, forskolin- and KCl-stimulated GH release (P < 0.001) but had no effect on phorbol myristate acetate (PMA)-stimulated GH release. Verapamil (voltage-dependent Ca2+ channel blocker) inhibited the GHRH effects on GH release (P < 0.0002) but did not influence forskolin or PMA actions. These data suggest that Ca(2+)-dependent pathways converge with cyclic AMP-dependent pathways before or with the activation of PKA. The data also suggest that PKA activation by cyclic AMP alone is insufficient to reproduce either the effects of GHRH stimulation or the combined effects of Ca2+ influx plus PKA activation on GH release. A calmodulin blocker, W7, reduced GHRH-stimulated GH release, a reduction equivalent to the Ca2+ effect on GH release. This suggests that Ca2+ activates calmodulin, which in turn enhances adenylyl cyclase and/or PKA activity to release GH from the sheep pituitary.

Animals↗
PubMed2005

Subcutaneous administration of pulsatile gonadotropin-releasing hormone decreases serum follicle-stimulating hormone and luteinizing hormone levels in women with polycystic ovary syndrome: a preliminary study.

OBJECTIVE: The main objectives of this study were to investigate whether [1] subcutaneous (SC) administration of pulsatile gonadotropin-releasing hormone (GnRH) decreases the increased levels of luteinizing hormone (LH) observed in women with polycystic ovary syndrome (PCOS); and [2] GnRH administration modifies the pattern of LH secretion observed in these patients. DESIGN: Serum follicle-stimulating hormone (FSH) and LH levels and LH pulse amplitude and pulse interval were determined in 13 patients with PCOS during the first 3 days of the cycle following the administration of 10 mg of medroxyprogesterone acetate during 5 days. SETTING: Infertility clinic. PATIENT(S): Thirteen women with PCOS. INTERVENTION(S): Determination of FSH and LH serum levels after SC administration of pulsatile GnRH. MAIN OUTCOME MEASURE(S): The FSH and LH levels in serum. RESULT(S): Mean FSH and LH levels in serum decreased following the administration of subcutaneous pulsatile GnRH in all treated women compared with baseline values. The LH pulse amplitude and pulse interval decreased in all patients following the administration of pulsatile GnRH. CONCLUSION(S): The SC administration of pulsatile GnRH in women with PCOS significantly decreases FSH and LH levels in serum. A decrease in the secretion of gonadotropins, without reaching the intense suppression observed with GnRH analogues, could be of great utility in in vitro fertilization (IVF) treatments.

Adult↗
PubMed2005

Luteinizing hormone, follicle stimulating hormone, and gonadotropin releasing hormone mRNA expression of Xenopus laevis in response to endocrine disrupting compounds affecting reproductive biology.

Environmental pollutants can interfere with the endocrine system of a variety of animals and are suggested to contribute to the worldwide decline of amphibians. In this study, the effects of endocrine disrupting compounds (EDC) on the hypothalamus-pituitary-gonad axis, regulating reproduction, were investigated in Xenopus laevis by determining their potential impact on gene expression of gonadotropin releasing hormone (GnRH), luteinizing hormone beta-subunit (LHbeta) and follicle-stimulating hormone beta-subunit (FSHbeta) in brain and pituitary using semi-quantitative reverse transcription polymerase chain reaction (RT-PCR). One environmental sample and four model compounds, ethinylestradiol (EE2), tamoxifen (TAM), methyldihydrotestosterone (MDHT), and flutamide (FLU), corresponding to (anti)estrogenic and (anti)androgenic modes of action were used at 10(-8)M during a four weeks exposure of adults of both sexes. In general, males had a higher LHbeta mRNA level compared to females, while the mRNA expression of FSHbeta and GnRH did not differ between both sexes. EE2 and MDHT treatment decreased LHbeta mRNA expression in the brain of male X. laevis, while only EE2 but not MDHT reduced LHbeta mRNA in females indicating classical negative feed-back mechanisms on hypophyseal gonadotropin expression. TAM increased LHbeta mRNA and FSHbeta mRNA expression in female X. laevis while none of the other treatments showed an effect on FSHbeta mRNA expression. GnRH expression was not changed by any treatment and exposure of X. laevis to Lambro river water had no significant effect on any of the genes examined. It is reported for the first time in amphibians that gonadotropin mRNA expression is differentially regulated by (anti)estrogenic and (anti)androgenic EDC and that gender-specific patterns of gene expression exist.

Animals↗
PubMed2000

Low growth hormone response to growth hormone-releasing hormone in child depression.

