Dataset Information

Chronic Insufficient Sleep Has a Limited Impact on Circadian Rhythmicity of Subjective Hunger and Awakening Fasted Metabolic Hormones.

ABSTRACT: Weight gain and obesity have reached epidemic proportions in modern society. Insufficient sleep-which is also prevalent in modern society-and eating at inappropriate circadian times have been identified as risk factors for weight gain, yet the impact of chronic insufficient sleep on the circadian timing of subjective hunger and physiologic metabolic outcomes are not well understood. We investigated how chronic insufficient sleep impacts the circadian timing of subjective hunger and fasting metabolic hormones in a 32-day in-laboratory randomized single-blind control study, with healthy younger participants (range, 20-34?years) randomized to either Control (1:2 sleep:wake ratio, 6.67?h sleep:13.33?h wake, n?=?7, equivalent to 8?h of sleep per 24?h) or chronic sleep restriction (CSR, 1:3.3 sleep:wake ratio, 4.67?h sleep:15.33?h wake, n?=?8, equivalent to 5.6?h of sleep per 24?h) conditions. Participants lived on a "20?h day" designed to distribute all behaviors and food intake equally across all phases of the circadian cycle over every six consecutive 20?h protocol days. During each 20?h day, participants were provided a nutritionist-designed, isocaloric diet consisting of 45-50% carbohydrate, 30-35% fat, and 15-20% protein adjusted for sex, weight, and age. Subjective non-numeric ratings of hunger were recorded before and after meals and fasting blood samples were taken within 5?min of awakening. Subjective levels of hunger and fasting concentrations of leptin, ghrelin, insulin, glucose, adiponectin, and cortisol all demonstrated circadian patterns; there were no differences, however, between CSR and Control conditions in subjective hunger ratings or any fasting hormone concentrations. These findings suggest that chronic insufficient sleep may have a limited role in altering the robust circadian profile of subjective hunger and fasted metabolic hormones. Clinical Trial Registration:The study was registered as clinical trial #NCT01581125.

SUBMITTER: McHill AW

PROVIDER: S-EPMC6005823 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Chronic Insufficient Sleep Has a Limited Impact on Circadian Rhythmicity of Subjective Hunger and Awakening Fasted Metabolic Hormones.

McHill Andrew W AW Hull Joseph T JT McMullan Ciaran J CJ Klerman Elizabeth B EB

Frontiers in endocrinology 20180612

Weight gain and obesity have reached epidemic proportions in modern society. Insufficient sleep-which is also prevalent in modern society-and eating at inappropriate circadian times have been identified as risk factors for weight gain, yet the impact of chronic insufficient sleep on the circadian timing of subjective hunger and physiologic metabolic outcomes are not well understood. We investigated how chronic insufficient sleep impacts the circadian timing of subjective hunger and fasting metab ...[more]

PMID: 29946297

Similar Datasets

Project description:To address whether changes in gene expression in blood cells with sleep loss are different in individuals resistant and sensitive to sleep deprivation (SD). Blood draws every 4 hours during a 3-day study: 24-hour normal baseline, 38 hours of continuous wakefulness and subsequent recovery sleep, for a total of 19 time-points per subject, with every 2-hr psychomotor vigilance test (PVT) assessment when awake. Fourteen subjects who were previously identified as behaviourally resistant (n=7) or sensitive (n=7) to SD by PVT. Intervention consisted of 38 hours continuous wakefulness. We found 4,481 unique genes with a significant 24-hour diurnal rhythm during a normal sleep-wake cycle in blood (false discovery rate [FDR] <5%). Biological pathways were enriched for biosynthetic processes during sleep. After accounting for circadian effects, two genes (SREBF1 and CPT1A, both involved in lipid metabolism) exhibited small, but significant, linear changes in expression with the duration of SD (FDR<5%). The main change with SD was a reduction in the amplitude of the diurnal rhythm of expression of normally cycling probe sets. This reduction was noticeably higher in behaviourally resistant subjects than sensitive subjects, at any given p-value. Furthermore, blood cell type enrichment analysis showed that the expression pattern difference between sensitive and resistant subjects is mainly found in cells of myeloid origin, such as monocytes. Individual differences in behavioural effects of sleep deprivation are associated with differences in diurnal amplitude of gene expression for genes that show circadian rhythmicity. Blood draws were done every 4 hours during a 3-day (+1 baseline day) study: 24-hour normal baseline (6 time points: day 1 8hr, 12hr, 16hr, 20hr, day 2 0hr, 4hr), 38 hours of continuous wakefulness (10 time points: day 2 8hr, 12hr, 16hr, 20hr, day 3 0hr, 4hr, 8hr, 12hr, 16hr, 20hr) and subsequent recovery sleep (3 time points: day 4 0hr, 4hr, 8hr), for a total of 19 time-points per subject, with every 2-hr psychomotor vigilance test (PVT) assessment when awake. The missing/failed samples were as following: Resistant subjects (total 10 samples): BH006 day 2 20hr, 12hr, BH003 day 2 12hr, 4hr, BH003 day 3 4hr, BH008 day 4 0hr, BH008 day 1 16hr, BH008 day 3 16hr 20hr, BH010 day 4 0hr; Sensitive subjects (total 7 samples): BH004 day 2 12hr and 1 more missing sample, BH026 day 2 4hr, BH007 day 2 20hr and 1 more missing sample, BH016 day 2 4hr, BH015 day 3 0hr.

