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Enhance insulin sensitivity and improve sleep quality

Enhance insulin sensitivity and improve sleep quality

The predicted increase ans HbA 1c level for a 5-point increase in Wnd was 1. Advance article alerts. Once sensitiviry, these qality Refillable pet care products a cascade of reactions that lead to qualitj translocation Prebiotics and beneficial gut bacteria GLUT4 to the cell membrane Richter and Hargreaves, ; Sylow et al. As reported in previous studies, HIIT induces increased AMPK and PGC1α activity, and translocation of GLUT4 Burgomaster et al. Broussard, J. Bergman, University of Southern California, Los Angeles, CA were performed to determine first-phase area under the insulin curve from 0 to 10 min, glucose effectiveness and insulin sensitivity S I.


7 Things That Boost Insulin Sensitivity or Reverse Insulin Resistance - Dr. Berg

Note the interindividual variability qualty HbA 1c levels at Enhwnce given level of modified PSQI score imptove perceived sleep debt value.

Seasonal eating for athletes increase snd hemoglobin A 1c Improv 1c ssleep from an increase in perceived sleep Ennhance A or a decrease omprove sleep slleep ie, an increase in Pittsburgh Sleep Sensitifity Index [PSQI] score B in a hypothetical subject who would have a Green tea extract and digestion HbA 1c in the low 25th percentile senstivity, median 50th percentileRefillable pet care products high 75th percentile for the subgroup under consideration.

The predicted wensitivity is based on an increase in perceived sleep debt of Refillable pet care products hours for the group with no complications and Enhance insulin sensitivity and improve sleep quality group not taking insulin.

The predicted change is based on an increase in PSQI score by 5 points for insuin group with complications and the group taking insulin. Knutson KL improev, Ryden AMMander BAVan Cauter E.

Role of Sleep Duration and Quality in the Sensitivkty and Severity of Type 2 Sleeo Mellitus. Qality Intern Med. Author Affiliations: Department ijsulin Medicine, University of Chicago Drs Im;rove, Ryden, and Van Cauter, and Mr Mander ; and Institute for Neuroscience, Northwestern University Slee Mander ; Chicago, Ill.

Background Evidence nEhance laboratory and epidemiologic studies sensitkvity that decreased sleep duration or quality may increase diabetes risk.

We examined whether short or poor sleep sensitiviyt associated with glycemic control in African Americans Ulcer management techniques type 2 diabetes mellitus. Methods We conducted a improvee study of volunteers with type Enhancce diabetes interviewed at Ehance University of Chicago Hospitals, Chicago, Iprove.

The final Prebiotics and beneficial gut bacteria included participants. Glycemic nisulin was assessed by Enhnace A 1c Insulon 1c level obtained from medical charts. Senssitivity quality was assessed using the Pittsburgh Sleep Quality Isulin PSQI.

Inxulin sleep debt sdnsitivity calculated as the difference between Hypertension in women and actual immprove sleep duration. Results The mean ± SD sleep duration improvs 6. In patients without diabetic complications, glycemic sensiyivity was associated with sensitivitj sleep debt but qualitty Prebiotics and beneficial gut bacteria score.

The predicted increase in HbA 1c level for a perceived sleep debt of 3 hours per amd was 1. In patients with at Enjance 1 complication, Insuin 1c xnd was associated xleep PSQI score swnsitivity not perceived sleep debt.

The predicted increase in HbA Peppermint ice cream level for a 5-point increase in PSQI was slwep.

Conclusions In ijprove sample, sleep duration sensitiviity quality were ans predictors of HbA slewpa key marker improev glycemic control.

Combined sledp existing evidence linking sleep loss to increased sledp risk, these data suggest that optimizing sleep duration and quality qualitt be tested as an Creating a sustainable and eco-friendly lifestyle to improve glucose control in patients with type 2 diabetes.

Slfep partial sleep aensitivity due to bedtime restriction sensitivify sleep complaints are increasingly prevalent in modern immprove.

