Sleep-promoting effects of growth hormone-releasing hormone in normal men

1993 ◽  
Vol 264 (4) ◽  
pp. E594-E598 ◽  
Author(s):  
M. Kerkhofs ◽  
E. Van Cauter ◽  
A. Van Onderbergen ◽  
A. Caufriez ◽  
M. O. Thorner ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Sleep Deprivation ◽  
Rem Sleep ◽  
Fold Increase ◽  
Growth Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Gh Secretion ◽  
Normal Men ◽  
Sleep Propensity ◽  
Sleep In Animals

Growth hormone-releasing hormone (GHRH) promotes rapid-eye-movement (REM) and non-REM sleep in animals, but there is little direct evidence for a hypnogenic action of GHRH in humans. In the present study, the possible somnogenic effects of intravenous bolus injections of a dose of GHRH eliciting physiological elevations of GH secretion in healthy young men were investigated. GHRH (0.3 micrograms/kg body wt) was given in early sleep [i.e., 1st slow-wave (SW) period], late sleep (i.e., 3rd REM period), and early sleep after sleep deprivation until 0400 h (i.e., 1st SW period). In the absence of sleep deprivation, injection of GHRH in early sleep did not modify SW sleep but increased REM sleep. GHRH administration in the third REM period was followed by a marked decrease of wake and an almost 10-fold increase in SW sleep. When GHRH was administered during the first SW period after sleep deprivation until 0400 h, the duration of wake decreased. Thus GHRH has sleep-promoting effects in young adults, particularly when given at a time of decreased sleep propensity.

Growth hormone-releasing hormone antibodies suppress sleep and prevent enhancement of sleep after sleep deprivation

1992 ◽  
Vol 263 (5) ◽  
pp. R1078-R1085 ◽  
Author(s):  
F. Obal ◽  
L. Payne ◽  
M. Opp ◽  
P. Alfoldi ◽  
L. Kapas ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Sleep Deprivation ◽  
Slow Wave ◽  
Brain Temperature ◽  
Wave Activity ◽  
Slow Wave Activity ◽  
Base Line ◽  
Light Cycle ◽  
Growth Hormone Releasing Hormone ◽  
Releasing Hormone

Previous reports suggest that the hypothalamic growth hormone-releasing hormone (GHRH) promotes sleep, especially non-rapid-eye-movement sleep (NREMS). To evaluate the role of endogenous GHRH in sleep regulation, the effects of antibodies to rat GHRH (GHRH-ab) were studied on normal sleep, brain temperature (Tbr), and GH secretion in experiment I and on enhanced sleep after sleep deprivation in experiment II. In experiment I, affinity-purified GHRH-ab (50 and 200 micrograms) raised in goats and a control goat immunoglobulin G (IgG) preparation were injected intracerebroventricularly (icv) in rats 1 h before the onset of the light cycle, and sleep-wake activity and Tbr were recorded for the next 12 or 23 h. Both doses of GHRH-ab suppressed NREMS and REMS throughout the light cycle. Sleep durations at night were normal. Electroencephalographic (EEG) slow-wave activity, characterized by EEG slow-wave amplitudes, was reduced after GHRH-ab during both the light and the dark cycles. Plasma GH concentrations measured 6-12 h after injection of GHRH-ab (200 micrograms) were diminished. Both the control IgG and GHRH-ab elicited fever. In experiment II, the sleep-wake activity and Tbr of rats were recorded for 24 h in three experimental conditions: base-line with icv injection of IgG, 3-h sleep deprivation with icv IgG injection, and 3-h sleep deprivation with icv GHRH-ab (200 micrograms). After sleep deprivation (+IgG), a prompt increase in EEG slow-wave activity (power density analysis) and late increases in NREMS and REMS durations were found.(ABSTRACT TRUNCATED AT 250 WORDS)

Growth hormone-releasing hormone in the diagnosis and treatment of growth hormone deficient children

1986 ◽  
Vol 113 (4_Suppl) ◽  
pp. S123-S129
Author(s):  
R.J.M. ROSS ◽  
A. GROSSMAN ◽  
G.M. BESSER ◽  
M.O. SAVAGE
Keyword(s):  
Growth Hormone ◽  
Linear Growth ◽  
Gh Deficiency ◽  
Venous Blood ◽  
Alternative Therapy ◽  
Normal Subjects ◽  
Growth Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Gh Secretion ◽  
Depot Preparations

ABSTRACT A growth hormone-releasing hormone (GHRH) has recently been extracted and synthesised, and appears to be identical to human hypothalamic GHRH. Immunoreactive GHRH is found in the venous blood of normal subjects and GH-deficient children, but is probably not hypothalamic in origin and therefore not important in GH regulation. GHRH is a potent specific stimulator of GH secretion in man, and provides a valuable diagnostic test in differentiating hypothalamic from pituitary causes of GH deficiency. Preliminary data suggests that GHRH may promote linear growth in some GH deficient children. GHRH may well prove an important alternative therapy for GH deficient children especially if depot preparations or intranasal administration prove effective.

scholarly journals Molecular evolution of the growth hormone-releasing hormone/pituitary adenylate cyclase-activating polypeptide gene family. Functional implication in the regulation of growth hormone secretion

2000 ◽  
Vol 25 (2) ◽  
pp. 157-168 ◽  
Author(s):  
M Montero ◽  
L Yon ◽  
S Kikuyama ◽  
S Dufour ◽  
H Vaudry
Keyword(s):  
Growth Hormone ◽  
Molecular Evolution ◽  
Adenylate Cyclase ◽  
Gene Family ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Growth Hormone Releasing Hormone ◽  
Releasing Hormone ◽  
Gh Secretion ◽  
Pituitary Adenylate Cyclase

