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PubMed1993

Effect of naloxone and pulsatile luteinizing-hormone-releasing hormone infusions on oestradiol-induced luteinizing hormone surges in immature gilts.

The aim of the study was to understand why immature 60-day-old gilts produce delayed low amplitude luteinizing hormone (LH) surges in response to oestradiol benzoate. In Expt 1, gilts (n = 36) were challenged with oestradiol benzoate and subsequently received either no further treatment or were infused with saline or various doses of the opioid antagonist, naloxone, for 6-48 h during the expected LH surge (48-96 h after oestradiol benzoate). No differences were observed among groups in the magnitude or duration of the LH surge. In contrast to the other groups, LH concentrations in gilts infused for 48 h with naloxone did not decrease after the surge period. In Expt 2, gilts (n = 34) were challenged with oestradiol benzoate or sesame oil and subsequently received pulses of luteinizing-hormone-releasing hormone (LHRH) or saline solution during the expected surge period. Two other groups were fed methallibure to pharmacologically suppress the oestradiol benzoate-induced LH surge. In addition, one of these groups was given pulses of an LHRH agonist (LHRH-A) during the surge period. Within 2 h of the start of pulsatile LHRH infusion, LH increased in sesame oil-treated gilts, but not in oestradiol benzoate-treated gilts, suggesting that the pituitary responsiveness to LHRH in immature gilts is decreased by oestrogen before the onset of the LH surge. Pulsatile LHRH infusion did not enhance the amplitude of oestradiol benzoate-induced LH surges nor did it advance its onset. Feeding methallibure suppressed the oestradiol benzoate-induced LH surge.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1980

Suppression of the luteinizing hormone releasing effect of luteinizing hormone releasing hormone by arginine-vasotocin in immature male dogs.

Arginine-vasotocin (0.1 or 10 ng/kg body wt) was administered into the carotid artery of anaesthetized immature male dogs 3 h before the administration of a standard dose of luteinizing hormone releasing hormone (LH-RH, 5 microgram/kg body wt) into the same vessel. The rate of secretion of 17-oxosteroids by the testes in vivo served as an index of luteinizing hormone (LH) secretion. The administration of LH-RH into the carotid artery of control dogs which had been injected with isotonic saline caused a slight but definite increase in the secretion of testicular 17-oxosteroids. This effect of LH-RH on the testicular secretion of steroids was markedly reduced by pretreatment with arginine-vasotocin. However, the testicular response to the i.v. administration of human chorionic gonadotrophin (5 i.u./kg body wt) was unaffected by pretreatment with arginine-vasotocin (10 ng/kg body wt). These results indicate that in immature male dogs, arginine-vasotocin is able to inhibit the action of LH-RH by acting directly on the anterior pituitary gland.

17-Ketosteroids↗
PubMed1983

Effects of oestradiol, phenobarbitone and luteinizing hormone releasing hormone upon the isoelectric profile of pituitary follicle-stimulating hormone in ovariectomized hamsters.

Anterior pituitary glands were removed from ovariectomized hamsters after specific endocrine treatments. The presence and relative proportions of the multiple species of FSH present within them were assessed by radioimmunoassay after separation by chromatofocusing. This technique is superior to polyacrylamide gel-isoelectric focusing, as it can accommodate a greater sample volume and has increased resolution. Endocrine conditions which decreased hypothalamic LH releasing hormone (LHRH) release or the sensitivity of the pituitary gland to that neurohormone (phenobarbitone treatment or short-term oestradiol exposure) caused an increase in the relative proportions of the more acidic forms (isoelectric points (pI) 5.1-3.8) of pituitary FSH and a concomitant reduction in the more basic (pI values 6.0-5.3) forms of FSH. During times of increased pituitary LHRH exposure (immediately before the oestradiol-induced gonadotrophin surge or after injection of synthetic LHRH) an increase was observed in the relative proportion of the more basic forms of pituitary FSH. Treatment of ovariectomized hamsters with an inhibin-containing preparation reduced serum FSH concentrations as well as the relative proportion of the more basic forms of pituitary FSH. We have previously shown that the more studies suggest that the existing hormonal milieu, in particular LHRH and oestradiol, influences the types of FSH produced and (presumably) secreted. Thus, through hormonal interactions, the pituitary gland regulates not only the absolute amount but also the potency of the FSH signal to the ovaries.