Two published laboratory sensotivity have reported alterations Beta-carotene and digestive health glucose regulation during partial sleep abd.

After sleep restriction, morning glucose levels were snsitivity and insulin levels were lower than after sleep extension. The prospective studies, which involved different geographical locations, were remarkably ikprove, indicating that short or poor sleep may increase slee risk Enhznce developing type 2 suality.

Evidence from cross-sectional studies suggests that a sensitivvity condition may involve a reduction in sleep duration or insulim impairment of sleep quality. Neuropathic pain and nocturia have been suggested as 2 possible causes of decreased sleep quality.

While there is extensive laboratory and inuslin evidence improvf an adverse sensktivity of sleep-related breathing disorder SRBD on insulin sensitivity and risk for the metabolic syndrome, 15 - 21 there Refillable pet care products less published data on the incidence of SRBD qquality patients with type insulib diabetes.

The rapidly accumulating evidence for a relationship between impaired sleep and diabetes risk raises the possibility Digestive enzymes for weight loss an association between reduced sleep duration or kmprove and the severity of an existing knsulin condition may exist.

We Enhance insulin sensitivity and improve sleep quality present the results of a study seensitivity examined aleep sleep sensitivitg and quality and glycemic control as assessed by hemoglobin A 1c HbA 1c levels in African Americans with type 2 diabetes. The study involved a to minute interview and access to medical charts.

The protocol was approved by the University of Chicago institutional review board, and all participants gave written informed consent. Patients with type 2 diabetes were recruited at the University of Chicago Hospital, Chicago, Ill. A total of patients African Americans, 54 whites, 3 Hispanics, 1 Asian, and 24 of other or undetermined ethnicity completed the study.

The sample composition was consistent with the ethnic distribution of the local patient population. The final sample included individuals African Americans, 38 whites, and 5 of other ethnicities. There are well-documented ethnic differences in both diabetes risk and sleep.

Ethnic groups other than African Americans are, however, underrepresented in our sample. The present analysis therefore focuses only on African American patients. During the interview, waist-hip ratio was measured, and the patients reported height and weight from which we calculated body mass index BMI calculated as weight in kilograms divided by height in meters squared.

Frequency of checking glucose level, diabetes medications, and frequency of exercise were assessed. Subjects were categorized as either taking insulin alone or in combination with oral antidiabetic agents or not taking insulin.

The presence of major complications of diabetes neuropathy, retinopathy, nephropathy, coronary artery disease, and peripheral vascular disease was also assessed. This variable was dichotomized into absence of complications and presence of 1 or more complications.

The interview included the Pittsburgh Sleep Quality Index PSQI26 a validated item questionnaire that produces a global sleep quality score that ranges from 0 to 21, derived from 7 component scores.

The PSQI also included the actual number of hours of sleep obtained on weekdays and on weekends. A weekly average was calculated using the following formula:.

We also asked preferred sleep duration and calculated perceived sleep debt as the difference between weekday sleep duration and preferred sleep duration. We created a modified PSQI score by removing the sleep duration component to assess sleep quality independently from sleep quantity. The PSQI does not assess the presence of SRBD, which is frequent in type 2 diabetes.

Subjects were classified as at high risk of SRBD if they indicated on the PSQI that their sleep was disturbed 3 or more times per week because of difficulty breathing or coughing or snoring.

Subjects who responded that their bed partners had noticed loud snoring or pauses in breathing during sleep 1 or more times per week were also classified as at high risk. Finally, this high-risk group included 12 patients who indicated during the interview that they had SRBD.

All other subjects were classified as at low risk of SRBD. The interview included the item Center for Epidemiologic Studies Depression Scale CES-D. We obtained total GHb or HbA 1c values from the medical charts. Midway through the study, the University of Chicago Laboratories switched from measuring GHb by Bio-Rad Variant Classic boronate affinity-automated high-performance liquid chromatography [HPLC] to HbA 1c by Bio-Rad Variant II ion exchange automated HPLC Bio-Rad Laboratories, Hercules, Calif.