Growth hormone-releasing hormone (GHRH) and pituitary adenylate cyclase-activating polypeptide (PACAP) belong to the same superfamily of regulatory neuropeptides and have both been characterized on the basis of their hypophysiotropic activities. This review describes the molecular evolution of the GHRH/PACAP gene family from urochordates to mammals and presents the hypothesis that the respective roles of GHRH and PACAP in the control of GH secretion are totally inverted in phylogenetically distant groups of vertebrates. In mammals, GHRH and PACAP originate from distinct precursors whereas, in all submammalian taxa investigated so far, including birds, amphibians and fish, a single precursor encompasses a GHRH-like peptide and PACAP. In mammals, GHRH-containing neurons are confined to the infundibular and dorsomedial nuclei of the hypothalamus while PACAP-producing neurons are widely distributed in hypothalamic and extrahypothalamic areas. In fish, both GHRH- and PACAP-immunoreactive neurons are restricted to the diencephalon and directly innervate the adenohypophysis. In mammals and birds, GHRH plays a predominant role in the control of GH secretion. In amphibians, both GHRH and PACAP are potent stimulators of GH release. In fish, PACAP strongly activates GH release whereas GHRH has little or no effect on GH secretion. The GHRH/PACAP family of peptides thus provides a unique model in which to investigate the structural and functional facets of evolution.

Growth hormone response to growth hormone-releasing hormone (GHRH), insulin, clonidine and arginine after GHRH pretreatment in obese children: evidence of somatostatin increase?

1995 ◽  
Vol 132 (6) ◽  
pp. 716-721 ◽  
Author(s):  
Cecilia Volta ◽  
Sergio Bernasconi ◽  
Lorenzo lughetti ◽  
Lucia Ghizzoni ◽  
Maurizio Rossi ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Normal Weight ◽  
Growth Hormone Response ◽  
Growth Hormone Releasing Hormone ◽  
Hormone Response ◽  
Obese Children ◽  
Normal Children ◽  
Insulin Hypoglycemia ◽  
Releasing Hormone ◽  
Gh Secretion

Volta C. Bernasconi S, lughetti L, Ghizzoni L, Rossi M, Costa M, Cozzini A. Growth hormone response to growth hormone-releasing hormone (GHRH), insulin, clonidine and arginine after GHRH pretreatment in obese children: evidence of somatostatin increase? Eur J Endocrinol 1995; 132:716–21. ISSN 0804–4643 To clarify the possible neuroendocrine mechanisms underlying the impairment in growth hormone (GH) secretion present in obesity, the GH response to GH-releasing hormone (GHRH, N = 6), insulin hypoglycemia (N = 6), clonidine (N = 7) and arginine (N = 8) after GHRH pretreatment (1 μg/kg iv 2 h before the tests) was evaluated in 27 obese peripubertal children and in a group of normal-weight short-normal children (N = 26). Growth hormone-releasing hormone pretreatment and all further stimuli elicited a statistically significant GH response in both obese and short-normal children; in the latter group arginine did not induce a significant GH response. No differences were found among the GH responses after the second stimuli in obese children, while in short-normal children the arginine peak and area values were lower than after GHRH and clonidine. Comparison between the two groups showed similar baseline but higher stimulated GH levels in normal-weight children after all tests except ariginine, after which no difference was present. In conclusion, the neuroregulation of GH release seems to be similar qualitatively in normal-weight and obese youngsters; the different behavior observed after arginine, which is supposed to act through somatostatin inhibition, might be due to a chronic increase in somatostatinergic tone responsible for the lower stimulated GH levels in obesity. Sergio Bernasconi, Clinica Pediatrica, Via Gransci 14, 43100 Parma, Italy

Sleep deprivation increases rat hypothalamic growth hormone-releasing hormone mRNA

1998 ◽  
Vol 275 (6) ◽  
pp. R1755-R1761 ◽  
Author(s):  
Jianyi Zhang ◽  
Zutang Chen ◽  
Ping Taishi ◽  
Ferenc Obál ◽  
Jidong Fang ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Sleep Deprivation ◽  
Mrna Expression ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Mrna Levels ◽  
Growth Hormone Releasing Hormone ◽  
Sleep Regulation ◽  
Releasing Hormone ◽  
Sleep Homeostasis

Much evidence indicates that growth hormone-releasing hormone (GHRH) is involved in sleep regulation. We hypothesized that GHRH mRNA would increase and somatostatin (SRIH) mRNA would decrease during sleep deprivation. With the use of RT-PCR and truncated internal standards, rat hypothalamic GHRH mRNA and SRIH mRNA levels were evaluated after sleep deprivation. After 8 or 12 h of sleep deprivation there was a significant increase in rat hypothalamic GHRH mRNA expression compared with time-matched control samples. Hypothalamic GHRH mRNA levels were not significantly different from control values after 1 or 2 h of recovery after 8 h of sleep deprivation or after 2 h of recovery after 12 h of sleep deprivation. In control animals, variations in hypothalamic GHRH mRNA levels were observed. GHRH mRNA expression was significantly higher in the afternoon than at dark onset or during the dark period. SRIH mRNA levels were significantly suppressed at the termination of an 8-h sleep deprivation period and were significantly higher after dark onset than in the morning. The alterations in GHRH and SRIH mRNA expressions after sleep deprivation and recovery support the notion that GHRH plays an important role in sleep homeostasis and suggest that these neuropeptides may interact reciprocally in modulating sleep as they do in the control of growth hormone secretion.

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