BACKGROUND: This study examined growth hormone (GH) response to growth hormone-releasing hormone (GHRH) in a large sample of depressed children compared with normal control children. Within-subject comparisons were also performed in control subjects to examine test-retest reliability and in depressed children comparing episode versus clinical recovery. METHODS: The sample included depressed children (n = 82) and normal control children (n = 55) group-matched for age, gender, and pubertal status; the mean ages were 11.2 +/- 1.7 and 11.2 +/- 1.8 years, respectively. We gave GHRH (0.1 mcg/Kg) at 9 AM, and serum GH levels were determined every 15 min from -30 min through +90 min of the GHRH infusion. A subgroup of normal control subjects (n = 11) repeated the protocol for test-retest reliability within a 2-month interval. A subgroup of depressed children (n = 20) were restudied off all medications following full clinical remission from depression. RESULTS: The mean GH response to GHRH was significantly lower in the depressed group (8.7 ng/mL +/- SEM 0.9) compared with normal control children [12.2 ng/mL +/- SEM 1.3; t(135) = 2.59, p =.01 effect size 0.44]. The test-retest reliability of GH response to GHRH was stable (intraclass correlation =.93 for mean post-GH). The GH response to GHRH remained low in subjects restudied during clinical remission from depression. CONCLUSIONS: Depressed children show low GH response to GHRH. The measure appears to be reliable, and the low GH response continues following clinical remission. Further studies are needed to explore the mechanism and relative specificity of this finding.

Child↗
PubMed1998

Effects of beta-adrenergic agonists and antagonists on the growth hormone response to growth hormone-releasing hormone in anorexia nervosa.

BACKGROUND: In anorexia nervosa (AN), growth hormone (GH) hypersecretion and low insulin-like growth factor I (IGF-I) levels are present. It is unclear whether this is due to a peripheral GH resistance and a reduced IGF-I negative feedback on GH secretion or to a primary hypothalamic dysfunction. In AN, in contrast to normal subjects, cholinergic antagonists and agonists, whose action is somatostatin (SS)-mediated, have reduced and absent effects on the GH response to growth hormone-releasing hormone (GHRH). Since arginine, another substance acting via inhibition of SS, maintains its potentiating effect on GH secretion in AN, it has been hypothesized that somewhat specific alteration of the SS-mediated cholinergic influence may be present in this condition. To further clarify the neural control of AH secretion in AN, we evaluated the effects of beta-adrenergic agonists and antagonists, which are known to inhibit and increase, respectively, the GHRH-induced GH secretion in normal subjects. METHODS: We studied the effect of atenolol (ATE), a beta 1-adrenergic antagonist, and salbutamol (SALB), a beta 2-adrenergic agonist, on the GHRH-induced GH release in 10 patients with AN and in 10 normal age-matched women (NW). RESULTS: Basal GH levels were higher, whereas IGF-I were lower in AN than in NW. The GHRH-induced GH rise in AN was higher than that in NW. ATE significantly enhanced the GH response to GHRH in NW, but not in AN. The GH responses to GHRH after ATE pretreatment were similar in NW and in AN. The GH response to GHRH was inhibited by SALB in both NW and AN. The GH responses to GHRH after SALB pretreatment were similar in NW and AN. CONCLUSIONS: These data reveal an exaggerated somatotrope responsiveness to GHRH in AN that is not further increased by beta-adrenergic blockade, while is abolished by beta-adrenergic activation. This suggests that an impairment of beta-adrenergic influence on GH secretion is present in anorexia nervosa.

Adolescent↗
PubMed2002

Effect of the opioid blockade on the feeding-induced growth hormone response to growth hormone-releasing hormone in women with polycystic ovary syndrome.

OBJECTIVE: To investigate the effect of naloxone, an opioid receptor antagonist, on the release of growth hormone (GH) induced by the growth hormone-releasing hormone (GHRH) in normal-weight and obese women with PCOS in relation to feeding. DESIGN: Prospective clinical study. SETTING: Academic research center. PATIENT(S): Seventeen women with PCOS (10 who were normal weight and 7 who were obese) and 14 control women (7 who were normal weight and 7 who were obese). INTERVENTION(S): A GHRH test (50 microg i.v.) and, on a different day, a GHRH test during a naloxone infusion (1.6 mg/h) during fasting. The same tests were repeated after a standard meal. MAIN OUTCOME MEASURE(S): GH response to GHRH (expressed as the area under the curve [AUC]) in different experimental conditions. RESULT(S): All normal-weight women showed a significantly higher AUC-GH compared with obese women in the fasting state. Normal-weight controls had a decrease in GH response to GHRH after feeding, and naloxone did not reverse the decrease. In obese controls, feeding increased the GH response but naloxone induced a decrease in the AUC. In fasting, normal-weight women with PCOS, naloxone significantly decreased the AUC-GH; in these patients, food intake induced an inhibition of GH response to GHRH, reversed by naloxone infusion. In obese PCOS patients, GH levels did not increase significantly after GHRH stimulation, either in the fasting state or after a meal, and naloxone did not affect these responses. CONCLUSION(S): Factors other than obesity and insulin may be involved in disruption of GH secretion in women with PCOS.

Adult↗
PubMed1978

The effect of acutely elevated blood glucose levels on luteinizing hormone and follicle-stimulating hormone release following an intravenous gonadotropin-releasing hormone injection.

