Nocturnal Growth Hormone Secretion Research Articles

Discordance Between Stimulated and Spontaneous Growth Hormone Levels in Short Children Is Dependent on Cut-Off Level and Partly Explained by Refractoriness.

BackgroundA growth hormone (GH) stimulation test is the recommended method for evaluating GH levels in children with possible GH deficiency (GHD). However, serial measurements of nocturnal spontaneous GH secretion are also performed. Divergent results from these tests have been reported, but with variable frequencies.ObjectivesTo investigate whether performing one or two GH tests is associated with the probability to diagnose a child with GHD; the frequency of divergent results in the arginine-insulin tolerance test (AITT) and the nocturnal spontaneous test using different cut-off levels, and whether refractoriness may explain some of the discordance.MethodsIn a population-based setting, the medical records of all short children evaluated for possible GHD during January 1993–February 2017 were reviewed. Twenty-one patients had been evaluated with one GH test only and 102 children had been evaluated with a spontaneous nocturnal GH test followed immediately by a complete AITT. Divergent results were defined as having a pathological response on only one of the tests when using 3, 5, 7, and 10 µg/L as cut-offs for peak GH on both tests, 1.1 and 3.3 µg/L for mean nocturnal values and receiver operating characteristic curves-derived cut-offs for nocturnal values.ResultsChildren evaluated with one test only were more often diagnosed with GHD compared with children evaluated with both tests (48 vs. 19%, p = 0.019). Divergent results were found in 6–42% of the patients, with higher frequencies seen when higher cut-offs were applied. A higher proportion of patients with stimulated peak values ≤ 7 and ≤ 5 µg/L had a spontaneous peak within 2 h before the start of the AITT compared with patients with higher stimulated peak values (68 vs. 45%, p = 0.026, and 77 vs. 48%, p = 0.033, respectively).ConclusionsDivergent results between AITT and nocturnal spontaneous secretion are common in short children, dependent on the cut-offs applied and partly due to refractoriness. Performing both tests decreases the risk of over diagnosing GHD in short children.

P1.03: Intravenous glucose nocturnal infusion reduces growth hormone secretion in children on total parenteral nutrition

Introduction: Most children with intestinal failure (IF) benefit from home parenteral nutrition (HPN). It allows a familial life with normal children activities such as going to school, sports, and being at home. In order to do so, PN is provided with cyclic infusion at night. Children with IF on HPN should have normal growth. However, some children grow under their genetic target height and present with decreased height velocity. Methods: We report the case of two children on HPN who presented with decreased height velocity while their weight gain was normal. After ruling out usual etiology (insufficient protein intake, acidosis, sodium deficiency, IFALD…), growth hormone (GH) deficiency was considered. Extensive testings were performed such as IgF1 levels, GH secretion stimulation test and nocturnal GH secretion. PN dependency was assessed using the PN/REE index (parenteral nutrition non-protein energy intake divided by resting energy expenditure calculated using Schofield equation, expressed in percentage). Results: These two children needed extremely high PN caloric intake to achieve a normal weight gain with a PN dependency index of 163% and 150%. Table 1 shows their clinical characteristics. Table 2 shows the results of the biological testings. These two children showed a normal GH peak under stimulation, but a low nocturnal GH secretion meaning they were able to produce GH under stimulation, but their nocturnal physiological secretion was inhibited. Their mean glycemia during PN perfusion was high compared to fasting glycemia which should normally be observed at night in children. Hyperglycemia is a well known inhibitor of GH secretion. Conclusion: Children with very high PN dependency are at risk of developing reduced height. In some children, GH secretion seems to be inhibited by nocturnal high glucose infusion. A longer PN infusion time can be proposed and/or a decrease in glucose intake with an increase in lipid intake. Also, growth hormone supplementation might be discussed and should be evaluated in this setting.

Aromatized Estrogens Amplify Nocturnal Growth Hormone Secretion in Testosterone-Replaced Older Hypogonadal Men.

