scholarly journals Simultaneous stimulation of slow-wave sleep and growth hormone secretion by gamma-hydroxybutyrate in normal young Men.

1997 ◽  
Vol 100 (3) ◽  
pp. 745-753 ◽  
Author(s):  
E Van Cauter ◽  
L Plat ◽  
M B Scharf ◽  
R Leproult ◽  
S Cespedes ◽  
...  
1999 ◽  
Vol 41 (2) ◽  
pp. 192-194 ◽  
Author(s):  
Kuniaki Iyoda ◽  
Hitoshi Tobiume ◽  
Susumu Kanzaki ◽  
Syouko Takano2 And Yoshiki Seino

1987 ◽  
Vol 27 (3) ◽  
pp. 355-361 ◽  
Author(s):  
P. ADLARD ◽  
F. BUZI ◽  
J. JONES ◽  
R. STANHOPE ◽  
M. A. PREECE

2004 ◽  
pp. 561-566 ◽  
Author(s):  
SK Jessup ◽  
BA Malow ◽  
KV Symons ◽  
AL Barkan

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.


1976 ◽  
Vol 82 (2) ◽  
pp. 460-466 ◽  
Author(s):  
C. Lucke ◽  
B. Höffken ◽  
A. von zur Mühlen

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.


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 ◽  
...  

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.


1990 ◽  
Vol 27 (5) ◽  
pp. 497-509 ◽  
Author(s):  
David B. Jarrett ◽  
Joel B. Greenhouse ◽  
Jean M. Miewald ◽  
Iva B. Fedorka ◽  
David J. Kupfer

Science ◽  
1969 ◽  
Vol 163 (3868) ◽  
pp. 705-705
Author(s):  
Lawrence A. Frohman ◽  
Lee L. Bernardis ◽  
Kenneth J. Kant

Science ◽  
1968 ◽  
Vol 162 (3853) ◽  
pp. 580-582 ◽  
Author(s):  
L. A. Frohman ◽  
L. L. Bernardis ◽  
k. J. Kant

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