Reductions in circulating anabolic hormones induced by sustained sleep deprivation rats

Department of Neurology, The Medical College of Wisconsin, Milwaukee, WI 53295, USA.
AJP Endocrinology and Metabolism (Impact Factor: 3.79). 07/2004; 286(6):E1060-70. DOI: 10.1152/ajpendo.00553.2003
Source: PubMed


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 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.

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    • "Factors affecting body weight in these animals include altered hormonal profiles and feeding behavior and increased metabolic rate. In sleep-deprived animals, anabolic hormones such as testosterone (TESTO) [4], growth hormone (GH), insulin-like growth factor-1 (IGF-1) [5], and thyroid hormones T3 and T4 [6] are decreased along with increased activity of the hypothalamic-pituitary-adrenal axis (HPA axis) [1]. High levels of corticotrophin-releasing hormone (CRH) after 96 h of SD may contribute to considerable increase in metabolic rate and insufficient food ingestion, leading to weight loss [1] [7]. "
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    ABSTRACT: Objective. Describe multicompartmental changes in the fat and various muscle fiber types, as well as the hormonal profile and metabolic rate induced by SD in rats. Methods. Twenty adult male Wistar rats were equally distributed into two groups: experimental group (EG) and control group (CG). The EG was submitted to SD for 96 h. Blood levels of corticosterone (CORT), total testosterone (TESTO), insulin like growth factor-1 (IGF-1), and thyroid hormones (T3 and T4) were used to assess the catabolic environment. Muscle trophism was measured using a cross-sectional area of various muscles (glycolytic, mixed, and oxidative), and lipolysis was inferred by the weight of fat depots from various locations, such as subcutaneous, retroperitoneal, and epididymal. The metabolic rate was measured using oxygen consumption ([Formula: see text]O2) measurement. Results. SD increased CORT levels and decreased TESTO, IGF-1, and T4. All fat depots were reduced in weight after SD. Glycolytic and mixed muscles showed atrophy, whereas atrophy was not observed in oxidative muscle. Conclusion. Our data suggest that glycolytic muscle fibers are more sensitive to atrophy than oxidative fibers during SD and that fat depots are reduced regardless of their location.
    International Journal of Endocrinology 03/2015; 2015:908159. DOI:10.1155/2015/908159 · 1.95 Impact Factor
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    • "In spite of not having certainty about its true purpose, there are several indications which infer that sleep is indeed functionally important: (1) sleep is ubiquitous among mammals, birds, and reptiles; (2) sleep has persisted in evolution even though it is apparently maladaptive with respect to other functions; (3) accommodations are made to permit sleep in different environments and life styles; (4) sleep is homeostatically regulated (sleep deprivation is followed by sleep compensation); (5) serious physiological changes result from prolonged sleep deprivation of animals [4] [5]. It has been reported that sleep deprivation represents a serious physiological issue since it causes a state of high caloric ingestion without weight gaining [5] [6] [7] [8] [9], reduction in anabolic hormones [10], opportunistic infections, and eventually death [11], among other physiological challenges. Different approaches of prolonged wakefulness have been employed to study the physiological impact of sleep deprivation on neurobiological functions. "
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    ABSTRACT: Because the function and mechanisms of sleep are partially clear, here we applied a meta-analysis to address the issue whether sleep function includes antioxidative properties in mice and rats. Given the expansion of the knowledge in the sleep field, it is indeed ambitious to describe all mammals, or other animals, in which sleep shows an antioxidant function. However, in this article we reviewed the current understanding from basic studies in two species to drive the hypothesis that sleep is a dynamic-resting state with antioxidative properties. We performed a systematic review of articles cited in Medline, Scopus and Web of Science until March 2015 using the following search terms: Sleep or sleep deprivation and oxidative stress, lipid peroxidation, glutathione, nitric oxide, catalase or superoxide dismutase. We found a total of 266 studies. After inclusion and exclusion criteria, 44 articles were included, which are presented and discussed in this study. The complex relationship between sleep duration and oxidative stress is discussed. Further studies should consider molecular and genetic approaches to determine whether disrupted sleep promotes oxidative stress.
    Oxidative medicine and cellular longevity 03/2015; DOI:10.1155/2015/234952 · 3.36 Impact Factor
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    • "The lack of effect of PSD at ZT0 may be explained by a ceiling effect on orexin levels at this time-point (Pedrazzoli et al., 2004). As for the animals' body weight, our results are consistent with previous findings in the literature, showing the unequivocal weight loss (Everson and Crowley, 2004; Koban and Stewart, 2006; Martins et al., 2006; Suchecki et al., 2003), particularly in the first day of PSD. This weight loss is directly related to the intense state of catabolism displayed by these animals, which present a negative energy balance, with greater energy expenditure (Bergmann et al., 1989; Hipolide et al., 2006), increased oxygen consumption and expression of uncoupling protein-1 in brown adipose tissue (Koban and Swinson, 2005), increased catecholamine (Andersen et al., 2005) and reduced body fat (Hipolide et al., 2006), also coinciding with the peak release of corticosterone (Galvão et al., 2009), an important catabolic hormone. "
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    ABSTRACT: Studies have shown a gradual reduction of sleep time in the general population, accompanied by increased food intake, representing a risk for developing obesity, type II diabetes and cardiovascular disease. Rats subjected to paradoxical sleep deprivation (PSD) exhibit feeding and metabolic alterations, both of which are regulated by the communication between peripheral signals and the hypothalamus. This study aimed to investigate the daily change of 96 h of PSD-induced food intake, body weight, blood glucose, plasma insulin and leptin concentrations and the expression of their receptors in the hypothalamus of Wistar rats. Food intake was assessed during the light and dark phases and was progressively increased in sleep-deprived animals, during the light phase. PSD produced body weight loss, particularly on the first day, and decreased plasma insulin and leptin levels, without change in blood glucose levels. Reduced leptin levels were compensated by increased expression of leptin receptors in the hypothalamus, whereas no compensations occurred in insulin receptors. The present results on body weight loss and increased food intake replicate previous studies from our group. The fact that reduced insulin levels did not lead to compensatory changes in hypothalamic insulin receptors, suggests that this hormone may be, at least in part, responsible for PSD-induced dysregulation in energy metabolism.
    Hormones and Behavior 10/2014; 66(5). DOI:10.1016/j.yhbeh.2014.08.015 · 4.63 Impact Factor
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