Testosterone (T) increases GH secretion in older men with a relative lack of T, in hypogonadal men of all ages, and in patients undergoing sex reassignment. The role of estradiol (E2) in men is less well defined. To assess the contribution of aromatization of T to spontaneous nocturnal and stimulated GH secretion. Four groups of healthy older men (N = 74, age range 57 to 77 years) were studied. The gonadotropic axis was clamped with the gonadotropin-releasing hormone antagonist degarelix. Three groups received T and one group placebo addback. Two T-replaced groups were treated with anastrozole (an aromatase inhibitor) and either placebo or E2 addback. Ten-minute GH concentration profiles were quantified by deconvolution analysis, after overnight (2200 to 0800 hours) sampling, and after combined IV injection of GHRH (0.3 µg/kg) and GHRH-2 (0.3 µg/kg) and withdrawal of a 2-hour somatostatin infusion (1 µg/kg/h). E2 addback during aromatase inhibition increased basal (P = 0.046), pulsatile (P = 0.020), and total (P = 0.018) GH secretion by 60% to 70%. E2 did not potentiate GH secretory stimuli. Logarithmically transformed pulsatile GH secretion correlated strongly and positively with concurrent E2 concentrations overall (P = 0.028) and under anastrozole treatment (P = 0.005). E2 administration in older men transdermally stimulates overnight pulsatile GH secretion. The exact site of E2 action cannot be ascertained from these experiments but may include hypothalamic loci involved in GH regulation, especially because GH secretagogue effects on somatotrope pituitary cells were not affected.

Pilot study: an acute bout of high intensity interval exercise increases 12.5h GH secretion.

The purpose of this study was to test the hypothesis that high‐intensity interval exercise (HIE) significantly increases growth hormone (GH) secretion to a greater extent than moderate‐intensity continuous exercise (MOD) in young women. Five young, sedentary women (mean ± SD; age: 22.6±1.3 years; BMI: 27.4±3.1 kg/m2) were tested during the early follicular phase of their menstrual cycle on three occasions. For each visit, participants reported to the laboratory at 1700 h, exercised from 1730–1800 h, and remained in the laboratory until 0700 h the following morning. The exercise component consisted of either 30‐min of moderate‐intensity continuous cycling at 50% of measured peak power (MOD), four 30‐s “all‐out” sprints with 4.5 min of active recovery (HIE), or a time‐matched sedentary control using a randomized, cross‐over design. The overnight GH secretory profile of each trial was determined from 10‐min sampling of venous blood from 1730–0600 h, using deconvolution analysis. Deconvolution GH parameters were log transformed prior to statistical analyses. Calculated GH AUC (0–120 min) was significantly greater in HIE than CON (P = 0.04), but HIE was not different from MOD. Total GH secretory rate (ng/mL/12.5 h) was significantly greater in the HIE than the CON (P = 0.05), but MOD was not different from CON or HIE. Nocturnal GH secretion (ng/mL/7.5 h) was not different between the three trials. For these women, in this pilot study, a single bout of HIE was sufficient to increase 12.5 h pulsatile GH secretion. It remains to be determined if regular HIE may contribute to increased daily GH secretion.

The Effect of Adenotonsillectomy on Growth in Prepubertal Children

Adenotonsillar hypertrophy (ATH) is the most common cause of obstructive sleep apnea syndrome in children,1 and the prevalence of obstructive sleep apnea syndrome (OSAS) were at least 1–3% in children.2 Sleep disordered breathing (SDB) is often associated with loud snoring, daytime sleepiness, and daytime mouth breathing. Complications of SDB may include failure to thrive, nocturnal enuresis, sweating during sleep, reduced neurocognition, behavioral problem, and school performances.3-5 Several possible mechanisms for failure to thrive have been assessed. Interruption of the insulin-like growth factor-I axis secondary to abnormal nocturnal growth hormone secretion,6 low caloric intake caused by poor appetite and dysphagia,7 recurrent tonsillitis,8 and high energy expenditure as a consequence of increased work of breathing during sleep9 had been proposed as causes. Also many studies had suggested and proved that growth failures were improved after adenotonsillectomy in children with ATH.10-12 On the other hand, obesity could be one of the risk factor for SDB in children.13 There were few studies about the effect of adenotonsillectomy in obesity children, instead it was reported that children who undergo adenotonsillectomy could be at risk to develop overweight in the years after surgery.14 The effect of SDB and adenotonsillectomy on children might be different according to the growth status, but little is known in this aspect. Received: June 8, 2016 Revised: June 17, 2016 Accepted: June 20, 2016

