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Am J Physiol Endocrinol Metab (February 10, 2004). doi:10.1152/ajpendo.00553.2003
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Submitted on December 5, 2003
Accepted on February 2, 2004

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

Carol A. Everson1* and William R. Crowley2

1 Department of Neurology, The Medical College of Wisconsin, Milwaukee, WI, USA
2 Department of Pharmacology and Toxicology, University of Utah Health Sciences Center, Salt Lake City, UT, USA

* To whom correspondence should be addressed. E-mail: ceverson{at}mcw.edu.

The 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 due to 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-1(IGF- 1) 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. And lastly, 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-1, 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-1, indicate failed negative feedback and point to hypothalamic mechanisms as containing the foci responsible for peripheral signs.




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