Innate Immunity Promotes Sleep through Epidermal Antimicrobial Peptides.
Current biology : CB
Wounding and infection trigger a protective innate immune response that includes the production of antimicrobial peptides in the affected tissue as well as increased sleep. Little is known, however, how peripheral wounds or innate immunity signal to the nervous system to increase sleep. We found that, during C. elegans larval molting, an epidermal tolloid/bone morphogenic protein (BMP)-1-like protein called NAS-38 promotes sleep. NAS-38 is negatively regulated by its thrombospondin domain and acts through its astacin protease domain to activate p38 mitogen-activated protein (MAP)/PMK-1 kinase and transforming growth factor β (TGF-β)-SMAD/SMA-3-dependent innate immune pathways in the epidermis that cause STAT/STA-2 and SLC6 (solute carrier)/SNF-12-dependent expression of antimicrobial peptide (AMP) genes. We show that more than a dozen epidermal AMPs act as somnogens, signaling across tissues to promote sleep through the sleep-active RIS neuron. In the adult, epidermal injury activates innate immunity and turns up AMP production to trigger sleep, a process that requires epidermal growth factor receptor (EGFR) signaling that is known to promote sleep following cellular stress. We show for one AMP, neuropeptide-like protein (NLP)-29, that it acts through the neuropeptide receptor NPR-12 in locomotion-controlling neurons that are presynaptic to RIS and that depolarize this neuron to induce sleep. Sleep in turn increases the chance of surviving injury. Thus, we found a novel mechanism by which peripheral wounds signal to the nervous system to increase protective sleep. Such a cross-tissue somnogen-signaling function of AMPs might also boost sleep in other animals, including humans.
10.1016/j.cub.2020.10.076
Greater Sleep Fragmentation Is Associated With Less Physical Activity in Adults With Cystic Fibrosis.
Cox Narelle S,Pepin Véronique,Holland Anne E
Journal of cardiopulmonary rehabilitation and prevention
BACKGROUND:Sleep quality in people with cystic fibrosis (CF) is known to be poor, whereas participating in regular physical activity is associated with less decline in lung function (forced expiratory volume in 1 sec [FEV1]). The relationship between sleep quality and physical activity in people with CF is unknown. METHODS:Secondary analysis of sleep and activity data collected via actigraphy. Adults with CF in stable health, participating in a study of physical activity (including assessment of exercise capacity), completed 7 d of activity and sleep assessment (SenseWear Armband [SWA]; BodyMedia). Sleep characteristics were derived from accelerometer positional data and registration of sleep state by the SWA, determined by energy expenditure. RESULTS:Sleep and activity data were available for 47 participants [n = 28 male; mean ± standard deviation age = 29 ± 8 yr; median (IQR) FEV1 = 60 (50, 82) % predicted]. More fragmented sleep was associated with poorer exercise capacity (rs = -0.303, P = .04), less time spent in moderate-vigorous physical activity (rs = -0.337, P = .020), and poorer FEV1 (rs = -0.344, P = .018). Regression analysis showed that less fragmented sleep was an independent predictor of more total daily activity time (β = -1.0, standard error [SE] of β = .4, P = .02) and trended toward significance for more moderate-vigorous physical activity (β = -.3, SE of β = -.26, P = .08). Greater total sleep time and sleep efficiency were related to better exercise capacity and lung function (P < .05). CONCLUSION:This secondary analysis demonstrated a modest relationship between sleep parameters and physical activity and exercise capacity in adults with CF. Future studies of interventions to promote physical activity participation in this group should consider the relationship between sleep and activity performance.
10.1097/HCR.0000000000000363
Melatonin improves inflammatory cytokine profiles in lung inflammation associated with sleep deprivation.