Detailed studies of growth hormone secretion in cystinosis patients

Cystinosis is an autosomal recessive disorder characterized by intralysosomal cystine accumulation. Growth retardation is more pronounced in cystinosis than in other chronic kidney diseases and is mostly not corrected by cysteamine. Growth was evaluated in nine cystinosis patients, all treated with cysteamine, both after cysteamine and recombinant human growth hormone (rhGH) therapy initiation. Growth hormone (GH) secretion was studied by nocturnal GH measurements in four of nine patients and by glucagon test in four of nine patients. RhGH was administered to seven of nine patients. At rhGH initiation, height was below -2 SDS in five of seven patients, final height was above -2 SDS in six of seven. In two patients not treated with rhGH, final height remained below -4 SDS despite cysteamine treatment being started at the age of 6.1 and 8.1 years, respectively. Nocturnal GH secretion was normal in all patients. Glucagon tests revealed GH deficiency in one patient; two of four patients had abnormal GH peak timing. We present the first reported case of GH deficiency in cystinosis. Although no overt GH deficiency was detected in other patients, abnormal GH peak timing can indicate a subclinical GH secretion problem. RhGH significantly improved growth in cystinosis patients and should be initiated early in life.

Decreased nocturnal growth hormone secretion and sleep fragmentation in combat-related posttraumatic stress disorder; potential predictors of impaired memory consolidation

Healthy sleep facilitates the consolidation of newly acquired memories. Although patients with posttraumatic stress disorder (PTSD) often complain of sleep disturbances and memory deficits, the interrelatedness of these symptoms is not well understood. Sleep may be disturbed in PTSD by increased awakenings during sleep, which has been associated with decreased growth hormone (GH) secretion. We conducted a controlled study in which we assessed sleep fragmentation, nocturnal secretion of GH, and memory consolidation in patients with PTSD. While sleep EEG was being monitored, 13 veterans with PTSD, 15 trauma controls (TC) and 15 healthy controls (HC) slept with an iv catheter, through which blood was collected every 20 min from 23:00 h to 08:00 h. Declarative memory encoding was assessed with the 15 word task before sleep, and consolidation was assessed the next morning by a free recall. Sleep was more fragmented in patients with PTSD, with more awakenings in the first half of the night (p<0.05). Plasma levels of GH during the night were significantly decreased in PTSD compared with HC (p<0.05). Furthermore, GH secretion and awakenings were independent predictors for delayed recall, which was lower in PTSD compared to HC (p<0.05). These data show that PTSD is associated with increased awakenings during sleep and decreased nocturnal GH secretion. Furthermore, decreased GH secretion may be related to sleep fragmentation and both variables may exert a negative effect on sleep dependent memory consolidation.

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

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.

Normal growth hormone secretion in overweight young adults with Down syndrome

Down syndrome (DS) is associated with short stature and obesity. Adults with DS have several features in common with growth hormone (GH) deficient adult subjects. The aim of this study was to investigate GH secretion in young adults with DS and its relation to body composition as well as glucose and lipid metabolism. Ten young adults with DS (aged 24–32 years; 5 F) and ten controls matched for age and sex were examined regarding spontaneous nocturnal GH secretion and body composition. Stable isotope tracers were used to study glucose and lipid metabolism in the DS subjects. There was no difference in secretion of GH between the DS subjects and controls. The DS subjects had a higher BMI, fat mass proportion and HOMA (homeostasis model assessment) index compared with the controls. The rates of production of glucose and glycerol (reflecting lipolysis) in the DS subjects were increased (15.5 ± 5.07 and 3.5 ± 1.68 μmol/kg/min, respectively). The DS subjects showed normal GH secretion despite increased BMI and fat mass. The increased HOMA index and high rate of glucose production indicate peripheral and hepatic insulin resistance in adult DS subjects.