Animals↗
PubMed1982

Interaction of estradiol and luteinizing hormone releasing hormone on follicle stimulating hormone release in cattle.

To study the mechanism by which estradiol induces a preovulatory surge of follicle stimulating hormone (FSH), we concluded experiments designed to determine: (1) the time course of change in luteinizing hormone releasing hormone (LHRH)-induced FSH release after estradiol in vivo, and (2) whether LHRH is required to trigger the FSH surge. Steers were given 1 microgram LHRH at 20-min intervals for 10 h, beginning 2, 8, 12 or 20 h after estradiol. During this period, serum samples were collected every 2 h (just before every sixth injection). The magnitude of LHRH-induced FSH release from baseline to peak was 40 ng/ml in oil-treated controls and increased (P less than .05) to 77 ng/ml when estradiol was given 2 h earlier. When LHRH was given starting at 8, 12 or 20 h after estradiol, the FSH response to LHRH was further augmented (P less than .001) so that the increment from baseline was about 150 ng/ml. To determine whether estradiol alters LHRH-induced FSH release in ovariectomized (ovx) cows as it does in steers, we gave ovx cows 1 microgram LHRH every 20 min beginning 2 or 8 h after estradiol. Serum samples were collected every 80 min (just before every fourth injection). When LHRH treatment began 2 h after estradiol, LHRH-induced FSH release was blocked (P less than .025) at 80 min after LHRH, but increased thereafter. When LHRH was given starting at 8 h after estradiol, concentrations of FSH increased 156 ng/ml above baseline. This release of FSH exceeded (P less than .001) the comparable value for cows given LHRH after oil (37 ng/ml). Furthermore, the LHRH-induced FSH release initiated 8 h after estradiol resembled the preovulatory and estradiol-induced FSH surges in magnitude (greater than 180 ng/ml), duration (8 to 10 h) and general shape. These results demonstrate that estradiol initially inhibits, then augments the capacity of the pituitary to secrete FSH in response to LHRH stimuli. The pituitary attains peak sensitivity long before the expected surge. Thus, we hypothesize that increased LHRH secretion triggers the FSH surge.

Animals↗
PubMed1988

A luteinizing hormone-releasing hormone-induced serum luteinizing hormone surge is not detectable in the milk of cows.

Six lactating Holstein cows were used to determine whether a serum luteinizing hormone (LH) surge induced by luteinizing hormone-releasing hormone (LHRH) could be detected in milk. A double antibody radioimmunoassay was evaluated for measuring LH in whole milk. Cows (d 10 of the estrous cycle) were injected with saline (time zero), followed by LHRH 12 h later. Blood samples were collected hourly for 12 h via jugular cannula following each injection; milk removal was accomplished every 2 h by a portable milking machine. On d 10 of the next estrous cycle, treatment, order was switched, with the same cows receiving LHRH at time zero and saline 12 h later. Approximately 2 h following LHRH treatment, serum LH levels peaked at 29 ng/ml and remained elevated for 5 h. There was no corresponding change in milk LH detected during the 12-h to 24-h period following the induced serum LH surge. Our conclusion is that the measurement of LH in the milk of cows shows little promise for predicting ovulation time in the cow.

Animals↗
PubMed1989

Luteinizing hormone concentrations in serum of postpartum beef cows injected with microencapsulated luteinizing hormone-releasing hormone analog.

Twenty-five cows were divided equally into five groups to determine whether [D-Trp6]-luteinizing hormone releasing hormone (LHRH-A) microencapsulated in poly (DL-lactide co-glycolide) would increase basal serum concentrations of LH during the postpartum period. On d 5 postpartum, cows were injected i.m. with 2 ml of vehicle alone (Group 1) or vehicle containing microcapsules calculated to release .4, 1.6, 6.4 or 25.6 micrograms LHRH-A per day for approximately 30 d (Groups 2, 3, 4 and 5, respectively). Cows were bled every 15 min for 4 h immediately before and after injection and every 15 min for 4 h at weekly intervals for the next 4 wk to evaluate serum profiles of LH. Estrus was determined by twice daily observations and confirmed by serum progesterone. More cows in Groups 2, 3, 4 and 5 exhibited pulsatile patterns of LH after LHRH-A injection than in Group 1 (P less than .06). More pulses of LH were observed after LHRH-A injection in Groups 4 and 5 than in Group 1 (P less than .01). Mean concentrations of LH within treatment groups did not change during the initial injection, except in Group 5. All cows in Group 5 had a surge of LH immediately after injection. The induced surge of LH in two cows in Group 5 cows resulted in progesterone profiles similar to those during a normal luteal phase. Days to first postpartum estrus were not different among the five treatment groups. Microencapsulated LHRH-A given at a dose estimated to release 25 micrograms LHRH-A/d was effective in elevating LH concentrations following injection. However, effectiveness of this hormonal treatment in shortening postpartum anestrus was not substantiated.