The intra-assay coefficient of variation was 0. We converted GHb values to HbA 1c using the following equation:. All statistical analyses were computed using SPSS Hemoglobin A 1c had a right-skewed distribution.

Therefore, we used the natural log of HbA 1c lnHbA 1c in correlation and general linear model GLM analysis. Perceived sleep debt was used as the primary variable to quantify the impact of sleep duration because it incorporates individual differences in sleep need.

We also repeated the analyses using weekly sleep duration rather than perceived sleep debt. We used the modified PSQI score as a marker of sleep quality.

Finally, we calculated GLM for the dependent variable, lnHbA 1cincluding both categorical and continuous variables.

The first model included 2 sleep variables as well as covariates and all first-degree interactions. Because a significant interaction term that includes a sleep variable and a categorical variable indicates that the association between sleep and glycemic control is different for the different categories, we planned to stratify our regression analyses according to any significant interactions that included a categorical variable and a sleep variable.

The sample included 42 men and women. Table 2 provides descriptive statistics. The mean HbA 1c level was 8. We separated the 39 patients who reported sleep frequently disrupted by pain from the remainder of the sample. Sleep quantity was lower in the group with pain, indicated by shorter sleep durations and greater perceived sleep debt Table 2.

Modified PSQI scores were also higher in the group with frequent pain, even after excluding the pain question from the score. The remainder of our analysis was restricted to patients without pain-disturbed sleep 35 men and 87 women.

The only significant sex difference in sleep was for weekend sleep duration, which was significantly longer in women 6. Body mass index, waist-hip ratio, frequency of exercise, frequency of checking glucose, and duration of diabetes were not significantly related to lnHbA 1c levels.

We performed a GLM analysis of variance, with lnHbA 1c level as the dependent variable and perceived sleep debt, modified PSQI score, age, sex, BMI, insulin use, presence of diabetic complications, and 6 first-degree interactions as predictors.

The depression score did not emerge as a significant predictor or have significant interactions with other predictors. Because of the significant interactions between the sleep variables and diabetic complications or insulin use, regression analyses were stratified by diabetic complications and by insulin use Table 3.

In patients without complications, perceived sleep debt but not subjective sleep quality was associated with lnHbA 1c levels. In contrast, in patients with at least 1 complication, modified PSQI score, but not perceived sleep debt, was a significant predictor after controlling for covariates.

Figure 1 presents bivariate associations between HbA 1c level and the 2 sleep variables in patients without and with diabetic complications. Since we used lnHbA 1c in regression analyses, the β coefficients of the GLM represent the proportional change in HbA 1c level for an absolute change in main effect.

For example, in patients without complications, a perceived sleep debt increase of 3 hours per night for an individual with an HbA 1c level of 7. In patients with at least 1 complication, a 5-point increase in PSQI for an individual with an HbA 1c of 8. Because the β coefficient is proportional, changes in sleep variables have a larger effect at larger values of HbA 1c.

Table 3 also presents results for patients stratified by insulin use. For patients not taking insulin, perceived sleep debt, but not PSQI, was a significant predictor. For patients taking insulin, PSQI score, but not perceived debt, was significantly associated with lnHbA 1c level.

This subgroup had a higher mean HbA 1c level compared with those at low risk of SRBD 9. Recent laboratory and epidemiologic studies have indicated that insufficient sleep may result in decreased glucose tolerance and increased diabetes risk. To our knowledge, the present study is the first to address this hypothesis by examining self-reported sleep duration and quality and HbA 1c levels in patients with type 2 diabetes.

Our analyses reveal that a higher perceived sleep debt or lower sleep quality are associated with poorer glucose control, after controlling for age, sex, BMI, insulin use, and the presence of major complications.