Overtrained horses alter their resting pulsatile growth hormone secretion

The influence of intensified and reduced training on nocturnal growth hormone (GH) secretion and elimination dynamics was studied in young (1.5 yr) Standardbred geldings to detect potential markers indicative for early overtraining. Ten horses trained on a treadmill for 32 wk in age-, breed-, and gender-matched fixed pairs. Training was divided into four phases (4, 18, 6, and 4 wk, respectively): 1) habituation to high-speed treadmill trotting, 2) normal training, in which speed and duration of training sessions were gradually increased, 3) in this phase, the horses were divided into 2 groups: control (C) and intensified trained (IT) group. In IT, training intensity, duration, and frequency were further increased, whereas in control these remained unaltered, and 4) reduced training (RT). At the end of phases 2, 3, and 4, blood was sampled overnight every 5 min for 8 h for assessment of GH secretory dynamics using pulse detection, deconvolution analysis, and approximate entropy (ApEn). Intensified training induced overtraining (performance decreased by 19% compared with C), which was associated with an increase in concentration peaks number (3.6 vs. 2.0, respectively), a smaller peak secretion pattern with a prolonged half-life (15.2 vs. 7.3 min, respectively), and an increased ApEn (0.89 vs. 0.49, respectively). RT did not lead to full recovery for the overtrained horses. The increased irregularity of nocturnal GH pulsatility pattern is indicative of a loss of coordinated control of GH regulation. Longer phases of somatostatin withdrawal are hypothesized to be the underlying mechanism for the observed changes in GH pulsatility pattern.

Effects of Exercise Training Intensity on Nocturnal Growth Hormone Secretion in Obese Adults with the Metabolic Syndrome

Abdominal adiposity is associated with reduced spontaneous GH secretion, and an increased incidence of the metabolic syndrome, type 2 diabetes, and cardiovascular disease. Exercise training increases GH secretion, induces abdominal visceral fat loss, and has been shown to improve the cardiometabolic risk factor profile. However, little is known about the effects of endurance training intensity on spontaneous GH release in obese individuals. Our objective was to examine the effects of 16 wk endurance training on spontaneous 12-h overnight GH secretion in adults with the metabolic syndrome. This randomized, controlled exercise intervention was conducted at the University of Virginia. A total of 34 adults with the metabolic syndrome (mean +/- sem: age: 49.1 +/- 1.8 yr) participated. Participants were randomized to one of three groups for 16 wk: no exercise training (control), low-intensity exercise training, or high-intensity training. Change in nocturnal integrated GH area under the curve (AUC) was calculated. Both exercise training conditions augmented within-group nocturnal GH AUC pretrain to post-training (low-intensity exercise training approximately (upward arrow) 49%, P < 0.05; and high-intensity training approximately (upward arrow) 65%, P < 0.01), and these changes were also greater than the changes in the control group (P < 0.01). The change in nocturnal GH AUC was inversely associated with the change in fat mass across the entire sample (r = -0.34; P = 0.051; n=34) but was not significantly associated with the change in abdominal visceral fat (r = 0.02; P = 0.920; n = 34). Sixteen wk of supervised exercise training in adults with the metabolic syndrome increases spontaneous nocturnal GH secretion independent of exercise training intensity.

