Neurobiology of Sleep and Circadian Rhythms最新文献

{"title":"Circadian rhythm and sleep-wake systems share the dynamic extracellular synaptic milieu","authors":"Joanna M. Cooper,&nbsp;Kathryn A. Halter,&nbsp;Rebecca A. Prosser","doi":"10.1016/j.nbscr.2018.04.001","DOIUrl":"10.1016/j.nbscr.2018.04.001","url":null,"abstract":"<div><p>The mammalian circadian and sleep-wake systems are closely aligned through their coordinated regulation of daily activity patterns. Although they differ in their anatomical organization and physiological processes, they utilize overlapping regulatory mechanisms that include an assortment of proteins and molecules interacting within the extracellular space. These extracellular factors include proteases that interact with soluble proteins, membrane-attached receptors and the extracellular matrix; and cell adhesion molecules that can form complex scaffolds connecting adjacent neurons, astrocytes and their respective intracellular cytoskeletal elements. Astrocytes also participate in the dynamic regulation of both systems through modulating neuronal appositions, the extracellular space and/or through release of gliotransmitters that can further contribute to the extracellular signaling processes. Together, these extracellular elements create a system that integrates rapid neurotransmitter signaling across longer time scales and thereby adjust neuronal signaling to reflect the daily fluctuations fundamental to both systems. Here we review what is known about these extracellular processes, focusing specifically on areas of overlap between the two systems. We also highlight questions that still need to be addressed. Although we know many of the extracellular players, far more research is needed to understand the mechanisms through which they modulate the circadian and sleep-wake systems.</p></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"5 ","pages":"Pages 15-36"},"PeriodicalIF":0.0,"publicationDate":"2018-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nbscr.2018.04.001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37358826","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mathematical modeling of sleep state dynamics in a rodent model of shift work","authors":"Michael J. Rempe ,&nbsp;Janne Grønli ,&nbsp;Torhild Thue Pedersen ,&nbsp;Jelena Mrdalj ,&nbsp;Andrea Marti ,&nbsp;Peter Meerlo ,&nbsp;Jonathan P. Wisor","doi":"10.1016/j.nbscr.2018.04.002","DOIUrl":"10.1016/j.nbscr.2018.04.002","url":null,"abstract":"<div><p>Millions of people worldwide are required to work when their physiology is tuned for sleep. By forcing wakefulness out of the body’s normal schedule, shift workers face numerous adverse health consequences, including gastrointestinal problems, sleep problems, and higher rates of some diseases, including cancers. Recent studies have developed protocols to simulate shift work in rodents with the intention of assessing the effects of night-shift work on subsequent sleep (Grønli et al., 2017). These studies have already provided important contributions to the understanding of the metabolic consequences of shift work (<span>Arble et al., 2015</span>; <span>Marti et al., 2016</span>; <span>Opperhuizen et al., 2015</span>) and sleep-wake-specific impacts of night-shift work (Grønli et al., 2017). However, our understanding of the causal mechanisms underlying night-shift-related sleep disturbances is limited. In order to advance toward a mechanistic understanding of sleep disruption in shift work, we model these data with two different approaches. First we apply a simple homeostatic model to quantify differences in the rates at which sleep need, as measured by slow wave activity during slow wave sleep (SWS) rises and falls. Second, we develop a simple and novel mathematical model of rodent sleep and use it to investigate the timing of sleep in a simulated shift work protocol (Grønli et al., 2017). This mathematical framework includes the circadian and homeostatic processes of the two-process model, but additionally incorporates a stochastic process to model the polyphasic nature of rodent sleep. By changing only the time at which the rodents are forced to be awake, the model reproduces some key experimental results from the previous study, including correct proportions of time spent in each stage of sleep as a function of circadian time and the differences in total wake time and SWS bout durations in the rodents representing night-shift workers and those representing day-shift workers. Importantly, the model allows for deeper insight into circadian and homeostatic influences on sleep timing, as it demonstrates that the differences in SWS bout duration between rodents in the two shifts is largely a circadian effect. Our study shows the importance of mathematical modeling in uncovering mechanisms behind shift work sleep disturbances and it begins to lay a foundation for future mathematical modeling of sleep in rodents.