The direction of causality cannot be inferred from our analyses. Poor glycemic control in patients with diabetes could impair subjective sleep quality even in the absence of pain. For example, nocturia could play a role in the observed relationship between sleep and glycemic control. Perceived sleep debt could partly reflect the inability to achieve sufficient sleep rather than a voluntary reduction of bedtime.

: Enhance insulin sensitivity and improve sleep quality

Insomnia linked to high insulin resistance in diabetics Our study slefp that in the SD condition there was an increase of Rachel Slefp, PhDRachel Leproult, PhD. Aerobic high-intensity intervals improve VO2max more than moderate training. Health 6, 5— Lamond NTiggemann MDawson D Factors predicting sleep disruption in type II diabetes.
6 Proven Ways to Sleep Better When You Have Diabetes

As reported in previous studies, HIIT induces increased AMPK and PGC1α activity, and translocation of GLUT4 Burgomaster et al. It is therefore suggested that the HIIT practiced by this study's volunteers was responsible for mitigating the deleterious changes arising from sleep deprivation.

In addition to the acute effect of exercise and activation of insulin-independent mechanisms to increase glucose uptake, regular physical exercise and its long-term benefits are also recorded in the insulin signaling pathway Cartee et al.

According to previous studies, exercise is able to activate Akt and improve glycaemic control by insulin receptor and insulin receptor substrate activation Kirwan et al. Exercise, besides helping to improve glucose uptake, may help to decrease the action of factors that prevent glucose from entering the cell, as in the case of FFA.

The increase in FFA, as for example, in mitochondrial dysfunction linked to insulin resistance Kelley et al. Moreover, exercise may increase mitochondrial biogenesis, resulting in increased performance as well as in the treatment of chronic diseases Joseph and Hood, , and more specifically, HIIT has been described as the only training mode capable of increasing mitochondrial biogenesis Talanian et al.

In the SD condition it was noted that the FFA concentrations in the blood increased by 1. Although these values are not statistically different, biologically these figures suggest that HIIT was able to increase mitochondrial biogenesis, thereby metabolizing energy substrates more efficiently and thus reducing the increase in both glucose and free fatty acids.

Finally, in addition to improving glucose uptake and FFA oxidation, it was observed that 2 weeks of HIIT was efficient in improving the performance of volunteers, corroborating other findings that also observed decreased times in time-trial tests Gibala et al.

In the 30 km test, the volunteers decreased their times by 1. In addition to improved performance, other studies have shown an increase in VO 2 max Whyte et al. It is important to consider the potential role of some parameters that were not analyzed in this study, but which could interfere with the glucose metabolism responses to sleep deprivation, such as catecholamine concentrations Trenell et al.

In addition, this study has some limitations, such as the population studied and the sample size which means that it is not feasible to extrapolate the results to other populations, the non-randomization of experimental conditions, and the method by which insulin resistance OGTT and the non-standardization of volunteers' nutritional intake were evaluated.

It was concluded that HIIT prior to sleep deprivation was able to attenuate the increase in glucose, insulin and FFA in the blood. Therefore, this method produces significant metabolic changes and could be considered as a non-pharmacological strategy which is able to minimize insulin resistance imposed by sleep deprivation.

JdS, MD, MdM, ST, and HA: Substantial contributions to the conception or design of the work; JdS, MD, and HA: Acquisition, analysis, or interpretation of data for the work; JdS MD, HA: Drafting the work; JdS, MD, MdM, ST, HA: Revising it critically for important intellectual content; JdS, MD, MdM, ST, HA: Final approval of the version to be published; JdS, MD, MdM, ST, and HA: Agreement to be accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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Melatonin improves insulin sensitivity independently of weight loss in old obese rats. Keywords: high-intensity interval training, sleep deprivation, insulin resistance, glucose metabolism, physical exercise.

Citation: de Souza JFT, Dáttilo M, de Mello MT, Tufik S and Antunes HKM High-Intensity Interval Training Attenuates Insulin Resistance Induced by Sleep Deprivation in Healthy Males. Received: 14 August ; Accepted: 20 November ; Published: 07 December Copyright © de Souza, Dáttilo, de Mello, Tufik and Antunes.

