Human Growth Hormone Release: Relation to Slow-Wave Sleep and Sleep-Waking Cycles

Sassin, Jon F.; Parker, Donal C.; Mace, John; Gotlin, Ronald W.; Johnson, Laverne C.; Rossman, Lawrence G.

doi:10.1126/science.165.3892.513

Cited by 402 publications

(152 citation statements)

References 6 publications

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“…GH is secreted in a series of pulses throughout 24 h; within the usual nighttime sleep and daytime wake routine, a major pulse occurs shortly after sleep onset in temporal association with slow-wave sleep (10,17,28). The classic endocrine effect of pituitary-secreted GH is the induction of IGF-I and IGFBP-3 synthesis.…”

Section: The Experimental Modelmentioning

confidence: 99%

“…The plasma concentration of many hormones displays sleep-related variations, suggesting that sleep influences hormone secretion. Slow-wave sleep function is critical for the neuroendocrine consequences of anabolism, GH secretion, and maintenance of growth (28). We assume that alterations in sleep function, mainly reduction of slow wave sleep function, as a result of CAL, lead to suppression of global GH level.…”

Section: The Experimental Modelmentioning

confidence: 99%

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Chronic upper airway resistive loading induces growth retardation via the GH/IGF-I axis in prepubescent rats

Tarasiuk¹,

Segev²

2007

Journal of Applied Physiology

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Tarasiuk A, Segev Y. Chronic upper airway resistive loading induces growth retardation via the GH/IGF-I axis in prepubescent rats. J Appl Physiol 102: [913][914][915][916][917][918] 2007. First published November 30, 2006; doi:10.1152/japplphysiol.00838.2006.-The effect of upper airway loading on longitudinal bone growth and various components of the growth hormone (GH)/insulin-like growth factor I (IGF-I) axis has not been fully elucidated. In the present study, the effect of chronic resistive airway loading (CAL) in a prepubescent rat model on linear bone growth and weight gain was investigated. We hypothesize that CAL induced in prepubescent rats will lead to impaired longitudinal growth due to impairment in circulating and liver GH/IGF-I parameters. The tracheae of 22-day-old rats were obstructed by tracheal banding to increase inspiratory esophageal pressure. The GH/IGF-I markers were analyzed using ELISA, RT-PCR, and Western immunoblot analysis 14 days after surgery. Animals exhibited impaired longitudinal growth as demonstrated by reduction of tibia and tail length gains by 40% (P Ͻ 0.0001) and body weight gain by 24% (P Ͻ 0.0001). No differences were seen in total body energy balance, i.e., oxygen consumption, daily food intake, or arterial blood gases. Circulating GH, IGF-I, and IGF binding protein-3 (IGFBP-3) levels were reduced by 40% (P ϭ 0.037), 30% (P Ͻ 0.006), and 27% (P ϭ 0.02), respectively, in the CAL group. Liver IGF-I mRNA level decreased by 20% (P Ͻ 0.0002), whereas GH receptor mRNA and protein expression were unchanged. We conclude that impaired longitudinal growth in prepubescent CAL rats is related to a decrease in GH, IGF-I, and IGFBP-3 levels. chronic resistive loading; growth hormone; insulin-like growth factor I; insulin-like growth factor binding protein-3; prepuberty ONE OF THE CONSEQUENCES OF chronic resistive airway loading (CAL) in adult rats is malfunction in body weight gain (12, 27) without effect on longitudinal bone growth (35). The failure to gain weight was not related to decreased caloric intake (12) and was recently attributed to a decline in serum insulin-like growth factor I (IGF-I) levels (35). The endocrine effect of pituitary-secreted growth hormone (GH) is induction of IGF-I and IGF binding protein-3 (IGFBP-3) synthesis in various organs, including the liver; both are highly correlated with the 24-h mean GH levels (3, 7). This effect is mediated via activation of GH receptor (GHR), which is extensively distributed throughout many tissues (9). Impairment of the GH/IGF-I axis in prepubescent rats, before bone growth is completed, leads to skeletal growth retardation (31). The effect of CAL on the GH/IGF-I axis and longitudinal growth in prepuberty rats is not known.In the present study, the effect of CAL on longitudinal growth and weight gain was studied using the prepubescent rat model. We hypothesize that CAL will impair the GH/IGF-I axis, consequently leading to longitudinal growth retardation. We explored the effect of CAL on linear growth, serum GH, IGF-I, and ...