</p></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"5 ","pages":"Pages 37-51"},"PeriodicalIF":0.0,"publicationDate":"2018-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nbscr.2018.04.002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37358824","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of sleep duration and sleep disordered breathing in gestational diabetes mellitus","authors":"Joshua J. Gooley,&nbsp;Litali Mohapatra,&nbsp;Derek Chao Kuan Twan","doi":"10.1016/j.nbscr.2017.11.001","DOIUrl":"10.1016/j.nbscr.2017.11.001","url":null,"abstract":"<div><p>Many women experience sleep problems during pregnancy. This includes difficulty initiating and maintaining sleep due to physiologic changes that occur as pregnancy progresses, as well as increased symptoms of sleep-disordered breathing (SDB). Growing evidence indicates that sleep deficiency alters glucose metabolism and increases risk of diabetes. Poor sleep may exacerbate the progressive increase in insulin resistance that normally occurs during pregnancy, thus contributing to the development of maternal hyperglycemia. Here, we critically review evidence that exposure to short sleep duration or SDB during pregnancy is associated with gestational diabetes mellitus (GDM). Several studies have found that the frequency of GDM is higher in women exposed to short sleep compared with longer sleep durations. Despite mixed evidence regarding whether symptoms of SDB (e.g., frequent snoring) are associated with GDM after adjusting for BMI or obesity, it has been shown that clinically-diagnosed SDB is prospectively associated with GDM. There are multiple mechanisms that may link sleep deprivation and SDB with insulin resistance, including increased levels of oxidative stress, inflammation, sympathetic activity, and cortisol. Despite emerging evidence that sleep deficiency and SDB are associated with increased risk of GDM, it has yet to be demonstrated that improving sleep in pregnant women (e.g., by extending sleep duration or treating SDB) protects against the development of hyperglycemia. If a causal relationship can be established, behavioral therapies for improving sleep can potentially be used to reduce the risk and burden of GDM.</p></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"4 ","pages":"Pages 34-43"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nbscr.2017.11.001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37359405","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Differential effects of diet composition and timing of feeding behavior on rat brown adipose tissue and skeletal muscle peripheral clocks","authors":"Paul de Goede ,&nbsp;Satish Sen ,&nbsp;Johanneke E. Oosterman ,&nbsp;Ewout Foppen ,&nbsp;Remi Jansen ,&nbsp;Susanne E. la Fleur ,&nbsp;Etienne Challet ,&nbsp;Andries Kalsbeek","doi":"10.1016/j.nbscr.2017.09.002","DOIUrl":"10.1016/j.nbscr.2017.09.002","url":null,"abstract":"<div><p>The effects of feeding behavior and diet composition, as well as their possible interactions, on daily (clock) gene expression rhythms have mainly been studied in the liver, and to a lesser degree in white adipose tissue (WAT), but hardly in other metabolic tissues such as skeletal muscle (SM) and brown adipose tissues (BAT). We therefore subjected male Wistar rats to a regular chow or free choice high-fat-high sugar (fcHFHS) diet in combination with time restricted feeding (TRF) to either the light or dark phase. In SM, all tested clock genes lost their rhythmic expression in the chow light fed group. In the fcHFHS light fed group rhythmic expression for some, but not all, clock genes was maintained, but shifted by several hours. In BAT the daily rhythmicity of clock genes was maintained for the light fed groups, but expression patterns were shifted as compared with <em>ad libitum</em> and dark fed groups, whilst the fcHFHS diet made the rhythmicity of clock genes become more pronounced. Most of the metabolic genes in BAT tissue tested did not show any rhythmic expression in either the chow or fcHFHS groups. In SM <em>Pdk4</em> and <em>Ucp3</em> were phase-shifted, but remained rhythmically expressed in the chow light fed groups. Rhythmic expression was lost for <em>Ucp3</em> whilst on the fcHFHS diet during the light phase. In summary, both feeding at the wrong time of day and diet composition disturb the peripheral clocks in SM and BAT, but to different degrees and thereby result in a further desynchronization between metabolically active tissues such as SM, BAT, WAT and liver.</p></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"4 ","pages":"Pages 24-33"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nbscr.2017.09.002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37359404","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acute sleep disruption- and high-fat diet-induced hypothalamic inflammation are not related to glucose tolerance in mice","authors":"Jacqueline M. Ho ,&nbsp;Nicole H. Ducich ,&nbsp;Nhat-Quynh K. Nguyen ,&nbsp;Mark R. Opp","doi":"10.1016/j.nbscr.2017.09.003","DOIUrl":"10.1016/j.nbscr.2017.09.003","url":null,"abstract":"<div><p>Chronic insufficient sleep is a major societal problem and is associated with increased risk of metabolic disease. Hypothalamic inflammation contributes to hyperphagia and weight gain in diet-induced obesity, but insufficient sleep-induced neuroinflammation has yet to be examined in relation to metabolic function. We therefore fragmented sleep of adult male C57BL/6<!