The effects of an acute blood glucose increase on the capacity of the pituitary gland to release gonadotropins (luteinzing hormone [LH] and follicle-stimulating hormone [FSH]) were studied in 21 women. Each woman received two intravenous challenges of 100 microgram of gonadotropin-releasing hormone (GNRH). Between these injections the blood glucose level was increased in 10 of the women by orally adminstering 100 gm of glucose. Although there were significantly higher blood glucose and plasma insulin levels in the latter group, the LH and FSH response to the second GNRH injection was not different. There was also no significant relationship between the basal blood glucose level and the gonadotropin (LH and FSH) response to GNRH. Acute elevations of blood glucose do not appear to alter the ability of the anterior pituitary cells to release gonadotropins.

Adult↗
PubMed1978

Inhibition of ovarian luteinizing hormone (LH) and follicle-stimulating hormone receptor levels with an LH-releasing hormone agonist during the estrous cycle in the rat.

A single injection of the luteinizing hormone (LH)-releasing hormone (LHRH) agonist [D-Ala6,des-Gly-NH2(10)]LHRH ethylamide to female rats on diestrus I produced a marked reduction in ovarian LH/human chorionic gonadotropin (hCG) and follicle-stimulating hormone (FSH) receptor levels, uterine weight, and plasma progesterone levels measured 2 days later on expected proestrus. A maximal inhibitory effect was seen after a dose of only 40 ng of the peptide. No consistent effect of the LHRH analog was seen on ovarian prolactin receptors. When the analog was injected on day 7 of pregnancy, the inhibition of ovarian LH/hCG receptors was of shorter duration and was much less sensitive than that in nonpregnant animals. These data indicate that ovarian LH and FSH receptors levels are highly sensitive to changes in endogenous gonadotropin secretion and suggest that the gonadotropin surge occurring spontaneously on proestrus may play an important role in the regulation of ovarian gonadotropin receptors during the estrous cycle.

Animals↗
PubMed1983

Gonadotroph and corpus luteum responses to two successive intranasal doses of a luteinizing hormone-releasing hormone agonist at different days after the midcycle luteinizing hormone surge.

Two successive intranasal doses (300 micrograms at 8:00 A.M. and 6:00 P.M.) of the luteinizing hormone-releasing hormone (LH-RH) agonist (D-Ser[TBU]6-des-Gly-NH2(10))LH-RH ethylamide (Buserelin) were administered on days 1 to 10 after the midcycle luteinizing hormone (LH) surge in 33 normally cycling women. Maximal stimulation of gonadotropins was observed at 4 hours and was of higher amplitude in the first 2 days after the LH surge. The response to the second dose was markedly blunted, showing pituitary refractoriness. On each day of treatment there was a progressive increase of serum estradiol, which was maximal (threefold) 4 hours after the second dose of Buserelin. Serum progesterone (P) levels were not significantly changed on days 1 to 4, but they were increased by 50% at 10 hours on days 5 to 10. Daily blood samples revealed that following treatment on days 1 to 4 after the midcycle LH surge, serum P profiles were lower than in control cycles, without change in the length of the luteal phase. Starting on treatment day 5, a precocious luteolysis was induced, as illustrated by an early fall in serum P levels and shortening of the luteal phase (1 to 4 days). All posttreatment control cycles were normal. The results of this time study indicate that an appropriate treatment with an intranasal Buserelin administered at any time between days 1 to 10 after the midcycle LH surge impair luteal function and could lead to a new postcoital contraceptive approach.

Administration, Intranasal↗
PubMed1985

Serum luteinizing hormone-releasing hormone (LH-RH) and gonadotropic hormones in men after a bolus dose of LH-RH: comparison of different doses and routes of administration.

Serum levels of luteinizing hormone-releasing hormone (LH-RH), LH, and follicle-stimulating hormone (FSH) were measured for 60 minutes after 5- and 20-micrograms bolus doses of LH-RH given either intravenously or subcutaneously to 20 healthy men, for the study of LH-RH pharmacokinetics and the corresponding pituitary gonadotropin release. Intravenous (5- and 20-micrograms) LH-RH administration revealed much sharper LH-RH pulses, with significantly higher levels between 1 and 5 minutes (P less than 0.001) but lower levels between 30 and 60 minutes (P less than 0.05), compared with the subcutaneous route. No statistically significant differences were observed in the magnitude and time occurrence of maximum LH release or in the area under the LH response curves between intravenous and subcutaneous LH-RH administration, either in the 5-micrograms or in the 20-micrograms group. FSH responses were small and insignificant in all the performed tests. The intravenous route of administration seems preferential in therapeutic regimens that use pulsatile exogenous LH-RH, because the conditions of intermittent pituitary stimulation are more adequately fulfilled and the risk of dose accumulation is reduced. Furthermore, LH-RH doses of 5 micrograms are capable of producing adequate pituitary LH release, whereas increases in the pulse dose up to 20 micrograms seem to have no additional effects.

Adult↗