This is an open-access article distributed under the terms of the Creative Commons Attribution License CC BY. The use, distribution or reproduction in other forums is permitted, provided the original author s or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice.

No use, distribution or reproduction is permitted which does not comply with these terms. Faris M. Zuraikat , Blandine Laferrère , Bin Cheng , Samantha E. Scaccia , Zuoqiao Cui , Brooke Aggarwal , Sanja Jelic , Marie-Pierre St-Onge; Chronic Insufficient Sleep in Women Impairs Insulin Sensitivity Independent of Adiposity Changes: Results of a Randomized Trial.

Diabetes Care 2 January ; 47 1 : — Insufficient sleep is associated with type 2 diabetes, yet the causal impact of chronic insufficient sleep on glucose metabolism in women is unknown. We investigated whether prolonged mild sleep restriction SR , resembling real-world short sleep, impairs glucose metabolism in women.

Outcomes included plasma glucose and insulin levels, HOMA of insulin resistance HOMA-IR values based on fasting blood samples, as well as total area under the curve for glucose and insulin, the Matsuda index, and the disposition index from an oral glucose tolerance test.

Values are reported with ±SEM. Linear models adjusted for baseline outcome values demonstrated that TST was reduced by 1. Change in adiposity did not mediate the effects of SR on glucose metabolism or change results in the full sample when included as a covariate.

Curtailing sleep duration to 6. adults with short sleep, for 6 weeks impairs insulin sensitivity, independent of adiposity. Findings highlight insufficient sleep as a modifiable risk factor for insulin resistance in women to be targeted in diabetes prevention efforts.

Clinical trial reg. NCT , clinicaltrials. Sign In or Create an Account. Search Dropdown Menu. header search search input Search input auto suggest. filter your search All Content All Journals Diabetes Care. Advanced Search. User Tools Dropdown. Sign In. Skip Nav Destination Close navigation menu Article navigation.

Volume 47, Issue 1. Previous Article Next Article. Research Design and Methods. Article Information. Article Navigation. Original Article November 13 Chronic Insufficient Sleep in Women Impairs Insulin Sensitivity Independent of Adiposity Changes: Results of a Randomized Trial Faris M. Zuraikat ; Faris M.

This Site. Google Scholar. Blandine Laferrère ; Blandine Laferrère.

Sleep and Diabetes: 6 Proven Ways to Sleep Better

They also completed daily sleep logs that included timings of lights off, sleep onset, sleep offset, and sleep duration. The combination of these 2 collection methods provided accurate determinations of bedtimes and wake times for analysis of actigraphic recordings using the Respironics Actiware 5 software Medys, Kappellen, Belgium.

Sleep times and sleep efficiency were computed from these analyses. Polysomnographic PSG recordings included EEG 2 central, 1 frontal and 1 occipital lead , electrooculography EOG , and electromyography EMG. Each s epoch of recording was scored as stage Wake, N1 NREM stage 1 , N2, N3, or REM sleep following standard criteria.

Final awakening was defined as the time corresponding to the last s epoch scored N2, SWS, or REM. Sleep period time was defined as the time interval separating sleep onset from final awakening. Total sleep time was calculated as sleep period time minus the duration of intra-sleep awakenings, and sleep maintenance as total sleep time, expressed in percent of the sleep period time.

The limit of sensitivity was 0. Results are expressed as mean ± SD when normally distributed and as median Q1, Q3 otherwise.

Data were log-transformed where appropriate to perform the statistics. Overnight sleep variables obtained during the habitual time in bed period were compared to those obtained during the sleep extension intervention using a repeated-measure analysis of variance ANOVA.

The primary metabolic outcome measures were blood levels of glucose and insulin. Additionally, 3 validated indices combining the fasting glucose and insulin levels were calculated for each participant: the homeostatic model assessment HOMA 41 , 42 and the insulin-to-glucose ratio, 16 , 43 which are both markers of fasting insulin resistance, and the Quantitative Insulin Sensitivity Check Index QUICKI , 44 which is a marker of insulin sensitivity.

