Reductions in circulating anabolic hormones induced by sustained sleep deprivation in rats.
ABSTRACT 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.
SourceAvailable from: Marcos Mônico-Neto[Show abstract] [Hide abstract]
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 01/2015; 2015:908159. DOI:10.1155/2015/908159 · 1.52 Impact Factor
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ABSTRACT: Sleep loss may induce endothelial dysfunction, a key factor in cardiovascular risk. We examined the endothelial function during one week of sleep restriction and a recovery period (from 3-to-13days) in healthy subjects, and its link to autonomic, inflammatory and/or endocrine responses. 12 men were followed at baseline (B1, 8-h sleep), after 2 (SR2) and 6 (SR6) days of SR (4-h sleep: 02:00-06:00) and after 1 (R1) and 12 (R12) recovery nights (8h sleep). At 10:00, we assessed changes in: arm cutaneous vascular conductance (CVC) induced by local application of methacholine (MCh), cathodal current (CIV) and heat (44°C), finger CVC and skin temperature (Tfi) during local cold exposure (5°C, 20-min) and passive recovery (22°C, 20-min). Blood samples were collected at 08:00. Compared with baseline (B1), MCh and heat-induced maximal CVC values (CVCpeak) were decreased at SR6 and R1. No effect of SR was observed for Tfi and CVC during immersion whereas these values were lower during passive recovery on SR6 and R1. From SR2 to R12, plasma concentrations of insulin, IGF-1 (total and free) and MCP-1 were significantly increased while those of testosterone and prolactin were decreased. Whole-blood blood mRNA concentrations of TNF-α and IL-1β were higher than B1. No changes in noradrenaline concentrations, heart rate and blood pressure were observed. These results demonstrate that SR reduces endothelial-dependent vasodilatation and local tolerance to cold. This endothelial dysfunction is independent of blood pressure and sympathetic activity but associated with inflammatory and metabolic pathway responses (ClinicalTrials-NCT01989741). Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.International journal of cardiology 07/2015; 190. DOI:10.1016/j.ijcard.2015.04.119 · 6.18 Impact Factor
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ABSTRACT: Adult mammalian brains continuously generate new neurons, a phenomenon called neurogenesis. Both environmental stimuli and endogenous factors are important regulators of neurogenesis. Sleep has an important role in normal brain physiology and its disturbance causes very stressful conditions, which disrupt normal brain physiology. Recently, an influence of sleep in adult neurogenesis has been established, mainly based on sleep deprivation studies. This review provides an overview on how rhythms and sleep cycles regulate hippocampal and subventricular zone neurogenesis, discussing some potential underlying mechanisms. In addition, our review highlights some interacting points between sleep and neurogenesis in brain function, such as learning, memory and mood states, and provides some insights on the effects of antidepressants and hypnotic drugs on neurogenesis.Frontiers in Cellular Neuroscience 03/2015; 9:140. DOI:10.3389/fncel.2015.00140 · 4.18 Impact Factor