Project description:BACKGROUND: Nocturnal awakening is the most frequent insomnia complaint in the general population. In contrast to a growing knowledge based on adults, little is known about its prevalence, correlated factors, and associations with subjective sleep perception and daytime sleepiness in children. This study was designed to assess the prevalence and the correlate factors of frequent nocturnal awakening (FNA) among Chinese school-aged children. Furthermore, the associations of FNA with subjective sleep perception and daytime sleepiness were examined. METHODS: A random sample of 20,505 children aged 5.00 to 11.92 years old (boys: 49.5% vs. girls: 50.5%) participated in a cross-sectional survey, which was conducted in eight cities of China. Parent-administered questionnaires were used to collect information on children's sleep behaviors, sleep perception, and potential influential factors of FNA from six domains. Univariate and multivariate logistic regression models were performed. RESULTS: The prevalence of FNA was 9.8% (10.0% for boys vs. 8.9% for girls) in our sampled children. The prominent FNA-related factors inclued biological health problems, such as overweight/obesity (OR = 1.70), chronic pain during night (OR = 2.47), and chronic respiratory condition (OR = 1.23), poor psychosocial condition, such as poor mental and emotional functioning (OR = 1.34), poor sleep hygiene, such as frequently doing exciting activities before bedtime (OR = 1.24) and bedtime resistance (OR = 1.42), and parents' history of insomnia (OR = 1.31). FNA was associated with subjective poor sleep quality (OR = 1.24), subjective insufficient sleep (OR = 1.21), and daytime sleepiness (OR = 1.35). CONCLUSION: FNA was associated with poor sleep and daytime sleepiness. Compared to sleep environment and family susceptibility, chronic health problems, poor psychosocial condition, and poor sleep hygiene had greater impact on FNA, indicating childhood FNA could be partly prevented by health promotion, by psychological intervention, and by improving sleep hygiene routine.

Project description:In mammals, the suprachiasmatic nucleus (SCN) is the central pacemaker organizing circadian rhythms of behavior and physiology. At the cellular level, the mammalian clock consists of autoregulatory feedback loops involving a set of "clock genes," including the Cryptochrome (Cry) genes, Cry1 and Cry2. Experimental evidence suggests that Cry1 and Cry2 play distinct roles in circadian clock function. In mice, Cry1 is required for sustained circadian rhythms in dissociated SCN neurons or fibroblasts but not in organotypic SCN slices or at the behavioral level, whereas Cry2 is not required at any of these levels. It has been argued that coupling among SCN cellular oscillators compensates for clock gene defects to preserve oscillatory function. Here we test this hypothesis in Cry1(-/-) mice by first disrupting intercellular coupling in vivo using constant light (resulting in behavioral arrhythmicity) and then examining circadian clock gene expression in SCN slices at the single cell level. In this manner, we were able to test the role of intercellular coupling without drugs and while preserving tissue organization, avoiding the confounding influences of more invasive manipulations. Cry1(-/-) mice (as well as control Cry2(-/-) mice) bearing the PER2::LUC knock-in reporter were transferred from a standard light:dark cycle to constant bright light (~650 lux) to induce arrhythmic locomotor patterns. In SCN slices from these animals, we used bioluminescence imaging to monitor PER2::LUC expression in single cells. We show that SCN slices from rhythmic Cry1(-/-) and Cry2(-/-) mice had similarly high percentages of functional single-cell oscillators. In contrast, SCN slices from arrhythmic Cry1(-/-) mice had significantly fewer rhythmic cells than SCN slices from arrhythmic Cry2(-/-) mice. Thus, constant light in vivo disrupted intercellular SCN coupling to reveal a cell-autonomous circadian defect in Cry1(-/-) cells that is normally compensated by intercellular coupling in vivo.

Dataset Information

Chronic Insufficient Sleep Has a Limited Impact on Circadian Rhythmicity of Subjective Hunger and Awakening Fasted Metabolic Hormones.

Publications

Chronic Insufficient Sleep Has a Limited Impact on Circadian Rhythmicity of Subjective Hunger and Awakening Fasted Metabolic Hormones.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets