Suppression of nocturnal growth hormone secretion in epilepsy with continuous spike-waves during slow-wave sleep

1999 ◽  
Vol 41 (2) ◽  
pp. 192-194 ◽  
Author(s):  
Kuniaki Iyoda ◽  
Hitoshi Tobiume ◽  
Susumu Kanzaki ◽  
Syouko Takano2 And Yoshiki Seino
Keyword(s):  
Growth Hormone ◽  
Slow Wave ◽  
Slow Wave Sleep ◽  
Hormone Secretion ◽  
Growth Hormone Secretion

PHYSIOLOGICAL GROWTH HORMONE SECRETION DURING SLOW-WAVE SLEEP IN SHORT PREPUBERTAL CHILDREN

1987 ◽  
Vol 27 (3) ◽  
pp. 355-361 ◽  
Author(s):  
P. ADLARD ◽  
F. BUZI ◽  
J. JONES ◽  
R. STANHOPE ◽  
M. A. PREECE
Keyword(s):  
Growth Hormone ◽  
Slow Wave ◽  
Slow Wave Sleep ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Prepubertal Children

scholarly journals Blockade of endogenous growth hormone-releasing hormone receptors dissociates nocturnal growth hormone secretion and slow-wave sleep

2004 ◽  
pp. 561-566 ◽  
Author(s):  
SK Jessup ◽  
BA Malow ◽  
KV Symons ◽  
AL Barkan
Keyword(s):  
Growth Hormone ◽  
Slow Wave ◽  
Hormone Receptors ◽  
Slow Wave Sleep ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Nrem Sleep ◽  
Temporal Association ◽  
Sleep Stages ◽  
Sleep Study

OBJECTIVES: A temporal association between non-rapid eye movement (NREM) sleep stages 3 and 4 and nocturnal augmentation of GH release was found long ago, yet the precise mechanism for this association has not been identified. It has been shown, however that pulsatile GHRH administration increases both slow-wave sleep (SWS) and GH. Based on these data, a role for GHRH as an inducer of SWS was proposed. To test this hypothesis, we have performed the corollary experiment whereby the action of endogenous GHRH has been antagonized. DESIGN: Healthy men (20-33 years old) had an infusion of GHRH antagonist ((N-Ac-Tyr(1), D-Arg(2)) GHRH-29 (NH(2))) or saline for a 12-h period, between 2100 and 0900 h. An i.v. bolus of GHRH was given at 0700 h and GH samples were drawn from 0700 to 0900 h to document the efficacy of GH suppression by the GHRH antagonist. METHODS: A limited montage sleep study was recorded from 2300 to 0700 h during each admission. Plasma GH concentrations were analyzed by the use of a sensitive chemiluminometric assay. RESULTS: Effectiveness of the GHRH antagonist was validated in all subjects by demonstrating 93+/-1.8% (P=0.012) suppression of GH response to a GHRH bolus. Polysomnography demonstrated that the percentage of SWS was not different when saline and GHRH antagonist nights were compared (P=0.607); other quantifiable sleep parameters were also unchanged. CONCLUSIONS: We conclude that endogenous GHRH is indispensable for the nocturnal augmentation of GH secretion, but that it is unlikely to participate in the genesis of SWS.

STUDIES ON THE POSTPONED GROWTH HORMONE SECRETION FOLLOWING THE INFUSION OF SOMATOSTATIN

1976 ◽  
Vol 82 (2) ◽  
pp. 460-466 ◽  
Author(s):  
C. Lucke ◽  
B. Höffken ◽  
A. von zur Mühlen
Keyword(s):  
Growth Hormone ◽  
Slow Wave ◽  
Slow Wave Sleep ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Rapid Rise ◽  
Trigger Mechanism ◽  
Gh Secretion ◽  
Inhibiting Factor ◽  
Rebound Phenomenon

ABSTRACT It is well known and also confirmed in this study that somatostatin (growth hormone inhibiting factor, GHIF) prevents the nocturnal GH secretion, as long as the peptide is infused. Following the infusion a rapid rise in GH levels is seen in sleeping subjects with peak values of 26.8 ± 9.7 ng/ml compared to 31.7 ± 4.7 ng/ml (± sem) in control nights. Delayed GH peaks were seen even in the absence of slow wave sleep. No postponed GH rise was observed when subjects fell asleep again. These data demonstrate that the postponed nocturnal GH peak does not represent a rebound phenomenon to a previous trigger mechanism but is acutely sleep induced.