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Section: The Experimental Modelmentioning

confidence: 99%

Section: The Experimental Modelmentioning

confidence: 99%

Chronic upper airway resistive loading induces growth retardation via the GH/IGF-I axis in prepubescent rats

Tarasiuk¹,

Segev²

2007

Journal of Applied Physiology

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“…Such changes may reflect the different functions of sleep at different time points. While there is on--going debate as to the functions of sleep, sleep has been suggested to serve a variety of functions including facilitating learning and memory processes and brain plasticity (Maquet 2001), synaptic homeostasis (Tononi and Cirelli 2006), restoration of the brain and body through the release of growth hormone during slow wave sleep (SWS) (Sassin et al 1969), and energy conservation (Siegel 2009). While sleep is a largely automatic process, sleep disturbances 1 are common in childhood.…”

mentioning

confidence: 99%

Sleep in Childhood and Adolescence: Age-Specific Sleep Characteristics, Common Sleep Disturbances and Associated Difficulties

Barclay

Gregory

2013

Current Topics in Behavioral Neurosciences

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Sleep changes throughout the lifespan, with particularly salient alterations occurring during the first few years of life, as well as during the transition from childhood to adolescence. Such changes are partly the result of brain maturation; complex changes in the organisation of the circadian system; as well as changes in daily routine, environmental demands and responsibilities.Despite the automaticity of sleep, given that it is governed by a host of complex mechanisms, there are times when sleep becomes disturbed. Sleep disturbances in childhood are common and may stem from behavioural difficulties or abnormalities in physiological processes and, in some cases manifest into diagnosable sleep disorders. As well as occurring exclusively, childhood sleep disturbances often co--occur with other difficulties. The purpose of this chapter is to outline the neurobiology of typical sleep/wake processes, and describe changes in sleep physiology and architecture from birth to adulthood. Furthermore, common childhood sleep disorders are described as are their associations with other traits, including all of the syndromes presented in this handbook: ASDs, ADHD, schizophrenia, and emotional/ behavioural difficulties. Throughout, we attempt to explain possible mechanisms underlying these disorders and their associations.

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“…of the light phase. During 12 h SD by gentle handling in the dark only 3.8% of NREMS and no REMS was present according to This may be why densitometry appeared to be more sensitive than cell count in the analysis of the amount of mRNA in functions of a common regulatory mechanism in the brain (Sassin et al 1969;Obál et al 1992). Possibly this common brain nuclei.…”

Section: Discussionmentioning

confidence: 99%

Sleep deprivation increases somatostatin and growth hormone‐releasing hormone messenger RNA in the rat hypothalamus

Toppila

Alanko

Asikainen

et al. 1997

Journal of Sleep Research

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SUMMARYWe studied the effect of sleep deprivation (SD) on the amount of somatostatin (SRIF) and growth hormone-releasing hormone (GHRH) mRNA in rat hypothalamic nuclei. According to earlier studies SRIF possibly facilitates REM sleep and GHRH slowwave sleep. Adult male rats were sleep deprived by the gentle handling method either for 6 h during the first half of the light phase or for 12 h during the dark phase. Undisturbed rats sacrificed at the same time as the SD rats served as controls. After oligonucleotide in situ hybridization the amount of SRIF and GHRH mRNA was measured in brain sections by image analysis and cell count. SD increased the amount of SRIF mRNA in the arcuate nucleus (ARC). In the periventricular nucleus (PE) there was no effect. The amount of GHRH mRNA increased in the paraventricular nucleus (PA) in the 6 h SD group but no effect was detected in ARC. In the periventromedial hypothalamic area (pVMH) the amount of GHRH mRNA was higher in the control rats sacrificed in the morning (09.00 hours) than in the afternoon (15.00 hours), and SD had no effect. We conclude that SRIF cells in ARC and GHRH cells in PA are modulated by sleep loss, which is in accordance with the possible sleep regulatory function of these neuropeptides.

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Human Growth Hormone Release: Relation to Slow-Wave Sleep and Sleep-Waking Cycles

Cited by 402 publications

References 6 publications

Chronic upper airway resistive loading induces growth retardation via the GH/IGF-I axis in prepubescent rats

Chronic upper airway resistive loading induces growth retardation via the GH/IGF-I axis in prepubescent rats

Sleep in Childhood and Adolescence: Age-Specific Sleep Characteristics, Common Sleep Disturbances and Associated Difficulties

Sleep deprivation increases somatostatin and growth hormone‐releasing hormone messenger RNA in the rat hypothalamus

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