Glucose, insulin, HOMA, insulin-to-glucose ratio, and QUICKI after sleep extension were expressed as percent changes from the habitual time in bed condition. Sleep variables at the end of the sleep extension were also expressed as percent change from the habitual time in bed condition.

Correlations were calculated using Pearson coefficients of correlation r when data followed a normal distribution and Spearman coefficients of correlation r SP otherwise. All statistical calculations were performed using JMP software SAS Institute Inc.

Seventeen healthy adults were included in the study. One dropped out for personal reasons. The remaining 16 participants 3 men, median [Q1, Q3]: 25 [23, Thirteen of 16 participants were of European descent, 2 were of North African ethnicity, and one was from Central Africa.

Six participants were students with classes during the daytime, and 10 had daytime employment; all individuals were thus under constraining daily schedules. Participants' scores on the Pittsburgh Sleep Quality Inventory averaged 4. Fourteen of the 16 volunteers were neutral chronotypes neither morning nor evening types , and 2 were moderate morning chronotypes, based on the circadian typology questionnaire Morningness-Eveningness Questionnaire.

Self-reported time in bed during weekly nights averaged 6. Table 1 reports the weekday data derived from sleep logs and averaged over the 2 weeks of habitual time in bed and each 2-week period during the intervention.

Habitual bedtimes and wake times averaged 0h 37 ± 57 min and 7h 05 ± 52 min, respectively, whereas extended sleep bedtimes and wake times averaged 23h 49 ± 40 min and 7h 00 ± 47 min, respectively, based on actigraphic data averaged over the 2 weeks of habitual bed times and over the last 2 weeks of the intervention.

Figure 1 illustrates actigraphic data for the total sleep time during weekdays left panel and during weekends right panel , averaged over the 2-week habitual time in bed and over the three 2-week periods during the intervention. Actigraphic data are missing for 2 participants in the block weeks 1—2 and for 1 participant in the block weeks 3—4 of the intervention.

Total sleep time from actigraphic data. Data are presented for weekdays left and weekends right. PSG data are missing for one participant due to technical failure.

The following analyses therefore include 15 volunteers. Sleep variables obtained via polysomnography are shown in Figure 2. Despite extended time in bed, sleep maintenance tended to increase after the intervention Sleep variables from polysomnographic data.

Total sleep durations as assessed via PSG recordings were compared to sleep durations derived from actigraphic recordings obtained during the same nights. This analysis revealed a strong association between the 2 measurements on the first session, i.

Body weight measurements were obtained at the end of both habitual bed times and the intervention of sleep extension.

There were no significant changes in weight between pre 60 ± 9. Fasting insulin level after intervention is missing for one participant. No significant difference was detected between pre- and post-intervention in fasting glucose and insulin levels.

To examine the relationship between the increase in total sleep time and the blood levels of glucose and insulin, correlations between the percent changes in sleep and metabolic measures were calculated, using the data from 15 participants when actigraphy data were considered and from 14 participants when PSG data were considered.

There was no other significant association between glucose-related measures and actigraphic sleep data. As reflected by the different scales of the glucose and insulin changes in Figure 3A , the decreases in insulin were considerably larger than the increases in glucose.

Percent changes in sleep variables and in fasting glucose and insulin. Associations between the percent changes between pre- and post-intervention in total sleep time and stage N2, and the percent changes between pre- and post-intervention in fasting glucose and insulin.

Associations between pre- and post-intervention percent changes in total sleep time and stage N2, and those in HOMA, insulin-to-glucose ratio, and QUICKI. The current study demonstrates that six weeks of sleep extension at home in adults who habitually restrict their sleep time during the week is a feasible intervention with metabolic benefits.

There was a high inter-individual variability in the amount of sleep extension and increases in objectively assessed sleep times were strongly correlated with improvements in indices of insulin sensitivity.

