Effect of Prolonged Wakefulness on the Urinary Excretion of 17-Ketosteroids.

Tyler, David B.; Marx, Walter; Goodman, Joshua

doi:10.3181/00379727-62-15364

Cited by 11 publications

(8 citation statements)

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“…By comparison, in the present study, sleep-deprived rats showed only a mild tendency for increased corticosteroid concentrations by 50%, and not more than was recorded at various times for the other two groups. This result replicates previous findings (8,20) and corroborates the mild or unchanged values found in the results of human studies of selective sleep deprivation (37,38,70). Although changes in corticosteroid receptors, sensitivity, and catabolism cannot yet be ruled out, corticosterone concentration in sleep-deprived rats appears consistent with what may be expected to mobilize fuel to support metabolic and cellular requirements.…”

Section: Discussionsupporting

confidence: 81%

Reductions in circulating anabolic hormones induced by sustained sleep deprivation in rats

Everson¹,

Crowley²

2004

American Journal of Physiology-Endocrinology and Metabolism

179

136

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Everson, Carol A., and William R. Crowley. Reductions in circulating anabolic hormones induced by sustained sleep deprivation in rats. Am J Physiol Endocrinol Metab 286: E1060 -E1070, 2004. First published February 10, 2004 10.1152/ajpendo.00553.2003The main systemic disorders resulting from prolonged sleep deprivation in laboratory animals are a negative energy balance, low circulating thyroid hormones, and host defense impairments. Low thyroid hormones previously have been found caused by altered regulation at the level of the hypothalamus with possible pituitary involvement. The present studies investigated the effects of sleep deprivation on other major anabolic hormonal systems. Plasma growth hormone (GH) concentrations and major secretory bursts were characterized. Insulin-like growth factor I (IGF-I) was evaluated as an integrative marker of peripheral GH effector activity. Prolactin (PRL) was assessed by basal concentrations and by stimulating the pituitary with exogenous thyrotropin-releasing hormone. Leptin was studied for its linkage to metabolic signs of sleep loss and its correspondence to altered neuroendocrine regulation in other disease states. Last, plasma corticosterone was measured to investigate the degree of hypothalamic-pituitary-adrenal activation. Sleep deprivation was produced by the disk-over-water method, a well-established means of selective deprivation of sleep and noninterference with normal waking behaviors. Hormone concentrations were determined in sham comparisons and at intervals during baseline and experimental periods lasting at least 15 days in partially and totally sleep-deprived rats. The results indicate that high-amplitude pulses of GH were nearly abolished and that concentrations of GH, IGF-I, PRL, and leptin all were suppressed by sleep deprivation. Corticosterone concentration was relatively unaffected. Features of these results, such as low GH and low IGF-I, indicate failed negative feedback and point to hypothalamic mechanisms as containing the foci responsible for peripheral signs. growth hormone; thyroxine; prolactin; insulin-like growth factor I; leptin; corticosterone SLEEP IS CONSIDERED CRITICAL for the maintenance of health (2, 14, 49b, 77a) and support of life (18,35,54). Some of the clinical states associated with abnormal sleep include pulmonary and cardiovascular disorders, cerebrovascular disease, thrombotic disease, epilepsy, arthritis, mood disorders, chronic pain, and shortened life span (reviewed in Refs. 39 and 49a). The physical consequences of sleep deprivation have not been localized. Evidence from studies in laboratory animals suggest that multitropic factors in immune and hormonal systems contribute to the absence of localization.The three principal consequences of prolonged sleep deprivation in the rat are a progressively deepening negative energy balance (8,18,23), reduced thyroid hormone concentrations (8,19,20), and abnormal control of microorganisms (22). Sleep-deprived rats become strikingly and progressively hyperphagic but do not gain we...