--> <!-->J mice for 18<!--> <!-->h daily for 9 days to determine whether sleep disruption elicits inflammatory responses in brain regions that regulate energy balance and whether this relates to glycemic control. To additionally test the hypothesis that exposure to multiple inflammatory factors exacerbates metabolic outcomes, responses were compared in mice exposed to sleep fragmentation (SF), high-fat diet (HFD), both SF and HFD, or control conditions. Three or 9 days of high-fat feeding reduced glucose tolerance but SF alone did not. Transient loss of body mass in SF mice may have affected outcomes. Comparisons of pro-inflammatory cytokine concentrations among central and peripheral metabolic tissues indicate that patterns of liver interleukin-1β concentrations best reflects observed changes in glucose tolerance. However, we demonstrate that SF rapidly and potently increases Iba1 immunoreactivity (-ir), a marker of microglia. After 9 days of manipulations, Iba1-ir remains elevated only in mice exposed to both SF and HFD, indicating a novel interaction between sleep and diet on microglial activation that warrants further investigation.</p></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"4 ","pages":"Pages 1-9"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nbscr.2017.09.003","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36074087","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The impact of breaking up prolonged sitting on glucose metabolism and cognitive function when sleep is restricted","authors":"Grace E. Vincent ,&nbsp;Sarah M. Jay ,&nbsp;Charli Sargent ,&nbsp;Katya Kovac ,&nbsp;Corneel Vandelanotte ,&nbsp;Nicola D. Ridgers ,&nbsp;Sally A. Ferguson","doi":"10.1016/j.nbscr.2017.09.001","DOIUrl":"10.1016/j.nbscr.2017.09.001","url":null,"abstract":"<div><h3>Objectives</h3><p>To investigate the acute benefits of breaking up prolonged sitting with light-intensity physical activity on (i) glucose metabolism under conditions of sleep restriction, and (ii) cognitive deficits associated with sleep restriction.</p></div><div><h3>Methods</h3><p>This counterbalanced, crossover trial consisted of two five-day (5 night) experimental conditions separated by a two-week washout period. On the first night, participants were given a 9-h sleep opportunity to allow the collection of steady-state baseline measures the following day. This was followed by three consecutive nights of sleep restriction (5-h sleep opportunity). In the sitting condition (SIT), participants remained seated between 1000 and 1800 h. In the physical activity condition (ACT), participants completed 3-min bouts of light-intensity walking every 30 min on a motorised treadmill between 1000 and 1800 h. At all other times, in both conditions, participants remained seated, except when walking to the dining room or to use the bathroom (max distance = 32 m). Six physically inactive, healthy males were randomised to one of two trial orders, 1) SIT then ACT, or 2) ACT then SIT. Continuous measures of interstitial glucose were measured at 5-min intervals. A cognitive and subjective test battery was administered every two hours during wake periods. Analyses were conducted using a series of linear mixed-effect ANOVAs.</p></div><div><h3>Results</h3><p>No differences in interstitial glucose concentration or cognitive performance were observed between the SIT condition and the ACT condition. Participants reported higher levels of sleepiness, and felt less alert in the SIT condition compared with the ACT condition.</p></div><div><h3>Conclusions</h3><p>There were no observable benefits of breaking up prolonged sitting on glucose metabolism under conditions of sleep restriction. These findings have implications for behaviour change interventions. Future studies will need to include larger, less homogenous study populations and appropriate control conditions (i.e., 8–9 h sleep opportunities).</p></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"4 ","pages":"Pages 17-23"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nbscr.2017.09.001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37359403","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Daytime bright light exposure, metabolism, and individual differences in wake and sleep energy expenditure during circadian entrainment and misalignment","authors":"Edward L. Melanson ,&nbsp;Hannah K. Ritchie ,&nbsp;Tristan B. Dear ,&nbsp;Victoria Catenacci ,&nbsp;Karen Shea ,&nbsp;Elizabeth Connick ,&nbsp;Thomas M. Moehlman ,&nbsp;Ellen R. Stothard ,&nbsp;Janine Higgins ,&nbsp;Andrew W. McHill ,&nbsp;Kenneth P. Wright Jr","doi":"10.1016/j.nbscr.2017.12.002","DOIUrl":"10.1016/j.nbscr.2017.12.002","url":null,"abstract":"<div><p>Daytime