Kim Ju-Young,Lee Yang-Deok,Kim Byung-Joon,Kim Sang-Pil,Kim Dae-Hyun,Jo Kyung-Jin,Lee Seong-Kyu,Lee Ki-Ho,Baik Haing-Woon
Molecular medicine reports
Sleep disturbance has become an endemic behavior in modern countries, and its prevalence has also increased. Even a subtle sleep deficiency is related to health problems. Particularly, patients with pulmonary disease often complain of insomnia. We recently showed that sleep deprivation (SD) exacerbates existing acute lung inflammation, and that melatonin treatment attenuates it via anti-apoptotic and anti-oxidant action. In order to reinforce our previous report, the present study was designed to evaluate pro-inflammatory mediators in acute lung inflammation in SD mice. In addition, we investigated the infiltration of inflammatory cells into the lungs. Twenty-five ICR mice were divided into 5 groups (n=5/group): control, SD, lipopolysaccharide (LPS), LPS + SD and LPS + SD + melatonin. The SD mice were deprived of sleep for 96 h in a multiplatform water bath. LPS (5 mg/kg) and melatonin (5 mg/kg) were administered on day 2. The mice were sacrificed on day 3, and serum and bronchoalveolar lavage (BAL) fluid were collected. The serum levels of inflammatory cytokines were increased in the LPS + SD group. Interleukin-6, tumor necrosis factor-α and interferon-γ levels were also increased in BAL fluid in the LPS + SD group. Melatonin reduced inflammatory mediators in the serum and BAL fluid. The accumulation of leukocytes in the LPS and LPS + SD mice was elevated, however, melatonin inhibited the recruitment of inflammatory cells (p<0.05). Lymphocytes in the BAL fluid of the LPS + SD group were increased, and macrophage levels were decreased; however, the increment was attenuated by melatonin administration (p<0.05). In conclusion, this study indicates that melatonin has a protective effect against lung inflammation associated with SD.
10.3892/mmr.2012.814
Sleep deprivation predisposes allergic mice to neutrophilic lung inflammation.
Nunes Jethe O F,Apostolico Juliana de Souza,Andrade David A G,Ruiz Francieli S,Fernandes Edgar R,Andersen Monica L,Keller Alexandre C,Rosa Daniela S
The Journal of allergy and clinical immunology
BACKGROUND:Although different studies associated sleep deprivation (SD) with systemic inflammatory changes, the effect of sleep duration on the pathology of allergic chronic diseases is poorly understood. OBJECTIVE:We sought to evaluate the influence of SD on allergen-induced pulmonary inflammation. METHODS:Ovalbumin (OVA)-sensitized C57BL/6 mice were exposed to a first set of intranasal OVA challenge under SD or healthy sleep (HS) conditions, followed by a second OVA challenge, 1 week apart. Some groups were subjected to corticosteroid treatment with dexamethasone. RESULTS:OVA-sensitized mice with SD had more severe airway inflammation than the allergic group with HS. Analysis of lung parenchyma revealed that the inflammation in allergic mice with SD was marked by an influx of neutrophils (mainly) and eosinophils and secretion of IL-6, TNF-α, and IL-17 in contrast to the eosinophilic inflammation and IL-4 production observed in allergic mice with HS. The same cytokine profile was observed in ex vivo culture of cervical lymph node cells and splenocytes, indicating that in allergic mice SD favors immune responses toward a proinflammatory T17 profile. This idea is supported by the fact that disruption of IL-17 signaling (IL-17 receptor A) prevented airway neutrophilia in allergic mice with SD. Furthermore, allergic mice with SD became refractory to corticosteroid treatment in contrast to the allergic group with HS. CONCLUSION:Collectively, our data show that sleep quality participates in the progression of allergen-induced eosinophilic lung inflammation to corticosteroid-refractory neutrophilic manifestation.
10.1016/j.jaci.2017.06.025
Sleep deprivation-induced multi-organ injury: role of oxidative stress and inflammation.
Periasamy Srinivasan,Hsu Dur-Zong,Fu Yu-Hsuan,Liu Ming-Yie
EXCLI journal
Sleep deprivation affects all aspects of health. Adverse health effects by sleep deviation are still underestimated and undervalued in clinical practice and, to a much greater extent in monitoring human health. We hypothesized that sleep deprivation-induced mild organ injuries; oxidative stress and inflammation might play a crucial role in inducing multi-organ injury. Male C57BL/6J mice (n = 6-7) were sleep-deprived for 0-72 h using a modified multiple platform boxes method. Blood and tissue were collected. Liver, heart, kidney, lung, and pancreatic injuries were evaluated using biochemical and histological analyses. Glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), total billirubin (TBIL), creatine phosphokinase (CPK), creatine phosphokinase-myocardial band (CKMB), lactic dehydrogenase (LDH), creatinine (CRE), and blood urea nitrogen (BUN) were assayed in blood. Malondialdehyde (MDA), nitric oxide (NO), tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 levels were measured. Histology revealed mild-to-moderate liver and lung injury in sleep-deprived mice. Sleep-deprived mice had significantly higher GOT, GPT, TBIL, CPK, CKMB, LDH, BUN, and α-amylase (AMYL) levels, which indicated liver, heart, kidney, and pancreatic injuries. Serum IL-1β at 24 h and IL-6 at 72 h were significantly higher in sleep-deprived than in control mice. Hepatic TNF-α and IL-1β were significantly higher, but IL-6 significantly lower in mice that had been sleep-deprived for 72 h. Sleep deprivation-mediated inflammation may be associated with mild to moderate multi-organ damage in mice. The implication of this study indicates sleep deprivation in humans may induce multi-organ injury that negatively affects cardiovascular and gastrointestinal health.
