Impact of sleep and sleep loss on glucose homeostasis and appetite regulation.

Department of Health Studies, University of Chicago, Chicago, Illinois.
Sleep Medicine Clinics 07/2007; 2(2):187-197. DOI: 10.1016/j.jsmc.2007.03.004
Source: PubMed

ABSTRACT Over the past 30 years there has been an increase in the prevalence of obesity and diabetes, both of which can have serious consequences for longevity and quality of life. Sleep durations may have also decreased over this time period. This chapter reviews laboratory and epidemiologic evidence for an association between sleep loss and impairments in glucose metabolism and appetite regulation, which could increase the risk of diabetes or weight gain.

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    ABSTRACT: Recent increases in the prevalence of obesity and type 2 diabetes mellitus (T2DM) in modern societies have been paralleled by reductions in the time their denizens spend asleep. Epidemiological studies have shown that disturbed sleep-comprising short, low-quality, and mistimed sleep-increases the risk of metabolic diseases, especially obesity and T2DM. Supporting a causal role of disturbed sleep, experimental animal and human studies have found that sleep loss can impair metabolic control and body weight regulation. Possible mechanisms for the observed changes comprise sleep loss-induced changes in appetite-signaling hormones (e.g., higher levels of the hunger-promoting hormone ghrelin) or hedonic brain responses, altered responses of peripheral tissues to metabolic signals, and changes in energy intake and expenditure. Even though the overall consensus is that sleep loss leads to metabolic perturbations promoting the development of obesity and T2DM, experimental evidence supporting the validity of this view has been inconsistent. This Perspective aims at discussing molecular to behavioral factors through which short, low-quality, and mistimed sleep may threaten metabolic public health. In this context, possible factors that may determine the extent to which poor sleep patterns increase the risk of metabolic pathologies within and across generations will be discussed (e.g., timing and genetics). © 2015 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered.
    Diabetes 04/2015; 64(4):1073-1080. DOI:10.2337/db14-1475 · 8.47 Impact Factor
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    ABSTRACT: Objectives Short sleep duration, poor sleep quality, and insomnia frequently characterize sleep in pregnancy during all three trimesters. We aimed to review: (i) the clinical evidence of the association between conditions of sleep loss during pregnancy and adverse pregnancy outcomes; and (ii) to discuss the potential pathophysiological mechanisms that may be involved. Methods A systematic search of cross-sectional, longitudinal studies, using Medline, Embase, and PsychINFO, using MeSH headings and key words for conditions of sleep loss such as ‘insomnia’ or ‘poor sleep quality’ or ‘short sleep duration’ and ‘pregnancy outcome’ was made for papers published between January 1, 1960 and July 2013. Results Twenty studies met inclusion criteria for sleep loss and pregnancy outcome: seven studies on prenatal depression, three on gestational diabetes, three on hypertension, pre-eclampsia/eclampsia, six on length of labor/type of delivery, eight on preterm birth and three on birth grow/birth weight. Two main results emerged: (i) conditions of chronic sleep loss are related to adverse pregnancy outcomes; (ii) chronic sleep loss yields a stress-related hypothalamic–pituitary–adrenal axis and abnormal immune/inflammatory, reaction, which, in turn, influences pregnancy outcome negatively. Conclusion Chronic sleep loss frequently characterizes sleep throughout the course of pregnancy and it may contribute to adverse pregnancy outcomes. Common pathophysiological mechanisms emerged as being related to stress system activation. We propose that according to the allostatic load hypothesis, chronic sleep loss in pregnancy may also be regarded as both a result of stress and as a physiological stressor per se, leading to stress ‘overload’. It may account for adverse pregnancy outcomes and somatic and mental disorders in pregnancy.
    Sleep Medicine 08/2014; 15(8). DOI:10.1016/j.sleep.2014.02.013 · 3.10 Impact Factor

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