Morning Circadian Misalignment during Short Sleep Duration Impacts Insulin Sensitivity (original) (raw)
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Sleep, 2015
A workshop was held at the National Institute for Diabetes and Digestive and Kidney Diseases with a focus on the impact of sleep and circadian disruption on energy balance and diabetes. The workshop identified a number of key principles for research in this area and a number of specific opportunities. Studies in this area would be facilitated by active collaboration between investigators in sleep/circadian research and investigators in metabolism/diabetes. There is a need to translate the elegant findings from basic research into improving the metabolic health of the American public. There is also a need for investigators studying the impact of sleep/circadian disruption in humans to move beyond measurements of insulin and glucose and conduct more in-depth phenotyping. There is also a need for the assessments of sleep and circadian rhythms as well as assessments for sleep-disordered breathing to be incorporated into all ongoing cohort studies related to diabetes risk. Studies in hum...
Proceedings of the National Academy of Sciences of the United States of America, 2015
Glucose tolerance is lower in the evening and at night than in the morning. However, the relative contribution of the circadian system vs. the behavioral cycle (including the sleep/wake and fasting/feeding cycles) is unclear. Furthermore, although shift work is a diabetes risk factor, the separate impact on glucose tolerance of the behavioral cycle, circadian phase, and circadian disruption (i.e., misalignment between the central circadian pacemaker and the behavioral cycle) has not been systematically studied. Here we show-by using two 8-d laboratory protocols-in healthy adults that the circadian system and circadian misalignment have distinct influences on glucose tolerance, both separate from the behavioral cycle. First, postprandial glucose was 17% higher (i.e., lower glucose tolerance) in the biological evening (8:00 PM) than morning (8:00 AM; i.e., a circadian phase effect), independent of the behavioral cycle effect. Second, circadian misalignment itself (12-h behavioral cycl...
Sleep Health, 2018
This pilot study tested the independent and interactive effects of sleep and meal times, under identical sleep duration and feeding conditions, on insulin sensitivity (Si) in overweight adults. Participants underwent a 4-phase randomized crossover inpatient study differing in sleep times: normal (Ns: 0000-0800 hours) or late (Ls: 0330-1130 hours); and in meal times: normal (Nm: 1, 5, 11, and 12.5 hours after awakening) or late (Lm: 4.5, 8.5, 14.5, and 16 hours after awakening). An insulin-modified frequently sampled intravenous glucose tolerance test, at scheduled breakfast time, and a meal tolerance test, at scheduled lunch time, were performed to assess Si after 3 days in each condition. Six participants were enrolled (4 men, 2 women; mean age 25.1 ± [SD] 3.9 years, body mass index 29.2 ± 2.7 kg/m 2); only 1 failed to complete her last study phase. There were no effects of sleep and meal times or sleep × meal time interaction on Si (all P N .35), acute insulin response to intravenous glucose (all P N .20), and disposition index (all P N .60) after adjusting for sex and body mass index. Meal tolerance test glucose and insulin areas under the curve were lower during Nm (glucose P = .11; insulin P = .0088). There were a sleep × meal interaction and an effect of meal times on overnight glucose (P = .0040 and .012, respectively) and insulin (P = .0075 and .067, respectively). Sleep timing, without concomitant sleep restriction, does not adversely affect Si and glucose tolerance, but meal times may be relevant for health. Our results should be confirmed in a larger sample.
Modulation of glucose regulation and insulin secretion by circadian rhythmicity and sleep
Journal of Clinical Investigation, 1991
To define the roles of circadian rhythmicity (intrinsic effects of time of day independent of the sleep or wake condition) and sleep (intrinsic effects of the sleep condition, irrespective of the time of day) on the 24-h variation in glucose tolerance, eight normal men were studied during constant glucose infusion for a total of 53 h. The period of study included 8 h of nocturnal sleep, 28 h of continuous wakefulness, and 8 h ofdaytime sleep. Blood samples for the measurement of glucose, insulin, C-peptide, cortisol, and growth hormone were collected at 20-min intervals throughout the entire study. Insulin secretion rates were derived from C-peptide levels by deconvolution. Sleep was polygraphically monitored. During nocturnal sleep, levels of glucose and insulin secretion increased by 31±5% and 60±11%, respectively, and returned to baseline in the morning. During sleep deprivation, glucose levels and insulin secretion rose again to reach a maximum at a time corresponding to the beginning of the habitual sleep period. The magnitude of the rise above morning levels averaged 17±5% for glucose and 49±8% for calculated insulin secretion. Serum insulin levels did not parallel the circadian variation in insulin secretion, indicating the existence of an approximate 40% increase in insulin clearance during the night. Daytime sleep was associated with a 16±3% rise in glucose levels, a 55±7% rise in insulin secretion, and a 39±5% rise in serum insulin. The diurnal-variation in insulin secretion was inversely related to the cortisol rhythm, with a significant correlation of the magnitudes of their morning to evening excursions. Sleep-associated rises in glucose correlated with the amount of concomitant growth hormone secreted. These studies demonstrate previously underappreciated effects of circadian rhythmicity and sleep on glucose levels, insulin secretion, and insulin clearance, and suggest that these effects could be partially mediated by cortisol and growth hormone.