10.17179/excli2015-245
Cardiometabolic correlates of sleep-disordered breathing in renal transplant children.
Lendvai Zsófia,Pásti Krisztina,Szeifert Lilla,Molnár László D,Rusai Krisztina,Balassa Katalin,Reusz George,Szabó Attila J
Pediatric transplantation
Sleep-disordered breathing, a prevalent condition among adult renal transplant (RTx) recipients, has become an established independent risk factor of MetS, and furthermore, it might contribute to increased CV risk. Despite the proven correlations in adults, there is a lack of evidence for its significance in the pediatric RTx population. In this study, we aimed at assessing the prevalence and the clinical correlates of SDB in RTx children. Data of 13 patients (age [mean ± SD]: 14.2 ± 2.7 years) were analyzed. SDB was evaluated by PSG, as severity score OAHI was applied. Carbohydrate metabolism was characterized by OGTT, whereas CV status was studied by ABPM. Three composite end-points were calculated as sum of z-scores: daytime systolic and diastolic BP; nighttime systolic and diastolic BP; and glucose and insulin levels at 120 minutes. Eight patients (61.5%) were diagnosed with SDB of whom five patients (38.5%) had moderate or severe SDB. In linear regression analysis, OAHI during REM was associated with the CV variables (daytime BP P = 0.032, ß = 0.748; nighttime BP P = 0.041, ß = 0.715), and the correlations remained significant after adjustments for BMI. However, we did not confirm a significant association with the metabolic variables. The prevalence of SDB was high, and its severity during REM was a predictor of the BP suggesting that RTx children with SDB might be at risk of developing CV complications, especially HTN similarly to adults.
10.1111/petr.13529
Sleep loss induces differential response related to genotoxicity in multiple organs of three different mice strains.
Kahan Vanessa,Ribeiro Daniel Araki,Andersen Monica Levy,Alvarenga Tathiana Aparecida,Tufik Sergio
Basic & clinical pharmacology & toxicology
The purpose of the present study was to determine the genetic damage induced by paradoxical sleep deprivation (PSD) in three different male mice strains in peripheral blood, heart, kidney and liver tissues by the single cell gel (comet) assay. Swiss, C57BL/6j and hairless (HRS/j) mice were submitted to PSD by the multiple platform technique for 72 hr, and DNA damage was evaluated. Statistically significant differences in DNA damage were found in blood cells of the Swiss mice strain when compared to negative controls. By contrast, no statistically significant differences were found in the C57BL/6j or hairless mice strains. With regard to the liver, extensive genotoxic effects were found in the Swiss strain. The hairless and C57BL/6j mice strains did not show any signs of genotoxocity in this organ. The same lack of effect was noted in kidney and heart cells of all strains evaluated. In conclusion, our results reveal that sleep deprivation exerted genetic damage in the form of DNA breakage in blood and liver cells of the Swiss mice strain only. This type of approach should be considered when studying noxious activities on genetic apparatus induced by sleep deprivation in mice since the Swiss strain is more suitable for this purpose.
10.1111/j.1742-7843.2010.00540.x
The effects of short sleep duration on proteinuria and chronic kidney disease: a systematic review and meta-analysis.
