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      Obstructive sleep apnea and hormones – a novel insight

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          Abstract

          Obstructive sleep apnea (OSA), a disorder characterized by repetitive collapse of the upper respiratory tract during sleep, occurs in about 4% of middle-aged men and 2% of women. The incidence of the disorder is rising due to an increase in obesity and ageing of the population. Patients with obstructive sleep apnea are at elevated risk of some endocrinal and metabolic disorders, which may lead to serious consequences including shortening of life expectancy. The recognition and understanding of interactions between local upper airway dysfunction and its endocrinal consequences is therefore vital. In this review we will focus on the influence of OSA on bone metabolism and endocrine homeostasis.

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          Burden of sleep apnea: rationale, design, and major findings of the Wisconsin Sleep Cohort study.

          Mari Palta, F Nieto, P Peppard … (2009)
          Untreated sleep apnea is a prevalent but treatable condition of breathing pauses during sleep. With approximately 15% of the US population affected, understanding of the total health burden is necessary to guide policy, population initiatives, and clinical practice to reduce the prevalence of this condition. To outline the history and need for a population approach to understanding sleep apnea and provide a review of the first longitudinal population study of this disorder. The results of cross-sectional and longitudinal data from 1500 participants in the Wisconsin Sleep Cohort, initiated 2 decades ago, illustrate the population burden of sleep apnea. The prevalence of sleep apnea is increasing with trends of increased obesity. Prospective findings from 4- to 15-year follow-up data indicate untreated sleep apnea predicts increased blood pressure, hypertension, stroke, depression, and mortality. The high prevalence of untreated sleep apnea and links to serious morbidity and mortality underscore the population burden of this condition and the need for greater clinical recognition and strategies to reduce prevalence.
          Article 0 comments Cited 121 times – based on 0 reviews     Review now
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            Sleep, the hypothalamic-pituitary-adrenal axis, and cytokines: multiple interactions and disturbances in sleep disorders.

            George P. Chrousos, Alexandros N Vgontzas (2002)
            Sleep is an important component of mammalian homeostasis, vital for survival. Sleep disorders are common in the general population and are associated with significant medical, psychologic, and social disturbances. Sleep, in particular deep sleep, has an inhibitory influence on the HPA axis, whereas activation of the HPA axis or administration of glucocorticoids can lead to arousal and sleeplessness. Insomnia, the most common sleep disorder, is associated with a 24-hour increase of ACTH and cortisol secretion, consistent with a disorder of central nervous system hyperarousal. Sleepiness and fatigue are very prevalent in the general population, and recent studies have demonstrated that the proinflammatory cytokines IL-6 and/or TNF-alpha are elevated in disorders associated with excessive daytime sleepiness, such as sleep apnea, narcolepsy, and idiopathic hypersomnia. Sleep deprivation leads to sleepiness and daytime hypersecretion of IL-6. Combined, these findings suggest that the HPA axis stimulates arousal, while IL-6 and TNF-alpha are possible mediators of excessive daytime sleepiness in humans.
            Article 0 comments Cited 81 times – based on 0 reviews     Review now
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              Bmal1 and β-cell clock are required for adaptation to circadian disruption, and their loss of function leads to oxidative stress-induced β-cell failure in mice.

              Jeongkyung Lee, Mousumi Moulik, Zhe Fang … (2013)
              Circadian disruption has deleterious effects on metabolism. Global deletion of Bmal1, a core clock gene, results in β-cell dysfunction and diabetes. However, it is unknown if this is due to loss of cell-autonomous function of Bmal1 in β cells. To address this, we generated mice with β-cell clock disruption by deleting Bmal1 in β cells (β-Bmal1(-/-)). β-Bmal1(-/-) mice develop diabetes due to loss of glucose-stimulated insulin secretion (GSIS). This loss of GSIS is due to the accumulation of reactive oxygen species (ROS) and consequent mitochondrial uncoupling, as it is fully rescued by scavenging of the ROS or by inhibition of uncoupling protein 2. The expression of the master antioxidant regulatory factor Nrf2 (nuclear factor erythroid 2-related factor 2) and its targets, Sesn2, Prdx3, Gclc, and Gclm, was decreased in β-Bmal1(-/-) islets, which may contribute to the observed increase in ROS accumulation. In addition, by chromatin immunoprecipitation experiments, we show that Nrf2 is a direct transcriptional target of Bmal1. Interestingly, simulation of shift work-induced circadian misalignment in mice recapitulates many of the defects seen in Bmal1-deficient islets. Thus, the cell-autonomous function of Bmal1 is required for normal β-cell function by mitigating oxidative stress and serves to preserve β-cell function in the face of circadian misalignment.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Arch Med Sci
                Journal ID (iso-abbrev): Arch Med Sci
                Journal ID (publisher-id): AMS
                Title: Archives of Medical Science : AMS
                Publisher: Termedia Publishing House
                ISSN (Print): 1734-1922
                ISSN (Electronic): 1896-9151
                Publication date (Electronic): 05 August 2016
                Publication date (Print): June 2017
                Volume: 13
                Issue: 4
                Pages: 875-884
                Affiliations
                [1 ]Department of Endocrinology, Metabolism and Internal Medicine, Poznan University of Medical Sciences, Poznan, Poland
                [2 ]Department of Pulmonology, Allergology and Respiratory Oncology, Poznan University of Medical Sciences, Poznan, Poland
                Author notes
                Corresponding author: Barbara Bromińska MD, Department of Endocrinology, Metabolism and Internal Medicine, Poznan University of Medical Sciences, 49 Przybyszewskiego St, 60-355 Poznan, Poland. Phone: +48 61 869 1330. Fax: +48 61 869 1682. E-mail: barbarabrominska@ 123456gmail.com
                Article
                Publisher ID: 28078
                DOI: 10.5114/aoms.2016.61499
                PMC ID: 5507108
                PubMed ID: 28721156
                SO-VID: 33cc5f2c-e305-4717-b28c-c43c7ef85f7f
                Copyright © Copyright: © 2016 Termedia & Banach
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License, allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license.

                History
                Date received : 24 January 2016
                Date accepted : 07 June 2016
                Categories
                Subject: State of the Art Paper

                ScienceOpen disciplines: Medicine
                Keywords: inflammation,sleep apnea,hormone,metabolic disorders,bones
                Data availability:
                ScienceOpen disciplines: Medicine
                Keywords: inflammation, sleep apnea, hormone, metabolic disorders, bones

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