Abstract
Extremes in duration of sleep have been associated with adverse health, specifically with the symptomatology characteristic of the metabolic syndrome. Body homeostasis and circadian rhythm are thought to interact and to influence energy metabolism. Environmental cues, such as time of year and amplitude of seasonal changes (changes in photoperiod length) influence both sleep behavior and energy metabolism, supporting a link between these two systems. However, little is known about the molecular mechanism underlying the relationships of sleep and the metabolic syndrome symptoms, or the sleep–circadian phenotypes per se. In genetic association studies on sleep duration (candidate clock genes approach and genome-wide association studies), we identified genes that are functionally involved in the development of the metabolic syndrome symptomatology. Although the relationship between sleep duration and body mass index may partly be caused by environmental influences such as voluntary sleep restriction and circadian misalignment, the association of sleep duration with genes related to metabolism indicates that genetic factors are central to it. In this article, the latest evidence of a gene–environment influence on the relationship of sleep duration with the metabolic syndrome symptomatology is discussed. Greater understanding of a common genetic pathway linking sleep duration to metabolic dysfunction, and the role of environment in the mediation of this relationship, will lead to the development of new guidelines for treatment of obesity, which is a major health issues in our society.
Zusammenfassung
Extreme der Schlafdauer sind in den letzten Jahren mit negativen gesundheitlichen Folgen, die das metabolische Syndrom kennzeichnen, in Verbindung gebracht worden. Es wird vermutet, dass die Homöostase des Körpers sowie der zirkadiane Rhythmus interagieren und den Energiestoffwechsel beeinflussen. Umwelteinflüsse wie Jahreszeit und Amplitude jahreszeitlicher Veränderungen (Länge der Photoperiode) beeinflussen sowohl das Schlafverhalten als auch den Energiestoffwechsel, was den Zusammenhang zwischen diesen Systemen untermauert. Allerdings ist über die molekularen Mechanismen, die diesen Wechselwirkungen bzw. den Schlaf-/zirkadianen Phänotypen zugrunde liegen, nur wenig bekannt. In genetischen Assoziationsstudien über die Schlafdauer (Kandidaten-Uhrengene-Ansatz und genomweite Assoziationsstudien) haben wir Gene identifiziert, die an der Entwicklung der Symptomatik des metabolischen Syndroms funktionell beteiligt sind. Auch wenn der Zusammenhang von Schlafdauer und Body-Mass-Index teilweise durch Umwelteinflüsse, wie z. B. freiwillige Schlafrestriktion und zirkadiane Abweichung, erklärt werden mag, deutet das Verhältnis von Schlafdauer und mit dem Stoffwechsel verbundenen Genen darauf hin, dass genetische Faktoren hierbei eine zentrale Rolle spielen. In diesem Beitrag diskutieren wir die neuesten Erkenntnisse eines Gen-Umwelt-Einflusses auf den Zusammenhang zwischen Schlafdauer und Symptomatik des metabolischen Syndroms. Ein besseres Verständnis eines gemeinsamen molekularen Signalwegs, der Schlafdauer mit Stoffwechselstörungen verbindet, sowie der Rolle der Umwelt in der Vermittlung dieser Beziehung wird zur Entwicklung neuer Richtlinien für die Behandlung von Fettleibigkeit führen, welche eine der wichtigen Gesundheitsfragen in unserer Gesellschaft darstellt.
Abbreviations
- BMAL1:
-
brain and muscle aryl hydrocarbon receptor nuclear translocator (ARNT)-like
- CLOCK:
-
circadian locomotor output cycles kaput
- CRY:
-
cryptochromes are a class of blue light-sensitive flavoproteins found in plants and animals; encoded by the genes CRY1 and CRY2
- DBP:
-
D site of albumin promoter (albumin D-box) binding protein
- DEC2:
-
BHLHB3; class E basic helix–loop–helix protein 41
- Hyperkinetic:
-
encodes a beta subunit of Shaker potassium channels in Drosophila
- KCNAB1:
-
voltage-gated potassium channel subunit beta-1
- KIR :
-
inwardly rectifying potassium channels
- NPAS2:
-
neuronal PAS domain-containing protein 2
- ob/ob mice:
-
genetic model of leptin deficiency caused by a mutation in the gene (ob); mice eat excessively and become obese
- PER:
-
period; family of genes PER1, PER2, and PER3.
- PROK2:
-
prokineticin 2
- REM sleep:
-
rapid eye movement sleep
- Shaker:
-
a putative potassium channel gene from Drosophila
- Sleepless:
-
encodes a brain-enriched, glycosylphosphatidylinositol-anchored protein in Drosophila
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Allebrandt, K. Sleep duration and metabolic syndrome. Somnologie 17, 15–20 (2013). https://doi.org/10.1007/s11818-012-0599-0
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DOI: https://doi.org/10.1007/s11818-012-0599-0