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      Sleep duration and quality are not associated with brown adipose tissue volume or activity—as determined by 18F-FDG uptake, in young, sedentary adults

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          Abstract

          Study Objectives

          Short sleep duration and sleep disturbances have been related to obesity and metabolic disruption. However, the behavioral and physiological mechanisms linking sleep and alterations in energy balance and metabolism are incompletely understood. In rodents, sleep regulation is closely related to appropriate brown adipose tissue (BAT) thermogenic activity, but whether the same is true in humans has remained unknown. The present work examines whether sleep duration and quality are related to BAT volume and activity (measured by 18F-FDG) and BAT radiodensity in humans.

          Methods

          A total of 118 healthy adults (69% women, 21.9 ± 2.2 years, body mass index: 24.9 ± 4.7 kg/m 2) participated in this cross-sectional study. Sleep duration and other sleep variables were measured using a wrist-worn accelerometer for seven consecutive days for 24 hours per day. The Pittsburgh Sleep Quality Index was used to assess sleep quality. All participants then underwent a personalized cold exposure to determine their BAT volume, activity, and radiodensity (a proxy of the intracellular triglyceride content), using static positron emission tomography combined with computed tomography (PET/CI) scan.

          Results

          Neither sleep duration nor quality was associated with BAT volume or activity (the latter represented by the mean and peak standardized 18F-FDG uptake values) or radiodensity (all p > .1). The lack of association remained after adjusting the analyses for sex, date of PET/CT, and body composition.

          Conclusions

          Although experiments in rodent models indicate a strong relationship to exist between sleep regulation and BAT function, it seems that sleep duration and quality may not be directly related to the BAT variables examined in the present work.

          Clinical Trial Registration

          NCT02365129 ( ClinicalTrials.gov).

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          Most cited references42

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          The metabolic consequences of sleep deprivation.

          The prevalence of diabetes and obesity is increasing at an alarming rate worldwide, and the causes of this pandemic are not fully understood. Chronic sleep curtailment is a behavior that has developed over the past 2-3 decades. Laboratory and epidemiological studies suggest that sleep loss may play a role in the increased prevalence of diabetes and/or obesity. Current data suggest the relationship between sleep restriction, weight gain and diabetes risk may involve at least three pathways: (1) alterations in glucose metabolism; (2) upregulation of appetite; and (3) decreased energy expenditure. The present article reviews the current evidence in support of these three mechanisms that might link short sleep and increased obesity and diabetes risk.
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            Reduced number of hypocretin neurons in human narcolepsy.

            Murine and canine narcolepsy can be caused by mutations of the hypocretin (Hcrt) (orexin) precursor or Hcrt receptor genes. In contrast to these animal models, most human narcolepsy is not familial, is discordant in identical twins, and has not been linked to mutations of the Hcrt system. Thus, the cause of human narcolepsy remains unknown. Here we show that human narcoleptics have an 85%-95% reduction in the number of Hcrt neurons. Melanin-concentrating hormone (MCH) neurons, which are intermixed with Hcrt cells in the normal brain, are not reduced in number, indicating that cell loss is relatively specific for Hcrt neurons. The presence of gliosis in the hypocretin cell region is consistent with a degenerative process being the cause of the Hcrt cell loss in narcolepsy.
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              Brown adipose tissue as a secretory organ.

              Brown adipose tissue (BAT) is the main site of adaptive thermogenesis and experimental studies have associated BAT activity with protection against obesity and metabolic diseases, such as type 2 diabetes mellitus and dyslipidaemia. Active BAT is present in adult humans and its activity is impaired in patients with obesity. The ability of BAT to protect against chronic metabolic disease has traditionally been attributed to its capacity to utilize glucose and lipids for thermogenesis. However, BAT might also have a secretory role, which could contribute to the systemic consequences of BAT activity. Several BAT-derived molecules that act in a paracrine or autocrine manner have been identified. Most of these factors promote hypertrophy and hyperplasia of BAT, vascularization, innervation and blood flow, processes that are all associated with BAT recruitment when thermogenic activity is enhanced. Additionally, BAT can release regulatory molecules that act on other tissues and organs. This secretory capacity of BAT is thought to be involved in the beneficial effects of BAT transplantation in rodents. Fibroblast growth factor 21, IL-6 and neuregulin 4 are among the first BAT-derived endocrine factors to be identified. In this Review, we discuss the current understanding of the regulatory molecules (the so-called brown adipokines or batokines) that are released by BAT that influence systemic metabolism and convey the beneficial metabolic effects of BAT activation. The identification of such adipokines might also direct drug discovery approaches for managing obesity and its associated chronic metabolic diseases.
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                Author and article information