Growth and Factors Affecting it in Thalassemia Major

In our thalassemic (T) cohort, 45% of them had height standard deviation score (HtSDS) less than −2 and 56% of them had growth velocity standard deviation score (GVSDS) less than −1. Their mid-arm circumference and triceps skin-fold thickness were decreased versus normal controls. Their circulating insulin-like growth factor-I (IGF-I) concentrations were significantly lower than normal children. Growth hormone (GH) response to provocation with clonidine and glucagon was defective in half of the short T children (peak GH < 7 ng/dL). Some of the short T children, with normal GH response to provocation, had defective spontaneous nocturnal GH secretion. IGF-I generation after one GH injection was reduced in T children than those with GH deficiency (GHD) and constitutional delay of growth and puberty (CDGP). GH therapy for a year significantly increased IGF-I concentrations, GV, and HtSDS in T children but to a lower level compared to those with GHD or CDGP, suggesting partial GH insensitivity. Pubertal induction with human chorionic gonadotropin in T adolescents was associated with increased IGF-I concentrations, GV, and HtSDS.

The effect of mode of breathing on craniofacial growth--revisited

It has been maintained that because of large adenoids, nasal breathing is obstructed leading to mouth breathing and an 'adenoid face', characterized by an incompetent lip seal, a narrow upper dental arch, increased anterior face height, a steep mandibular plane angle, and a retrognathic mandible. This development has been explained as occurring by changes in head and tongue position and muscular balance. After adenoidectomy and change in head and tongue position, accelerated mandibular growth and closure of the mandibular plane angle have been reported. Children with obstructive sleep apnoea (OSA) have similar craniofacial characteristics as those with large adenoids and tonsils, and the first treatment of choice of OSA children is removal of adenoids and tonsils. It is probable that some children with an adenoid face would nowadays be diagnosed as having OSA. These children also have abnormal nocturnal growth hormone (GH) secretion and somatic growth impairment, which is normalized following adenotonsillectomy. It is hypothesized that decreased mandibular growth in adenoid face children is due to abnormal secretion of GH and its mediators. After normalization of hormonal status, ramus growth is enhanced by more intensive endochondral bone formation in the condylar cartilage and/or by appositional bone growth in the lower border of the mandible. This would, in part, explain the noted acceleration in the growth of the mandible and alteration in its growth direction, following the change in the mode of breathing after adenotonsillectomy.

Ghrelin enhances the nocturnal secretion of cortisol and growth hormone in young females without influencing sleep

Ghrelin was shown to increase slow wave sleep (SWS) and the secretion of growth hormone (GH) and cortisol in young males. In terms of sleep, such information for females, however, is lacking. Therefore, polysomnographies were recorded (23:00-07:00 h) and nocturnal (20:00-07:00 h) secretion profiles of GH and cortisol were determined in 10 healthy females (24.9+/-2.4 years, body mass index: 21.2+/-1.1) twice, receiving four boluses of 50 microg ghrelin or placebo at 22:00, 23:00, 00:00, and 01:00 h, in this single-blind, randomized, cross-over study. No significant differences of conventionally or quantitatively analyzed sleep were observed between ghrelin and placebo condition. First administration of ghrelin caused a marked mean increase of GH by 53.3 to 64.4+/-14.2 ng/ml (placebo: 5.9+/-1.5 ng/ml) and cortisol by 54.2 to 96.4+/-15.3 ng/ml (placebo: 27.5+/-4.7 ng/ml). The following ghrelin injections were associated with smaller increases of GH and cortisol. In the ghrelin condition, GH plasma levels remained significantly (P<0.05) higher from 22:20 to 02:00 h and cortisol plasma levels from 22:20 to 02:20 h. In contrast to findings in young men, ghrelin did not affect sleep in young women, indicating a sexual dimorphism. In accordance with the findings in young men, ghrelin stimulated secretion of GH and cortisol.