Reversibility of deficient sleep entrained growth hormone secretion in a boy with achondroplasia and obstructive sleep apnea

1987 ◽  
Vol 116 (1) ◽  
pp. 95-101 ◽  
Author(s):  
Steven J. Goldstein ◽  
Richard H. K. Wu ◽  
Michael J. Thorpy ◽  
Robert J. Shprintzen ◽  
Robert E. Marion ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Slow Wave ◽  
Slow Wave Sleep ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Hormone Release ◽  
Growth Hormone Release ◽  
Obstructive Sleep

Abstract. Obstructive sleep apnea may lead to disordered sleep architecture and impair the physiologic slow wave sleep related growth hormone release. Obstructive sleep apnea occurs with craniofacial syndromes and in children with airway narrowing, pharyngeal hypoplasia, tonsillar adenoidal hypertrophy, micrognathia and achondroplasia. To examine the relationship between disordered sleep and growth hormone release we studied a 9 year old male with achondroplasia, growth failure (3 cm/year) and obstructive sleep apnea. Polysomnography data and a 20 min sampling for sleep entrained growth hormone showed before therapeutic tracheostomy numerous apneic episodes, absent slow wave sleep and abnormal low growth hormone secretion during sleep. Normalized slow wave sleep entrained growth hormone secretion after tracheostomy led to a sustained increase in growth rate. Normal growth rate (> 5 cm/year) continues 2 years after tracheostomy. We conclude that obstructive sleep apnea may impair sleep related growth hormone release. Obstructive sleep apnea may be a useful model for other diseases in which growth failure and sleep disturbances are linked.

A reexamination of the relationship between growth hormone secretion and slow wave sleep using delta wave analysis

1990 ◽  
Vol 27 (5) ◽  
pp. 497-509 ◽  
Author(s):  
David B. Jarrett ◽  
Joel B. Greenhouse ◽  
Jean M. Miewald ◽  
Iva B. Fedorka ◽  
David J. Kupfer
Keyword(s):  
Growth Hormone ◽  
Slow Wave ◽  
Slow Wave Sleep ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Wave Analysis ◽  
Delta Wave ◽  
The Relationship

Sleep-endocrine effects of mifepristone and megestrol acetate in healthy men

1998 ◽  
Vol 274 (1) ◽  
pp. E139-E145 ◽  
Author(s):  
Klaus Wiedemann ◽  
Christoph J. Lauer ◽  
Margarete Hirschmann ◽  
Kristina Knaudt ◽  
Florian Holsboer
Keyword(s):  
Growth Hormone ◽  
Slow Wave Sleep ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Sleep Eeg ◽  
Megestrol Acetate ◽  
Simultaneous Administration ◽  
Healthy Men ◽  
Eeg Recordings ◽  
Time Awake

Administration of steroid hormones was demonstrated to modulate the sleep electroencephalogram (EEG) and sleep-associated hormonal secretion in specific ways. The present study was conducted to compare the effects of mifepristone (Mif), a mixed glucocorticoid (GR) and progesterone receptor (PR) antagonist, and megestrol acetate (Meg), a PR agonist. Nine healthy men were pretreated with either placebo or 200 mg Mif or 320 mg Meg, or a combination of both. Changes in plasma adrenocorticotropic hormone (ACTH), cortisol, and growth hormone concentrations were registered every 30 min; sleep EEG recordings were obtained continuously. Administration of Mif increased the morning plasma ACTH and cortisol surges, whereas Meg had the opposite effect. Growth hormone secretion was lowered by Mif pretreatment and enhanced by Meg. Simultaneous administration of both compounds led to largely compensated effects. The sleep EEG changes induced by Mif were a slight increase in the time awake and a delayed onset of slow-wave sleep. Meg led to a reduction of rapid-eye-movement sleep. Simultaneous administration of Mif and Meg showed a synergism in increasing time awake and shallow sleep: it therefore may be concluded that the sleep EEG effects are mediated by an interaction of GR and PR in unknown mechanisms.