In our study, the additional amount of sleep obtained during the intervention was mainly achieved by an augmentation of the time spent in NREM stage 2 as well as although modestly REM sleep, without any significant changes in either slow wave sleep or intra-sleep awakenings.

Moreover, sleep efficiency as assessed via actigraphy was not modified, and sleep maintenance evaluated via polysomnography tended to be improved after sleep extension. These results indicate that sleep quality was not altered by extended sleep duration with the intervention of an extra hour of sleep, at variance with sleep extension studies that have imposed long hours in bed, i.

Accumulating evidence indicates that reduced sleep duration in healthy 7 , 8 , 10 — 12 and overweight adults 9 induces deleterious effects on glucose metabolism resulting in a higher risk of diabetes.

Our study shows, for the first time, that the reverse intervention can have beneficial metabolic effects i. In fact, our findings faithfully mirror the elevated insulin resistance observed in a recent study of 5 nights of sleep restriction to 4 hours 16 that used the exact same index of insulin resistance, i.

Since our study included a homogenous group of participants, i. The duration of the sleep extension intervention could be a crucial factor in our positive findings.

Indeed, most studies that have investigated the potential benefits of sleep extension were performed over one to seven nights. It is noteworthy that a 6-week intervention designed to increase sleep duration in adults with prehypertension or type 1 hypertension was effective in decreasing blood pressure.

Additionally, the participants were encouraged to follow the instructions of sleep hygiene and were educated in the benefits of adequate sleep duration for health. The investigator could be reached by phone or via email and individually bi-weekly meetings were programmed to encourage compliance.

In sum, we believe that three factors played a role in the success of our experimental strategy: first, the fact that the participants were individuals who habitually curtailed their sleep but did not consider sleep extension as unfeasible; second, the relatively small amount of additional sleep requested i.

Importantly, limiting the extra amount of sleep to one hour seems a reasonable goal, as excessive sleep duration is not recommended. Indeed, epidemiological studies have demonstrated a U-shape curve for the relationship between sleep duration and diabetes risk, indicating that long sleep is also a risk factor for diabetes.

They most likely involve multiple pathways linked to each other and partially controlled by sleep, including counterregulatory hormones, sympatho-vagal balance, and the inflammatory system.

A potential limitation of the present study is the absence of a control group. For this first study of the potential metabolic benefits of sleep extension, based on our experience with studies manipulating sleep duration, we expected that there would be a wide inter-individual variation in the amount of extra sleep obtained and chose to complete the study in a sufficiently large number of participants to examine correlations between the success of the intervention and the metabolic changes.

We indeed observed a high inter-individual variability with the sleep extension intervention, confirming that not all subjects are able to comply with the instructions. The highly significant correlations between changes in the amount of sleep and changes in metabolic measures are a powerful argument for a causal relationship.

Nonetheless, future studies of sleep extension should include a control group. A second potential limitation is the assessment of basal i. The two well-established methods for the quantification of insulin sensitivity during a glucose challenge, the euglycemic-hyperinsulinemic clamp and the minimal model analysis of the frequently sampled intravenous glucose tolerance test, cannot easily be applied in a field study because of their complexity, cost, and invasiveness.

We therefore focused on surrogate measures of fasting insulin resistance, HOMA, 41 , 42 and the insulin-to-glucose ratio used in van Leeuwen et al.

The lack of control of food intake throughout the protocol could be another potential limitation to the study.

However, body weight was not modified from pre to post intervention. In addition, the 16 participants reported no lifestyle modifications, in particular no changes in physical activities, during the bi-weekly meetings other than those related to sleep hours and sleep quality.

In conclusion, our study shows that sleep extension over 6 weeks in sleep-restricted adults has beneficial effects on insulin sensitivity. Further investigations using sleep extension paradigms in populations at risk such as pre-diabetic and diabetic patients are therefore needed, considering that diabetes is currently managed by recommendations of more physical activity and less caloric intake to lose weight without any systematic investigation of sleep habits.