Anestrus↗
PubMed1993

Gonadotropin hormone-releasing hormone induced luteinizing hormone responses in young and old female C57BL/6J mice.

The estrogen-induced luteinizing hormone (LH) surge is markedly attenuated in old (24 months) female mice compared with young (6 months) females. To test whether or not this attenuated LH response is due to a diminished capacity of the pituitary to respond to hypothalamic gonadotropin hormone-releasing hormone (GnRH), the pituitary response to exogenous GnRH was measured in young (5-6 months), normally cycling (n = 6) and old (24 months), acyclic constant diestrus (n = 6) C57BL/6J female mice. Mice were ovariectomized and estrogen-treated for 7 days. After intrajugular catheterization on Day 6, serial blood samples were taken at 15-min intervals for 165 min on Day 7. Serum LH was measured in samples obtained before and after infusion of either saline or GnRH (5 micrograms/5 microliters saline/kg body wt) and 15 micrograms/15 microliters saline/kg body wt 1 hr apart). Saline-treated animals demonstrated no LH response in either young (0.09 +/- 0.02 ng/ml baseline) or old (0.11 +/- 0.01 ng/ml baseline) females. However, a significant release of LH was obtained in response to each challenge of GnRH in both young (0.3 +/- 0.04 ng/ml first challenge, 0.69 +/- 0.1 ng/ml second challenge) and old (0.78 +/- 0.1 ng/ml first challenge, 1.76 +/- 0.2 ng/ml second challenge) mice. The LH response in the aged group was significantly greater (P < 0.05, analysis of variance) than in the young group. These results show that pituitaries of old female mice were at least as capable of responding to exogenous stimulation by GnRH as those of young. We conclude that alteration in the capacity of the pituitary to respond to GnRH is not likely to be a factor contributing to altered LH secretion with age in C57BL/6J mice.

Aging↗
PubMed1993

Median eminence and anterior pituitary degradation of luteinizing hormone releasing hormone in hens undergoing changes in luteinizing hormone secretion.

Studies described in this report provide physiological evidence for a possible involvement of median eminence (ME) and anterior pituitary (AP) luteinizing hormone releasing hormone degrading activity (LHRH-DA) in the genesis of the hen's preovulatory surge of luteinizing hormone (LH). Serum LH and progesterone (P4), ME LHRH content and LHRH-DA, and AP LHRH-DA were determined in laying hens in the following reproductive conditions: 1) a "spontaneous" preovulatory LH surge; 2) a "premature" preovulatory LH surge; and 3) an ovulatory failure induced by feed withdrawal. The premature preovulatory surge of LH occurred 3 h after P4 administration and was preceded by an increase in both ME and AP LHRH-DA and by a decrease in ME LHRH content 1 h after P4 administration. However, the premature preovulatory LH surge was associated with a decrease in LHRH-DA back to control levels as ME LHRH content increased, even though LHRH was presumably being released from the ME at this time to maintain the preovulatory surge of LH. Although similar changes in LHRH-DA (an increase in both ME and AP LHRH-DA, followed by a decrease) also preceded the spontaneous preovulatory surge of LH, its profile was significantly blunted and no changes in ME LHRH content were associated with this LH surge. In contrast, ovulatory failure was correlated with a decrease in ME LHRH content but no changes in LHRH-DA. Therefore, in the hen, ME and AP enzymatic degradation of LHRH I might be involved in the genesis of a premature preovulatory surge of LH.

Animals↗
PubMed1975

Luteinizing hormone release in entire and castrated rams following injection of synthetic luteinizing hormone releasing hormone, and effect of testosterone propionate pre-treatment.