Nocturnal Secretion of Growth Hormone, Noradrenaline, Cortisol and Insulin in Cluster Headache Remission

We have previously shown decreased, nocturnal lipolysis in both phases of cluster headache (CH). Lipolysis is stimulated by noradrenaline (NA), growth hormone (GH) and cortisol, and inhibited by insulin, hormones which are directly or indirectly regulated by the hypothalamus. Our aim was to investigate the nocturnal secretion of NA, GH, cortisol and insulin in nine CH patients in remission and 10 healthy controls. Nocturnal venous blood samples were collected in hourly intervals for analysis of NA, cortisol and insulin and in 30-min intervals for GH. We found a reduced increase in GH between 24.00 h and 01.00 h (anova, P < 0.05) in CH patients. Nocturnal secretion of NA, cortisol and insulin did not differ significantly between the groups. The altered nocturnal GH pattern that was seen in CH patients in remission might in part explain the altered nocturnal lipolysis previously found and further indicate a permanent hypothalamic disturbance in CH.

The advantage of measuring spontaneous growth hormone (GH) secretion compared with the insulin tolerance test in the diagnosis of GH deficiency in young adults

Reassessment of GH status after the attainment of adult height has important clinical implications in the diagnosis and prognosis of GH deficiency (GHD) in adulthood. The current GH threshold for biochemical definition of GHD in young adults is still a subject of debate. To investigate the role of pharmacological stimulation tests compared with spontaneous 12-h nocturnal GH secretion in the diagnosis of permanent GHD in young adults with childhood-onset GHD. Forty-five young adults (25 males, 20 females) with childhood-onset GHD, height standard deviation score (SDS) -1.1 +/- 1.3 and body mass index (BMI) SDS 1.0 +/- 1.6, were re-evaluated at the age of 19.8 +/- 2.7 years. Sixteen subjects showed a normal pituitary gland on magnetic resonance imaging (MRI), while in 29, consistent structural hypothalamic-pituitary abnormalities were found. GH secretion was assessed by means of an insulin tolerance test (ITT) and a 12-h spontaneous nocturnal profile as well as by IGF-I assessment. The results were compared with those of 43 healthy controls. Mean 12-h spontaneous nocturnal GH secretion was < 3.1 microg/l (the lowest limit of the normal range) in 36 (80%) of the subjects and > 3.1 microg/l in nine (20%). Of these 36 patients, 29 (80%) had abnormal MRI findings and 20 (55%) had multiple pituitary hormone deficiencies (MPHD). All nine subjects with mean spontaneous GH secretion > 3.1 microg/l had a normal pituitary MRI, isolated GHD and a peak GH response to ITT > 5 microg/l. There was a discordance in 14 patients (31%), who showed a peak GH response to ITT > 5 microg/l but a reduced spontaneous GH secretory capacity; 10 had structural hypothalamic-pituitary abnormalities on MRI. Although the ITT provides valuable information and proves to be a sensitive index of permanent GHD, the results of this study emphasize the potential diagnostic value of assessment of 12-h spontaneous GH secretion in young adults with childhood-onset GHD.

Altered nocturnal growth hormone (GH) secretion in obsessive compulsive disorder

Nocturnal patterns of growth hormone (GH) in obsessive compulsive disorder (OCD), which is physiologically released predominantly during the first half of night, have not been reported. However, altered GH responses to pharmacological challenges suggest a disturbed function of the somatotropic axis in OCD. In this study, nine inpatients with a DSM-IV diagnosis of OCD without comorbid major depression (Yale-Brown Obsessive Compulsive Scale (Y-BOCS) score >15; HAMD-21 total score 16) and 9 healthy matched controls were included. Blood of patients (7 males, 31.8+/-9.3 years, Y-BOCS: 27.3+/-4.3, HAMD-21: 13.3+/-1.9) and controls (7 males, 31.6+/-9.1 years) was drawn every 20 min between 2300 and 0700 h during sleep using a long catheter for later GH analysis. Mean plasma GH levels peaked at 0040 h, however this peak was significantly blunted in patients (maximum 4.3+/-1.5 ng/ml) compared to controls (maximum 12.3+/-4.0 ng/ml; p<0.05). In patients but not controls two other, smaller peaks were observed (0220 and 0620 h). In patients but not in controls, GH values exceeding maximum GH values of the peak at 0040 h were observed already at 2300 h or during the second half of night. In conclusion, our results indicate that the nocturnal GH secretion in patients with OCD is altered compared to controls.