Cheungpasitporn Wisit,Thongprayoon Charat,Gonzalez-Suarez Maria L,Srivali Narat,Ungprasert Patompong,Kittanamongkolchai Wonngarm,Caples Sean M,Erickson Stephen B
Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association
BACKGROUND:The risks of proteinuria and chronic kidney disease (CKD) in adults who regularly have short sleep duration (short sleepers) are controversial. The aim of this meta-analysis was to assess the effects of short sleep duration on proteinuria and CKD. METHODS:A literature search was conducted using MEDLINE, EMBASE and the Cochrane Database of Systematic Reviews from the inception of the databases through November 2015. Studies that reported relative risks, odd ratios or hazard ratios comparing the risks of proteinuria and CKD in short sleepers were included. Pooled risk ratios (RR) and 95% confidence intervals (CI) were computed utilizing a random-effect, generic inverse variance method. RESULTS:Six observational studies with 252 075 individuals and three observational studies with 37 197 individuals were included in the analyses to assess the risks of CKD and proteinuria in short sleepers, respectively. The pooled RR of CKD in short sleepers was 1.51 (95% CI, 0.99-2.55). When meta-analysis was restricted only to studies with adjusted analysis for confounders assessing the risk of CKD in short sleepers, the pooled RR of CKD was 1.54 (95% CI, 0.80-2.95). The pooled RR of proteinuria in short sleepers was 1.47 (95% CI, 1.26-1.72). CONCLUSIONS:Despite the lack of significant association between short sleep duration and CKD, our meta-analysis suggests a potential association between short sleep duration and proteinuria, a surrogate marker for kidney disease progression. Future study is required to investigate if reversal of short sleep helps reduce proteinuria.
10.1093/ndt/gfw072
Estimating individual optimal sleep duration and potential sleep debt.
Scientific reports
In this study, we hypothesized that dynamics of sleep time obtained over consecutive days of extended sleep in a laboratory reflect an individual's optimal sleep duration (OSD) and that the difference between OSD and habitual sleep duration (HSD) at home represents potential sleep debt (PSD). We found that OSD varies among individuals and PSD showed stronger correlation with subjective/objective sleepiness than actual sleep time, interacting with individual's vulnerability of sleep loss. Furthermore, only 1 h of PSD takes four days to recover to their optimal level. Recovery from PSD was also associated with the improvement in glycometabolism, thyrotropic activity and hypothalamic-pituitary-adrenocortical axis. Additionally, the increase (rebound) in total sleep time from HSD at the first extended sleep would be a simple indicator of PSD. These findings confirmed self-evaluating the degree of sleep debt at home as a useful clinical marker. To establish appropriate sleep habits, it is necessary to evaluate OSD, vulnerability to sleep loss, and sleep homeostasis characteristics on an individual basis.
10.1038/srep35812
Human brain patterns underlying vigilant attention: impact of sleep debt, circadian phase and attentional engagement.
Maire Micheline,Reichert Carolin F,Gabel Virginie,Viola Antoine U,Phillips Christophe,Berthomier Christian,Borgwardt Stefan,Cajochen Christian,Schmidt Christina
Scientific reports
Sleepiness and cognitive function vary over the 24-h day due to circadian and sleep-wake-dependent mechanisms. However, the underlying cerebral hallmarks associated with these variations remain to be fully established. Using functional magnetic resonance imaging (fMRI), we investigated brain responses associated with circadian and homeostatic sleep-wake-driven dynamics of subjective sleepiness throughout day and night. Healthy volunteers regularly performed a psychomotor vigilance task (PVT) in the MR-scanner during a 40-h sleep deprivation (high sleep pressure) and a 40-h multiple nap protocol (low sleep pressure). When sleep deprived, arousal-promoting thalamic activation during optimal PVT performance paralleled the time course of subjective sleepiness with peaks at night and troughs on the subsequent day. Conversely, task-related cortical activation decreased when sleepiness increased as a consequence of higher sleep debt. Under low sleep pressure, we did not observe any significant temporal association between PVT-related brain activation and subjective sleepiness. Thus, a circadian modulation in brain correlates of vigilant attention was only detectable under high sleep pressure conditions. Our data indicate that circadian and sleep homeostatic processes impact on vigilant attention via specific mechanisms; mirrored in a decline of cortical resources under high sleep pressure, opposed by a subcortical "rescuing" at adverse circadian times.