Plasma luteinizing hormone (LH) levels and LH responses to intravenous administration of 100 mug luteinizing hormone releasing hormone (LH-RH) were studied in entire rams, long-term castrated animals (operation performed six months previously), long-term castrated animals treated with testosterone for the two prededing weeks and short-term castrated animals (castrated 3 h before LH-RH injection). LH was measured by radioimmunoassay in samples taken at 5 or 15 min intervals. Basal LH levels were lower in entire rams (0-9 ng/ml) than in long-term castrated animals (6-0 ng/nl). After LH-RH treatment the LH response was much smaller (peak level 9-6 ng/ml), total response 13-3 ng/ml/1 h) and slower (120 min to peak) in entire than in long-term castrated animals (peak level 61-8 ng/ml, total response 141-2 ng/ml/1 h, 29 min to peak). Testosterone treatment after long-term castration depressed the basal LH level and delayed the peak LH response after LH-RH to values similar to those for entire rams. After short-term castration the response to LH-RH was already as great (peak level 70-1 ng/ml, total response 133-6 ng/ml/1 h) as after long-term castration. The latency to peak LH level (82 min) was intermediate between that for untreated and testosterone-treated long-term castrated animals (130 min). Testosterone treatment was considered to have acted on the hypothalamus to depress basal levels. The results provided evidence for the presence of two inhibitory actions of the testis at the pituitary level in the ram: a qualitative delaying action of testosterone and a quantitative inhibitory action of the testis on LH release after LH-RH injection. The latter may also be related to plasma testosterone levels.

Animals↗
PubMed2005

Combined therapy with luteinizing hormone releasing hormone agonist (LHRHa) and growth hormone (GH) in central precocious puberty.

Luteinizing Hormone Releasing Hormone analogues (LHRHa) are considered the treatment of choice in central precocious puberty (CPP). Final height after therapy is usually higher than the predicted one before treatment, but about 60% of patients do not reach their genetic target. The association of Growth Hormone (GH) with LHRHa could be useful in a subgroup of children with CPP and low growth velocity in order to obtain a higher final height with a complete expression of genetic potential. Moreover, in children with early puberty adopted from developing countries, predicted adult height is significantly greater when the combined therapy, GH and LHRHa, is employed. In this paper the rationale for adding GH to LHRHa is discussed and the clinical reports from the literature are presented.

Drug Therapy, Combination↗
PubMed2003

Interactions between the thyroid hormones and the hormones of the growth hormone axis.

The normal secretion and action of the thyroid hormones and the hormones of the GH/IGF-I (growth hormone/ insulin-like growth factor I) axis are interdependent. Their interactions often differ in man from animal studies in rodents and sheep. Thus neonates with congenital hypothyroidism are of normal length in humans but IUGR (intrauterine growth retardation) in sheep. Postnatally normal GH/IGF-I secretion and action depends on an euthyroid state. Present knowledge on the interactions between the two axes is reviewed in states of hypo- and hyperthyroidism, states of GH/IGF-I deprivation and hypersecretion, as well as the relationship between IGF-I and thyroid cancer. Emphasis is given to data in children and aspects of linear growth and skeletal maturation.

Animals↗
PubMed1991

Inhibitory effect of calcitonin on growth hormone response to growth hormone releasing hormone in acromegaly.

1. A neuroendocrine role for calcitonin (CT) has been suggested by the finding of CT receptors in the hypothalamus. We have recently shown that salmon calcitonin (sCT) inhibits growth hormone releasing hormone (GHRH)-induced GH secretion in man by a mechanism apparently independent of changes in peripheral cortisol, glucose, calcium or parathyroid hormone levels. 2. We have further investigated the inhibitory action of sCT on GH secretion by studying the effects of sCT (100 MRC units, im) or placebo on basal and GHRH (1-29) NH2 (50 micrograms, iv) stimulated GH secretion in 6 acromegalic patients with active disease. 3. Basal GH levels were not altered by sCT administration (placebo: 136 +/- 99 micrograms/l vs sCT: 99 +/- 53 micrograms/l). However, the GH response to GHRH was decreased by sCT. The area under the curve was significantly smaller when patients were treated with sCT compared to placebo controls (placebo: 77202 +/- 57036 vs sCT: 64828 +/- 51909 micrograms min-1 l-1; P less than 0.02). No changes in glucose or calcium levels were observed. 4. These results demonstrate that sCT decreases GHRH-induced GH secretion in acromegalic patients. Although the mechanism of action of sCT on GH secretion is unknown, our results indicate that the inhibitory effect of this peptide on GH secretion is also observed in patients harboring pituitary adenomas.

Acromegaly↗
PubMed1977

Luteinizing hormone-releasing hormone and serum growth hormone in insulin-dependent diabetes.