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Section: Discussionsupporting

confidence: 81%

Reductions in circulating anabolic hormones induced by sustained sleep deprivation in rats

Everson¹,

Crowley²

2004

American Journal of Physiology-Endocrinology and Metabolism

179

136

View full text Add to dashboard Cite

show abstract

“…The abnormally low level appears compensatory and points to increased negative feedback to the brain and pituitary, perhaps serving a permissive action for effector functions that tend to be reciprocally related to glucocorticoid action (49). Corticosterone otherwise remained unchanged by sleep loss, consistent with earlier findings in laboratory rats studied under this paradigm (17,18,21), and with a lack of a cortisol stress response in human sleep deprivation or extended sleep restriction studies (2,9,31,41,42,51,52,55,62,64,71,72). Findings opposite to these, that is, decreased circulating leukocytes and marked increases in corticosterone, have been reported in laboratory rodents sleep deprived by the pedestal technique (73), also known as the platform or inverted flower-pot technique, which is considered nonspecific for sleep deprivation (48,66).…”

Section: Discussionsupporting

confidence: 78%

Phagocyte migration and cellular stress induced in liver, lung, and intestine during sleep loss and sleep recovery

Everson¹,

Thalacker²,

Hogg³

2008

American Journal of Physiology-Regulatory, Integrative and Comp

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“…12) is one candidate mechanism that may contribute to changes in granulocyte storage pools. In contrast, serum corticosteroids are not increased by sleep deprivation in rats (16,19) or humans (1,28,29,39,42,56,65), suggesting that glucocorticoid excess is not a leading mediator. Whether more neutrophils are moving from the circulation into marginal pools is not known, but preliminary evidence from our laboratory indicates high concentrations of myeloperoxidase, an enzyme considered virtually exclusive for neutrophils, in major organs of sleep-deprived rats.…”

Section: Discussionmentioning

confidence: 49%

“…Such abnormal control of opportunistic microorganisms is diagnostic of clinical immune suppression. The first suspected mediators of immune suppression, corticosteroids, remain unchanged or decrease in sleep-deprived rats (16,19) and humans (1,28,29,39,42,56,65) in studies that are controlled for extraneous variables that may elicit behavioral distress.…”

mentioning

confidence: 98%

Clinical assessment of blood leukocytes, serum cytokines, and serum immunoglobulins as responses to sleep deprivation in laboratory rats

Everson¹

2005

American Journal of Physiology-Regulatory, Integrative and Comp

114

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The specific systems and mechanisms affected by sleep deprivation that may perpetuate disease processes in humans still are speculative. In laboratory rats, prolonged sleep deprivation induces a state marked by abnormal control over indigenous bacteria that results in transient infections of internal tissues and eventual lethal septicemia. The present studies investigated changes in blood, serum, and bone marrow parameters that may provide diagnostic clues to immunopathology. Prolonged sleep deprivation was produced in rats by the disk-over-water method, a well-established and selective means that does not interfere with normal waking behaviors. Measurements included bone and blood differential white blood cell counts, multiple serum cytokines and chemokines, several major Ig classes and subclasses, and serum endotoxin concentrations. The results indicated mild, regenerative neutrophilia in sleep-deprived rats, initially accompanied by immature neutrophils and later by monocytosis. The corresponding serum cytokine profile revealed an evolving proinflammatory state, particularly by high incidence of interleukin-1beta, implicating mononuclear phagocytes and resident tissue cells as main intermediary sources. In addition, multiple serum Ig classes were increased by sleep deprivation without experimental administration of an exogenous antigen. Despite this immune activation, there was failure to eradicate invading bacteria and toxins, suggesting competing anti-inflammatory processes or interference with immune effector functions during sleep deprivation. Nearly all of the immune-related events that emerged as responses to sleep deprivation have been implicated as etiological or provocative factors in other disease processes and may provide means by which sleep deprivation as a risk factor in disease may become understood.

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Effect of Prolonged Wakefulness on the Urinary Excretion of 17-Ketosteroids.

Cited by 11 publications

References 0 publications

Reductions in circulating anabolic hormones induced by sustained sleep deprivation in rats

Reductions in circulating anabolic hormones induced by sustained sleep deprivation in rats

Phagocyte migration and cellular stress induced in liver, lung, and intestine during sleep loss and sleep recovery

Clinical assessment of blood leukocytes, serum cytokines, and serum immunoglobulins as responses to sleep deprivation in laboratory rats

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