light exposure has been reported to impact or have no influence on energy metabolism in humans. Further, whether inter-individual differences in wake, sleep, 24 h energy expenditure, and RQ during circadian entrainment and circadian misalignment are stable across repeated 24 h assessments is largely unknown. We present data from two studies: Study 1 of 15 participants (7 females) exposed to three light exposure conditions: continuous typical room ~100 lx warm white light, continuous ~750 lx warm white light, and alternating hourly ~750 lx warm white and blue-enriched white light on three separate days in a randomized order; and Study 2 of 14 participants (8 females) during circadian misalignment induced by a simulated night shift protocol. Participants were healthy, free of medical disorders, medications, and illicit drugs. Participants maintained a consistent 8 h per night sleep schedule for one week as an outpatient prior to the study verified by wrist actigraphy, sleep diaries, and call-ins to a time stamped recorder. Participants consumed an outpatient energy balance research diet for three days prior to the study. The inpatient protocol for both studies consisted of an initial sleep disorder screening night. For study 1, this was followed by three standard days with 16 h scheduled wakefulness and 8 h scheduled nighttime sleep. For Study 2, it was followed by 16 h scheduled wake and 8 h scheduled sleep at habitual bedtime followed by three night shifts with 8 h scheduled daytime sleep. Energy expenditure was measured using whole-room indirect calorimetry. Constant posture bedrest conditions were maintained to control for energy expenditure associated with activity and the baseline energy balance diet was continued with the same exact meals across days to control for thermic effects of food. No significant impact of light exposure was observed on metabolic outcomes in response to daytime light exposure. Inter-individual variability in energy expenditure was systematic and ranged from substantial to almost perfect consistency during both nighttime sleep and circadian misalignment. Findings show robust and stable trait-like individual differences in whole body 24 h, waking, and sleep energy expenditure, 24 h respiratory quotient—an index of a fat and carbohydrate oxidation—during repeated assessments under entrained conditions, and also in 24 h and sleep energy expenditure during repeated days of circadian misalignment.</p></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"4 ","pages":"Pages 49-56"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nbscr.2017.12.002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36200263","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rhythms of metabolism in adipose tissue and mitochondria","authors":"Yasemin Onder,&nbsp;Carla B. Green","doi":"10.1016/j.nbscr.2018.01.001","DOIUrl":"10.1016/j.nbscr.2018.01.001","url":null,"abstract":"<div><p>Circadian clocks synchronize the daily functions of organisms with environmental cues like light-dark cycles and feeding rhythms. The master clock in the suprachiasmatic nucleus in the hypothalamus of the brain and the many clocks in the periphery are organized in a hierarchical manner; the master clock synchronizes the peripheral clocks, and the peripheral clocks provide feedback to the master clock in return. Not surprisingly, it has been shown that circadian rhythms and metabolism are closely linked. Metabolic disorders like obesity have a large cost to the individual and society and they are marked by adipose tissue and mitochondrial dysfunction. Mitochondria are central to energy metabolism and have key functions in processes like ATP production, oxidative phosphorylation, reactive oxygen species production and Ca²⁺ homeostasis. Mitochondria also play an important role in adipose tissue homeostasis and remodeling. Despite the extensive research investigating the link between circadian clock and metabolism, the circadian regulation of adipose tissue and mitochondria has mostly been unexplored until recently, and the emerging data in this topic are the focus of this review.</p></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"4 ","pages":"Pages 57-63"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nbscr.2018.01.001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"36858461","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Eating on nightshift: A big vs small snack impairs glucose response to breakfast","authors":"Stephanie Centofanti ,&nbsp;Jillian Dorrian ,&nbsp;Cassie Hilditch ,&nbsp;Crystal Grant ,&nbsp;Alison Coates ,&nbsp;Siobhan Banks","doi":"10.1016/j.nbscr.2017.12.001","DOIUrl":"10.1016/j.nbscr.2017.12.001","url":null,"abstract":"<div><p>Shift work is a risk factor for chronic diseases such as Type 2 diabetes. Food choice may play a role, however simply eating at night when the body is primed for sleep may have implications for health. This study examined the impact of consuming a big versus small snack at night on glucose metabolism. N = 31 healthy subjects (21–35 y; 18 F) participated in a simulated nightshift laboratory study that included one baseline night of sleep (22:00 h-07:00<!