NOCTURNAL GROWTH HORMONE SECRETION: CORRELATION WITH SLEEPING EEG IN ADULTS AND PATTERN IN CHILDREN AND ADOLESCENTS WITH NON-PITUITARY DWARFISM, OVERGROWTH AND WITH OBESITY

1971 ◽  
Vol 67 (4) ◽  
pp. 767-783 ◽  
Author(s):  
H.-J. Quabbe ◽  
H. Helge ◽  
S. Kubicki
Keyword(s):  
Growth Hormone ◽  
Children And Adolescents ◽  
Slow Wave Sleep ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Immunoreactive Insulin ◽  
Normal Children ◽  
Pituitary Dwarfism ◽  
Continuous Eeg ◽  
Eeg Recordings

ABSTRACT Half-hourly blood samples and continuous EEG recordings were obtained during nocturnal sleep in ten adults in whom a special sampling system working from the adjacent room was used in order not to disturb the sleep. In nine of the ten adults the first D/E-stage during sleep was accompanied by a significant increase in plasma growth hormone (HGH) (2.5 to 31.8 ng/ml). Of 16 subsequent D/E-stages only three were accompanied by HGH peaks. Similar studies but without EEG recordings were done in 25 children and adolescents. HGH peaks comparable to those seen in adults occurred in normal children, children with constitutional or primordial dwarfism, with retarded growth associated with renal or with miscellaneous diseases and in children with overgrowth. These peaks frequently seemed to coincide with periods of deeper sleep as judged from observation of the children. There was no evidence that HGH peaks occurred less often or were smaller in dwarfed children or that children with overgrowth had higher or more frequent HGH peaks. However, fewer and smaller HGH peaks were seen in obese children, whether or not obesity was associated with overgrowth. There was no correlation between nocturnal HGH peaks and variations in the concentration of blood sugar (BS), free fatty acids (FFA) or immunoreactive insulin (IRI). No apparent correlation could be seen between the height of the nocturnal HGH peaks and the response of plasma HGH concentration to provocative stimuli. It is concluded that nocturnal HGH peaks are related to, but not exclusively determined by phases of slow-wave sleep. They are not due to disturbance of sleep by the sampling procedure. Their pattern is the same in adults, normal children and in children with non-pituitary dwarfism or overgrowth. Obese subjects often have fewer and smaller nocturnal HGH peaks even when obesity is associated with overgrowth.

Effect of sodium oxybate on growth hormone secretion in narcolepsy patients and healthy controls

2011 ◽  
Vol 300 (6) ◽  
pp. E1069-E1075 ◽  
Author(s):  
Claire E. H. M. Donjacour ◽  
N. Ahmad Aziz ◽  
Ferdinand Roelfsema ◽  
Marijke Frölich ◽  
Sebastiaan Overeem ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Slow Wave Sleep ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Approximate Entropy ◽  
Sodium Oxybate ◽  
Fat Percentage ◽  
Body Weight Reduction ◽  
Gh Secretion ◽  
Concentration Time Series

Hypocretin deficiency causes narcolepsy and may affect neuroendocrine systems and body composition. Additionally, growth hormone (GH) alterations my influence weight in narcolepsy. Symptoms can be treated effectively with sodium oxybate (SXB; γ-hydroxybutyrate) in many patients. This study compared growth hormone secretion in patients and matched controls and established the effect of SXB administration on GH and sleep in both groups. Eight male hypocretin-deficient patients with narcolepsy and cataplexy and eight controls matched for sex, age, BMI, waist-to-hip ratio, and fat percentage were enrolled. Blood was sampled before and on the 5th day of SXB administration. SXB was taken two times 3 g/night for 5 consecutive nights. Both groups underwent 24-h blood sampling at 10-min intervals for measurement of GH concentrations. The GH concentration time series were analyzed with AutoDecon and approximate entropy (ApEn). Basal and pulsatile GH secretion, pulse regularity, and frequency, as well as ApEn values, were similar in patients and controls. Administration of SXB caused a significant increase in total 24-h GH secretion rate in narcolepsy patients, but not in controls. After SXB, slow-wave sleep (SWS) and, importantly, the cross-correlation between GH levels and SWS more than doubled in both groups. In conclusion, SXB leads to a consistent increase in nocturnal GH secretion and strengthens the temporal relation between GH secretion and SWS. These data suggest that SXB may alter somatotropic tone in addition to its consolidating effect on nighttime sleep in narcolepsy. This could explain the suggested nonsleep effects of SXB, including body weight reduction.

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