Growth hormone (GH) responses were studied in 26 insulin-dependent diabetics after the intravenous administration of 100 microgram of synthetic luteinizing hormone-releasing hormone (LH-RH). Although the mean basal GH concentration was significantly higher than that of 20 matched non-diabetic controls, no significant increment occurred after the LH-RH injection. (The controls also showed no rise in GH.) It seems that the GH hypersecretion of insulin-requiring diabetics does not, as is frequently noted in acromegaly, respond to the injection of LH-RH.

Adolescent↗
PubMed1979

Serum luteinizing hormone and ovulatory response to luteinizing hormone-releasing hormone in the estrous and anestrous domestic cat.

A heterologous double antibody radioimmunoassay was developed to measure changes in serum luteinizing hormone (LH) concentrations in estrous and anestrous queens (female domestic cats), following a single injection of varying doses (0--25 microgram) of luteinizing hormone-releasing hormone (LH-RH). No increase in serum LH was detected in any of the estrous or anestrous queens following a single saline injection. Treatment with LH-RH resulted in a sharp increase in serum LH concentration in both estrous and anestrous queens. Ovulations as observed by the presence of corpora lutea at laparoscopy occurred in none of four, one of four, two of four and four of four estrous queens receiving 0, 5, 10 or 25 microgram of LH-RH, respectively. Mean serum LH concentration of the ovulating queens was maintained at a higher level and did not return to basal level at the same time as that of nonovulating queens. The data show that: LH-RH can cause release of LH in both estrous and anestrous queens and induce ovulation in the estrous cat; the magnitude of LH response is influenced by the stage of the reproductive cycle; and the duration during which LH is maintained above basal level may play a significant role in ovulation induction in this coitus-induced ovulatory species.

Anestrus↗
PubMed1984

Hormonal regulation of cyclic AMP-dependent protein kinase in cultured ovarian granulosa cells. Effects of follicle-stimulating hormone and gonadotropin-releasing hormone.

The hormonal regulation of cAMP-dependent protein kinase was examined in granulosa cells from diethylstilbestrol-implanted immature rats. Follicle-stimulating hormone (FSH) increased the number of available cAMP-binding sites in a dose- and time-dependent manner, with a maximum 4-6-fold increase at 50-100 ng/ml between 6 and 48 h of culture after a transient decrease in available sites during the first 6 h. The potent gonadotropin-releasing hormone (GnRH) agonist [D - Ala6]des - Gly10 - GnRH - N - ethylamide (GnRHa) reduced the FSH-induced increase in cAMP-binding sites by approximately 50% at 24 and 48 h of culture. Photoaffinity labeling with 8-azido-[32P] cAMP revealed the existence of one major cAMP-binding protein (Mr = 55,000 +/- 400) which appeared to be the regulatory (R) subunit of type II cAMP-dependent protein kinase. While FSH induced a 5-10-fold increase in the labeling of R II both in vivo and in vitro, GnRHa reduced the amount of R II induced by FSH in granulosa cells cultured for 48 h. The large increase in R II subunit was not accompanied by a corresponding increase in protein kinase activity, which was only enhanced by 50% after 48 h of culture with FSH. Fractionation of granulosa cell cytosol from FSH-treated ovaries on DEAE-cellulose showed a single peak of cAMP-dependent phosphokinase activity with the elution properties of a type II protein kinase. However, the peak of cAMP binding activity (eluted at 0.20 M KCl) was not coincident with the protein kinase activity. FSH transiently stimulated cAMP-dependent protein kinase activity during the first 10-30 min of culture. GnRHa impaired the FSH-induced early increase in protein kinase activity, causing a delay in activation until 60 min. These findings suggest that a large dose- and time-dependent increase in the content of cAMP-binding sites may be a major factor in cAMP-mediated differentiation of granulosa cells. The inhibitory effect of GnRHa on both FSH-induced protein kinase activation during the first minutes of culture and on FSH-induced R II synthesis during the subsequent 48 h of culture could be crucial events in the prevention of granulosa cell maturation by GnRH agonists.

Animals↗
PubMed1994

Regulation of luteinizing hormone-releasing hormone and luteinizing hormone secretion by hypothalamic amino acids.