--> <!-->h) and one night awake with allocation to either a big snack (2100<!--> <!-->kJ) or small snack (840<!--> <!-->kJ) group. The snack was consumed between 00:00–00:30<!--> <!-->h and consisted of low fat milk, a sandwich, chips and fruit (big snack) or half sandwich and fruit (small snack). Subjects ate an identical mixed meal breakfast (2100<!--> <!-->kJ) at 08:30<!--> <!-->h after one full night of sleep and a simulated nightshift. Interstitial glucose was measured continuously during the entire study using Medtronic Continual Glucose Monitors. Only subjects with identical breakfast consumption and complete datasets were analysed (N = 20). Glucose data were averaged into 5-minute bins and area under the curve (AUC) was calculated for 90<!--> <!-->min post-breakfast. Pre-breakfast, glucose levels were not significantly different between Day1 and Day2, nor were they different between snack groups (p &gt; 0.05). A snack group by day interaction effect was found (F_1,16 = 5.36, p = 0.034) and post-hocs revealed that in the big snack group, AUC response to breakfast was significantly higher following nightshift (Day2) compared to Day1 (p = 0.001). This translated to a 20.8% (SEM 5.6) increase. AUC was not significantly different between days in the small snack group. Consuming a big snack at 00:00<!--> <!-->h impaired the glucose response to breakfast at 08:30<!--> <!-->h, compared to a smaller snack. Further research in this area will inform dietary advice for shift workers, which could include recommendations on how much to eat as well as content.</p></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"4 ","pages":"Pages 44-48"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nbscr.2017.12.001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37358821","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lower nocturnal urinary 6-sulfatoxymelatonin is associated with more severe insulin resistance in patients with prediabetes","authors":"Sirimon Reutrakul ,&nbsp;Rungtip Sumritsopak ,&nbsp;Sunee Saetung ,&nbsp;Suwannee Chanprasertyothin ,&nbsp;La-or Chailurkit ,&nbsp;Thunyarat Anothaisintawee","doi":"10.1016/j.nbscr.2017.06.001","DOIUrl":"10.1016/j.nbscr.2017.06.001","url":null,"abstract":"<div><h3>Objective</h3><p>Melatonin, a neurohormone secreted by the pineal gland, controls circadian rhythmicity, modulates sleep and plays a role in glucose metabolism. Low secretion of nocturnal urinary 6-sulfatoxymelatonin (aMT6S) was associated with incident diabetes. Sleep disturbances have also been shown to be risk factors for diabetes. In this study, we explored the relationship between nocturnal urinary aMT6s and markers of glucose metabolism in prediabetes patients, considering sleep related factors.</p></div><div><h3>Methods</h3><p>Sixty two non-shift working patients with prediabetes [hemoglobin A1c (HbA1c) 5.7–6.49%] who were not on beta-blockers participated. Sleep duration and efficiency was recorded using 7-day actigraphy. Obstructive sleep apnea was evaluated using an overnight in-home monitoring device. Nocturnal urinary aMT6s/creatinine ratio was measured from an overnight urine sample. Oral glucose tolerance test (OGTT, 75-grams glucose) was performed, with measurements of insulin and glucose levels.</p></div><div><h3>Results</h3><p>Mean (SD) age was 55.3 (8.2) years and mean HbA1c level was 6.01 (0.2)%. Mean (SD) sleep duration 6.0 (0.9) h, sleep efficiency was 83.4 (6.6)% and a median (interquartile rage) apnea hypopnea index was 10.3 (3.6, 16.4). Median nocturnal urinary aMT6s was 17.4 (9.4, 28.2) ng/mg creatinine. Higher nocturnal urinary aMT6s significantly correlated with lower fasting insulin (p = 0.004), lower insulin response to OGTT (p = 0.027), and lower fasting and whole body insulin resistance as indicated by lower HOMA-IR and higher Matsuda insulin sensitivity index (p = 0.006 and p = 0.011, respectively), but it was not correlated with fasting glucose, glucose response to OGTT, or HbA1c. Sleep duration inversely correlated with HbA1c but no other correlations were found between other sleep variables and markers of glucose metabolism or nocturnal urinary aMT6s. After adjusting for body mass index, higher nocturnal urinary aMT6s significantly correlated with lower HOMA-IR (p = 0.025) and fasting insulin levels (p = 0.014).</p></div><div><h3>Conclusion</h3><p>Nocturnal urinary aMT6s inversely correlated with fasting insulin resistance and insulin levels in patients with prediabetes. These results support the role of melatonin in glucose metabolism.</p></div>","PeriodicalId":37827,"journal":{"name":"Neurobiology of Sleep and Circadian Rhythms","volume":"4 ","pages":"Pages 10-16"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.nbscr.2017.06.001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37359402","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}