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Prolonged sleep restriction induces changes in pathways involved in cholesterol metabolism and inflammatory responses
Department of Physiology, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
Department of Physiology, Faculty of Medicine, University of Helsinki, Helsinki, Finland; Genomics and Biomarkers Unit, Institute for Molecular Medicine FIMM, National Institute for Health and Welfare, Helsinki, Finland; Department of Psychiatry, Helsinki University Hospital, University of Helsinki, Helsinki, Finland; Stanford University Center for Sleep Sciences, Palo Alto CA, United States.
Department of Chronic Disease Prevention, Population Studies Unit, National Institute for Health and Welfare, Turku, Finland.
VTT Technical Research Centre of Finland, Espoo, Finland; Steno Diabetes Center A/S, Gentofte, Denmark.
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2016 (English)In: Scientific Reports, ISSN 2045-2322, E-ISSN 2045-2322, Vol. 6, article id 24828Article in journal (Refereed) Published
Abstract [en]

Sleep loss and insufficient sleep are risk factors for cardiometabolic diseases, but data on how insufficient sleep contributes to these diseases are scarce. These questions were addressed using two approaches: an experimental, partial sleep restriction study (14 cases and 7 control subjects) with objective verification of sleep amount, and two independent epidemiological cohorts (altogether 2739 individuals) with questions of sleep insufficiency. In both approaches, blood transcriptome and serum metabolome were analysed. Sleep loss decreased the expression of genes encoding cholesterol transporters and increased expression in pathways involved in inflammatory responses in both paradigms. Metabolomic analyses revealed lower circulating large HDL in the population cohorts among subjects reporting insufficient sleep, while circulating LDL decreased in the experimental sleep restriction study. These findings suggest that prolonged sleep deprivation modifies inflammatory and cholesterol pathways at the level of gene expression and serum lipoproteins, inducing changes toward potentially higher risk for cardiometabolic diseases.

Place, publisher, year, edition, pages
Nature Publishing Group, 2016. Vol. 6, article id 24828
National Category
Other Clinical Medicine
Identifiers
URN: urn:nbn:se:oru:diva-59377DOI: 10.1038/srep24828ISI: 000374588600001PubMedID: 27102866Scopus ID: 2-s2.0-84964253389OAI: oai:DiVA.org:oru-59377DiVA, id: diva2:1136160
Note

Funding Agencies:

EU  LSHM-CT-2005-518189  QLK6-CT-2000-00499 

Finska Läkaresällskapet  

Finnish Work Environment Fund  

Yrjo Jahnsson Foundation  

Orion Research Foundation  

Jenny and Antti Wihuri Foundation  

Finnish Foundation for Cardiovascular Research  

Liv och Hälsa Foundation  

Magnus Ehrnrooth Foundation  

Diabetes Research Foundation  

Sigrid Juselius Foundation  

Helsinki University Central Hospital research funds  TYH6254 

Carlos III Health Institute of the Spanish Ministry of Health  

Academy of Finland  118065  138201  283045  139635  137870  257545  250114  137575  134309  126925  121584  124282  129378  117797  41071 

Academy of Finland  

TEKES - the Finnish Funding Agency for Technology and Innovation  

Novo Nordisk Foundation  

Finnish Diabetes Research Foundation  

University of Oulu, Finland  

British Heart Foundation  

Welcome Trust  

Medical Research Council, UK  

Social Insurance Institution of Finland  

Kuopio, Tampere and Turku University Hospital Medical Funds  

Juho Vainio Foundation  

Paavo Nurmi Foundation  

Finnish Foundation of Cardiovascular Research  

Finnish Cultural Foundation  

Tampere Tuberculosis Foundation 

Emil Aaltonen Foundation

Available from: 2017-08-25 Created: 2017-08-25 Last updated: 2019-03-04Bibliographically approved

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Hyötyläinen, TuuliaOrešič, Matej

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