                Journal
                Sleep
                Sleep
                sleep
                Sleep
                Oxford University Press (US )
                0161-8105
                1550-9109
                December 2019
                13 August 2019
                13 August 2019
                : 42
                : 12
                : zsz177
                Affiliations
                [1 ] PROFITH “PROmoting FITness and Health through physical activity” Research Group, Department of Physical and Sports Education, Sport and Health University Research Institute (iMUDS), Faculty of Sports Science, University of Granada , Granada, Spain
                [2 ] Department of Medicine, Division of Endocrinology, and Einthoven Laboratory for Experimental Vascular Medicine, Leiden University Medical Center , Leiden, The Netherlands
                [3 ] Nuclear Medicine Services, “Virgen de las Nieves” University Hospital , Granada, Spain
                [4 ] Faculty of Medicine and Health Sciences, Department of Pharmacology-Physiology, Université de Sherbrooke and Centre de Recherche du Centre hospitalier universitaire de Sherbrooke , Quebec, Canada
                Author notes
                Corresponding author. Francisco M. Acosta, Department of Physical and Sports Education, Sport and Health University Research Institute (iMUDS), Faculty of Sports Science, University of Granada, Carretera de Alfacar, s/n, Granada 18071, Spain. Email: acostaf@ 123456ugr.es
                Author information
                http://orcid.org/0000-0002-4792-0969
                http://orcid.org/0000-0003-4455-2483
                http://orcid.org/0000-0001-8783-1859
                http://orcid.org/0000-0002-7207-9016
                http://orcid.org/0000-0002-8455-4988
                http://orcid.org/0000-0002-7548-7138
                Article
                zsz177
                10.1093/sleep/zsz177
                6930133
                31555815
                dd1985e9-4a00-49e6-8d2d-c93c6d46007f
                © Sleep Research Society 2019. Published by Oxford University Press [on behalf of the Sleep Research Society].

                This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License ( http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

                History
                : 22 April 2019
                : 21 May 2019
                : 26 September 2019
                Page count
                Pages: 10
                Funding
                Funded by: Spanish Ministry of Economy and Competitiveness
                Funded by: Fondo de Investigación Sanitaria del Instituto de Salud Carlos III
                Award ID: PI13/01393
                Award ID: PTA-12264
                Funded by: Retos de la Sociedad
                Award ID: DEP2016-79512-R
                Funded by: European Regional Development Fund 10.13039/501100008530
                Funded by: Spanish Ministry of Education
                Award ID: FPU13/04365
                Award ID: FPU 15/04059
                Funded by: Fundación Iberoamericana de Nutrición (FINUT)
                Funded by: Redes Temáticas de Investigación Cooperativa RETIC
                Award ID: RD16/0022
                Funded by: AstraZeneca HealthCare Foundation
                Funded by: University of Granada Plan Propio de Investigación 2016
                Funded by: Excellence actions: Unit of Excellence on Exercise and Health (UCEES)
                Funded by: Plan Propio de Investigación 2018—Programa Contratos-Puente
                Funded by: Junta de Andalucía, Consejería de Conocimiento, Investigación y Universidades
                Award ID: SOMM17/6107/UGR
                Categories
                Sleep, Health and Disease

                brown fat,cold-induced thermogenesis,energy balance,glucose uptake,sleep curtailment,thermoregulation

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