Diabetes Care, 2019
OBJECTIVE Sleep disturbances and circadian misalignment (social jet lag, late chronotype, or shift work) have been associated with worse glycemic control in type 2 diabetes (T2D). Whether these findings apply to adults with prediabetes is yet unexplored. We hypothesized that self-reported short sleep, poor sleep quality, and/or circadian misalignment are associated with higher glycemia, BMI, and blood pressure (BP) in adults with prediabetes or recently diagnosed, untreated T2D. RESEARCH DESIGN AND METHODS Our cohort included 962 overweight/obese adults ages 20–65 years with prediabetes or recently diagnosed, untreated T2D who completed a 2-h oral glucose tolerance test and validated sleep questionnaires. Independent associations of sleep and circadian variables with glycemia, BMI, and BP were evaluated with regression models. RESULTS The multiethnic cohort was 55% men, with mean ± SD age 52.2 ± 9.5 years and BMI 34.7 ± 5.5 kg/m2. Mean sleep duration was 6.6 ± 1.3 h. Poor sleep qual...
Metabolites
Circadian rhythms are generated by the circadian clock, a self-sustained internal timing system that exhibits 24-h rhythms in the body. Many metabolic, cellular, behavioral and physiological processes are regulated by the circadian clock in coordination with environmental cues. The present study is a comprehensive review of the currently existing evidence concerning the relationship between circadian rhythms and sleep, metabolic, and cardiovascular disorders. We thoroughly searched the online databases PubMed, Scopus, and Web of Science to find the existing clinical studies from the last twenty-three years (2000–2023). Circadian misalignment was found to be associated with an increase in the risk of metabolic disorders, cardiovascular diseases, and obesity, as well as inadequate sleep quality. In this review article, all the included studies had a strength protocol design and all of them were conducted on humans. However, the most common limitations of them were the small sample siz...
Influence of weeks of circadian misalignment on leptin levels
Nat. Sci. Sleep, 2010
The neurobiology of circadian, wakefulness-sleep, and feeding systems interact to influence energy homeostasis. Sleep and circadian disruptions are reported to be associated with increased risk of diabetes and obesity, yet the roles of energy balance hormones in these associations are largely unknown. Therefore, in the current study we aimed to assess the influence of several weeks of circadian misalignment (sleep and wakefulness occurring at an inappropriate biological time) on the anorexigenic adipocyte hormone leptin. We utilized data from a previous study designed to assess physiological and cognitive consequences of changes in day length and light exposure as may occur during space flight, including exploration class space missions and exposure to the Martian Sol (day length). We hypothesized that circadian misalignment during an exploration class spaceflight simulation would reduce leptin levels. Following a three-week ∼8 hours per night home sleep schedule, 14 healthy participants lived in the laboratory for more than one month. After baseline data collection, participants were scheduled to either 24.0 or 24.6 hours of wakefulness-sleep schedules for 25 days. Changes in the phase of the circadian melatonin rhythm, sleep, and leptin levels were assessed. Half of participants analyzed exhibited circadian misalignment with an average change in phase angle from baseline of ∼4 hours and these participants showed reduced leptin levels, sleep latency, stage 2 and total sleep time (7.3 to 6.6 hours) and increased wakefulness after sleep onset (all P 0.05). The control group remained synchronized and showed significant increases in sleep latency and leptin levels. Our findings indicate that weeks of circadian misalignment, such as that which occurs in circadian sleep disorders, alters leptin levels and therefore may have implications for appetite and energy balance.