10.1038/s41598-017-17022-9
Sleep debt induces skeletal muscle injuries in athletes: A promising hypothesis.
de Sousa Nogueira Freitas Luísa,da Silva Flavia Rodrigues,Andrade Henrique de Araújo,Guerreiro Renato Carvalho,Paulo Fernanda Viegas,de Mello Marco Túlio,Silva Andressa
Medical hypotheses
Sleep is a physiological state and it is fundamental for physical and cognitive recovery of athletes. Due to strenuous training and competitions, athletes may present sleep complaints compromising good quality and quantity of sleep. Studies have related sleep debt to the occurrence of musculoskeletal injuries in athletes, but the mechanisms that can lead to this are not entirely clear. Studies involving animals and humans have shown that poor sleep quality can cause significant changes in hormones and cytokines. Demonstrating that this hormones changes lead to a decrease of testosterone and growth hormone levels and increased cortisol levels, important hormones in the process of protein synthesis and degradation. In athletes, the sport itself is a risk factor of injuries, and sleep debt may result in overtraining syndrome associated with inflammatory markers and ultimately to immune system dysfunction. Thus, we hypothesize that athletes who have sleep debt are more susceptible to musculoskeletal injuries due to increased catabolic pathway signaling, i.e. protein degradation and decreased anabolic pathway signaling, compromising muscle integrity. In this sense, we indicate the relationship between musculoskeletal injuries and sleep debt involving new targets for immunological signaling pathways that start the reduction of the muscle recovery process.
10.1016/j.mehy.2020.109836
Sleep debt and prevalence of proteinuria in subjects with short sleep duration on weekdays: a cross-sectional study.
Aoki Katsunori,Yamamoto Ryohei,Shinzawa Maki,Kimura Yoshiki,Adachi Hiroyoshi,Fujii Yoshiyuki,Tomi Ryohei,Nakanishi Kaori,Taneike Manabu,Nishida Makoto,Kudo Takashi,Yamauchi-Takihara Keiko,Isaka Yoshitaka,Moriyama Toshiki
Clinical and experimental nephrology
STUDY OBJECTIVE:Short sleep duration is a risk factor of chronic kidney disease, along with cardiovascular diseases and all-cause mortality. Several studies reported that many people sleep longer on weekends than on weekdays, suggesting that they should be compensated for their sleep debt on weekdays on the weekends. Few studies have reported the clinical impact of sleep debt on the kidney. METHODS:This cross-sectional study included 5799 employees of Osaka University who visited its Health Care Center for their annual health examinations and answered ≤ 6 h of sleep duration on weekdays. The independent variable was the sleep debt index defined as a gap in self-reported sleep duration (≤ 5, 5-6, 6-7, 7-8, 8-9, and ≥ 9 h) between weekdays and weekends, which was categorized into ≤ 0, + 1, + 2, + 3 and ≥+4. An association between the sleep debt index and a prevalence of proteinuria defined as dipstick proteinuria of ≥ 1 + was assessed using logistic regression models adjusting for clinically relevant factors. RESULTS:More than four-fifths of the subjects had a positive sleep debt index (≤ 0, + 1, + 2, + 3, and ≥+4 recorded for 19%, 36%, 28%, 11%, and 6%, respectively). The multivariable-adjusted logistic regression models showed the sleep debt index ≥ 3 + was significantly associated with the prevalence of proteinuria (sleep debt index ≤ 0, adjusted odds ratio 1.13 [0.77, 1.65]; + 1, 1.00 [reference]; + 2, 1.29 [0.93, 1.79]; + 3, 1.54 [1.02, 2.33]; ≥ + 4, 1.87 [1.15, 3.05]). CONCLUSIONS:Sleep debt was associated with the prevalence of proteinuria in a dose-dependent manner.
10.1007/s10157-019-01808-4
Chronotype, social jet lag, sleep debt and food timing in inflammatory bowel disease.
Chakradeo Prachi S,Keshavarzian Ali,Singh Shubha,Dera Akram E,Esteban James Philip G,Lee Alice A,Burgess Helen J,Fogg Louis,Swanson Garth R
Sleep medicine
The preference of the sleep/wake cycle can be grouped into categories or chronotypes. Inflammatory bowel disease (IBD) has been linked to poor sleep quality which correlates with disease severity. Social jet lag (SJL) is the difference between sleep timing on work and free days and is a marker for circadian misalignment which has been linked to increased inflammation. We investigated whether chronotype, SJL, sleep debt (SD), and food timing were associated with an IBD specific complications and a lower quality of life. Overall, 191 subjects (115 IBD subjects and 76 healthy controls (HC)) completed the Pittsburgh Sleep Quality Index (PSQI), Morningness-Eveningness Questionnaire (MEQ), Munich ChronoType Questionnaire (MCTQ), Short Inflammatory Bowel Disease Questionnaire (SIBDQ), and a structured Food Timing Questionnaire. Later chronotype (by MEQ) was associated with a worse SIBDQ (r = -0.209; P < 0.05). SJL was increased in IBD at 1.32 h ± 1.03 vs. 1.05 h ± 0.97 in HC, P < 0.05, when adjusted for age. SJL (>2 h) was present in 40% of severe/complicated Crohn's patients (fistulizing or structuring Crohn's or history of Crohn's related surgery) compared to only 16% of uncomplicated Crohn's patients (P < 0.05). Sleep debt was increased in IBD subjects compared to HC at 21.90 m ± 25.37 vs. 11.49 m ± 13.58, P < 0.05. IBD subjects with inconsistent breakfast or dinner times had lower SIBDQ scores (4.78 ± 1.28 vs. 5.49 ± 1.02, P < 0.05; 4.95 ± 0.31 vs. 5.42 ± 0.32, P < 0.05 respectively). In summary, later chronotype, and markers of circadian misalignment (social jet lag, sleep debt, and inconsistent meal timing) were associated with IBD disease specific complications and/or lower quality of life.
10.1016/j.sleep.2018.08.002
Mouse Gambling Task reveals differential effects of acute sleep debt on decision-making and associated neurochemical changes.
Pittaras Elsa,Callebert Jacques,Dorey Rodolphe,Chennaoui Mounir,Granon Sylvie,Rabat Arnaud
Sleep
Sleep loss is associated with sleepiness, sustained attention, and memory deficits. However, vulnerability of higher cognitive processes (i.e. decision making) to sleep debt is less understood. Therefore, a major challenge is to understand why and how higher cognitive processes are affected by sleep debt. We had established in mice correlations between individual decision-making strategies, prefrontal activity, and regional monoaminergic levels. Now, we show that acute sleep debt (ASD) disturbs decision-making processes and provokes brain regional modifications of serotonin and dopamine that could explain why ASD promotes inflexible and more risk-prone behaviors. Finally, we highlight, for the first time, that in a large group of healthy inbred mice some of them are more sensitive to ASD by showing inflexible behavior and decision-making deficits. We were also able to predict mice that would be the most vulnerable to ASD depending of their behavior before ASD exposure.
10.1093/sleep/zsy168
Associations between sleep duration and sleep debt with insulin sensitivity and insulin secretion in the EGIR-RISC Study.
van Dijk D,Balkau B,Segrestin B,Gottsäter M,Gabriel R,Hatunic M,Mari A,Dekker J M,Rutters F,
Diabetes & metabolism
AIM:Extremes in sleep duration play an important role in the development of type 2 diabetes. We examined the associations between sleep duration and sleep debt with estimates of insulin sensitivity and insulin secretion. METHODS:Data were derived from the European multi-centre EGIR-RISC study. Sleep duration and sleep debt were derived from a sleep questionnaire asking about sleeping time during the week and during the weekend. Insulin sensitivity and insulin secretion were estimated from a 2-hour Oral Glucose Tolerance Test, with samples every 30 minutes. Associations between sleep duration and sleep debt with insulin sensitivity and insulin secretion, were analysed by multiple linear regression models corrected for possible confounders. RESULTS:Sleep data were available in 1002 participants, 46% men, mean age 48 ± 8 years, who had an average sleep duration of 7 ± 1 hours [range 3-14] and an average sleep debt (absolute difference hours sleep weekend days minus weekdays) of 1 ± 1 hour [range 0-8]. With regard to insulin sensitivity, we observed an inverted U-shaped association between sleep duration and the Stumvoll MCR in (mL/kg/min), with a corrected β (95% CI) of 2.05 (0.8; 3.3) and for the quadratic term -0.2 (-0.3; -0.1). Similarly, a U-shaped association between sleep duration and log HOMA-IR in (µU/mL), with a corrected βs of -0.83 (-1.4; -0.24) and 0.06 (0.02; 0.10) for the quadratic term. Confounders showed an attenuating effect on the associations, while BMI mediated 60 to 91% of the association between sleep duration and insulin sensitivity. No significant associations were observed between sleep duration with insulin secretion or between sleep debt with either insulin sensitivity or insulin secretion. CONCLUSIONS:Short and long sleep duration are associated with a lower insulin sensitivity, suggesting that sleep plays an important role in insulin resistance and may provide the link with development of type 2 diabetes.
10.1016/j.diabet.2018.11.001