1. The present review discusses the proposed roles of the amino acids glutamate and GABA in the central regulation of luteinizing hormone-releasing hormone (LHRH) and in luteinizing hormone (LH) secretion. 2. Descriptions of the mechanisms of action of these neurotransmitters have focused on two diencephalic areas, namely, the preoptic-anterior hypothalamic area where the cell bodies of LHRH neurons are located, and the medial basal hypothalamus which contains the nerve endings of the LHRH system. Increasing endogenous GABA concentration by drugs, GABA agonists, or blockade of glutamatergic neurotransmission by selective antagonists in rats and non-human primates prevents ovulation and pulsatile LH release, and blunts the LH surges induced by estrogen or an estrogen-progesterone combination. In contrast, glutamate and different glutamate agonists such as NMDA, AMPA and kainate, can increase LHRH/LH secretion. 3. The simultaneous enhancement of glutamatergic activity and a decrease of GABAergic tone may positively influence the maturation of the pituitary-gonadal system in rats and non-human primates. Administration of glutamate receptor agonists has been shown to significantly advance the onset of puberty. Conversely, glutamate antagonists or increased endogenous GABA levels may delay the onset of puberty. The physiological regulation of LHRH/LH secretion may thus involve a GABA-glutamate interaction and a cooperative action of the various types of ionotropic glutamate receptors. 4. The inhibitory actions of GABA on LH release and ovulation may be exerted at the level of afferent nerve terminals that regulate LHRH secretion. A likely candidate is noradrenaline, as suggested by the synaptic connections between noradrenergic nerve terminals and GABAergic interneurons in the preoptic area. Recent experiments have provided complementary evidence for the physiological balance between inhibitory and excitatory transmission resulting in modulation of the action of noradrenaline to evoke LHRH release.

Animals↗
PubMed1993

Effects of the opioid antagonist naltrexone-estrone azine on the luteinizing hormone-releasing hormone induced release of luteinizing hormone from the pituitary glands of ovariectomized rats.

The effects were studied of in vivo administration of the new opioid antagonist-estrogen hybrid, naltrexone-estrone azine (EH-NX), on subsequent luteinizing hormone-releasing hormone (LHRH)-stimulated luteinizing hormone (LH) release by the pituitary gland in vitro. It is well known that administration of estrogen exerts negative and positive effects on the pituitary LH response to LHRH, respectively after short-term and long-term treatment. Rats were injected subcutaneously with either 17 beta-estradiol-3-benzoate (EB), EH-NX or oil on days 18 and 19 (long-term treatment), and on day 21 (short-term treatment) following ovariectomy. Twenty minutes later the animals were killed and the pituitary glands were incubated in the presence of LHRH (1000 ng/ml) for 4 h. Whereas short-term treatment with EB on day 21 did not affect LH release in vitro, EH-NX significantly decreased the pituitary LH response to LHRH in oil pretreated rats. This inhibitory effect was partially blocked by the opioid antagonist naltrexone. After long-term EB or EH-NX, followed by short-term oil treatment, the pituitary LH response to LHRH was increased considerably, compared to the long-term oil controls. These observations demonstrate that the opioid antagonist estrogen hybrid EH-NX has estrogenic activity at the level of the pituitary gland. This hybridized drug is more effective in time than EB and an equimolar amount of EH (estrone hydrazone) to induce the negative estrogenic effect.

Animals↗
PubMed2002

Pulsatile growth hormone secretion persists in genetic growth hormone-releasing hormone resistance.

Growth hormone (GH) secretion is regulated by GH-releasing hormone (GHRH), somatostatin, and possibly ghrelin, but uncertainty remains about the relative contributions of these hypophysiotropic factors to GH pulsatility. Patients with genetic GHRH receptor (GHRH-R) deficiency present an opportunity to examine GH secretory dynamics in the selective absence of GHRH input. We studied circadian GH profiles in four young men homozygous for a null mutation in the GHRH-R gene by use of an ultrasensitive GH assay. Residual GH secretion was pulsatile, with normal pulse frequency, but severely reduced amplitude (<1% normal) and greater than normal process disorder (as assessed by approximate entropy). Nocturnal GH secretion, both basal and pulsatile, was enhanced compared with daytime. We conclude that rhythmic GH secretion persists in an amplitude-miniaturized version in the absence of a GHRH-R signal. The nocturnal enhancement of GH secretion is likely mediated by decreased somatostatin tone. Pulsatility of residual GH secretion may be caused by oscillations in somatostatin and/or ghrelin; it may also reflect intrinsic oscillations in somatotropes.

Adult↗