Ghrelin and sleep-wake regulation

peptides play a key role in the regulation of sleep-wake behavior ([11][1]). There are many hints that also the endogenous ligand of the growth hormone (GH) secretagogue (GHS) receptor ghrelin participates in the regulation of vigilance states. In a previous editorial focus ([10][2]) I wrote that

Nocturnal ghrelin, ACTH, GH and cortisol secretion after sleep deprivation in humans

Ghrelin is an endogenous ligand of the growth hormone (GH) secretagogue (GHS) receptor. It is hypothesised to play a key role in energy balance stimulating food intake and body weight. Besides GH-releasing hormone (GHRH) and somatostatin, it is thought to be a regulating factor of GH release. Ghrelin also appears to be involved in sleep regulation. We showed recently that ghrelin promotes slow-wave sleep and the nocturnal release of GH, cortisol and prolactin in humans. Similarly, promotion of non-rapid-eye-movement (NREM) sleep was reported in mice after systemic ghrelin. If ghrelin is a factor that induces and/or maintains sleep, it should be enhanced after a period of sleep deprivation (SD). To clarify this issue, nocturnal ghrelin, GH, ACTH and cortisol plasma concentrations were determined and simultaneously sleep electroencephalogram (EEG) was recorded (2300-0700 h) during sleep before and after 1 night of total SD in 8 healthy subjects. Compared to baseline, ghrelin levels increased earlier by a non-significant trend, already before the beginning of recovery sleep. Further a non-significant trend occurred, suggesting higher ghrelin secretion in the first half of the night. The ghrelin maximum was found significantly earlier after SD than at baseline. GH secretion during the first half of the night and total night after SD were elevated. ACTH and cortisol were also elevated, which was most pronounced during the second half of the night. No effects of SD on the time of the maximum were found for GH, ACTH and cortisol. The increase in ACTH after SD is a novel finding. Whereas the effects of SD on ghrelin levels were relatively weak, our findings are in line with the hypothesis that ghrelin is a sleep-promoting factor in humans. Ghrelin may be involved in sleep promotion after SD.

Sex Differences in Nocturnal Growth Hormone and Prolactin Secretion in Healthy Older Adults: Relationships With Sleep EEG Variables

To examine sex differences in nocturnal growth hormone and prolactin release in older adults. Sleep was polygraphically recorded for 2 consecutive nights, and blood was sampled at frequent intervals during the last 24 hours. The University of Chicago Clinical Research Center. Two groups of healthy nonobese older subjects: 10 men (59 +/- 2 years, mean +/- SEM), and 10 postmenopausal women (63 +/- 2 years). N/A. A spectral analysis of the electroencephalogram was performed in the delta and alpha bands. When delta activity was normalized for the activity in rapid eye movement sleep, women had lower delta activity than men. Growth hormone secretion was estimated by deconvolution. The prolactin profile was quantified by a best-fit curve. In both sexes, growth hormone was released both before and after sleep onset. In men, there was no relationship between presleep growth hormone release and subsequent sleep quality and postsleep growth hormone release correlated with delta activity. In women, presleep growth hormone release appeared to inhibit both postsleep growth hormone release and sleep consolidation. Prolactin release was related to rapid eye movement sleep and was lower in men than in women. Women with poor sleep maintenance had a lower prolactin acrophase. Major sex differences in the nocturnal profiles of growth hormone and prolactin and their relationship to sleep electroencephalogram variables are present in healthy older adults. Our analyses suggest that lower sleep-onset release of growth hormone in women as compared with men could be related to lower levels of delta activity. Improvements in the homeostatic control of sleep could have hormonal benefits in older adults.