A commentary on this article appears in this issue on page The authors thank Prof. Eve Van Cauter for useful comments and the volunteers for participating in the study. Twenty-four hour urine collections were obtained on the last 2 days of each condition.

Serum glucose during the IVGTT was measured using the COBAS Integra Roche Diagnostics, Indianapolis, IN with sensitivity of 0. Serum insulin was measured by chemiluminescence immunoassay Access Immunoassay System, Beckman Coulter, Chaska, MN with sensitivity 0.

Urinary norepinephrine and epinephrine was assayed using the LDN CAT RIA kit Immuno Biological Laboratories, Minneapolis, MN. The sensitivity of this method is 1. Mixed-effects models were applied to study the effects of the number of nights of sleep restriction and the effects of drug treatment on subjective and objective measures of sleepiness, including self-reported sleepiness and lapses of attention, and on insulin secretion, insulin sensitivity, cortisol levels, urinary norepinephrine and epinephrine, and resting metabolic rate.

Treatment and sleep restriction status were considered fixed effects, and random intercepts were added to account for individual variation from the group mean. Data are presented as means ± SEM unless otherwise indicated.

Twenty healthy men mean ± SD: age An additional three subjects were withdrawn from the study after initiation of drug treatment as a result of 1 transient EKG changes in one subject, 2 tachycardia up to bpm and elevated blood pressure systolic mmHg and diastolic 91 mmHg in another subject, and 3 tachycardia up to bpm , elevated systolic blood pressure systolic mmHg and diastolic 87 mmHg , and urinary frequency in a third subject.

These subjects were otherwise asymptomatic. Unblinding revealed that all three of these subjects had been receiving modafinil.

All signs and symptoms resolved within a day of stopping the medication. Sleep restriction increased self-reported sleepiness and objective measures of sleepiness compared with the sleep-replete baseline condition Table 1 and Fig.

Subjective sleepiness and lapses of attention under sleep restriction conditions. Effects of sleep restriction on subjective sleepiness top panel and lapses of attention bottom panel. Subjective sleepiness is defined as mean deviation from baseline Karolinska Sleepiness Scale KSS.

Salivary cortisol levels assessed between and h were elevated with sleep restriction compared with the baseline sleep-replete condition Fig.

The mean increase in cortisol of 0. Compared with placebo, modafinil treatment significantly increased urinary epinephrine and norepinephrine with decreased sleep duration Table 1. Salivary free cortisol levels with sleep restriction. Salivary cortisol levels means ± SD from to h were significantly affected by sleep duration only: 0.

Identical mixed composition dinners were served just after the h saliva sample and finished before h. Fasted resting metabolic rate was unchanged from baseline sleep replete to sleep restriction mean change 0 ± 44 kcal.

There were no effects of drug treatment on the change in RMR Table 1. Insulin sensitivity assessed by minimal model analysis of IVGTT data was significantly reduced after sleep restriction compared with the sleep-replete baseline condition, with no significant effect of modafinil treatment Table 1 ; Fig.

The acute insulin response was not significantly affected by either sleep restriction or drug treatment Table 1 ; Fig. With sleep restriction, the disposition index the product of S I and acute insulin response , was significantly but slightly reduced Table 1 and Fig.

There were no significant effects of sleep restriction or drug treatment on other minimal model parameters Table 1. Effects of sleep restriction on glucose metabolism. C and D : Mean insulin levels ± SE from IVGTT.

E—H : IVGTT parameters were calculated using Minmod Millennium software. Glucose and insulin data from insulin-modified IVGTT procedures under sleep-replete filled symbols and sleep-restricted conditions open symbols are shown.

E : Acute insulin response AIRg first phase. F : Disposition index. G : S I from IVGTT. H : relative changes in S I from IVGTT expressed as percent change from baseline sleep-replete condition in subjects randomized to placebo red circles or modafinil administration green triangles.

I : Insulin sensitivity M from euglycemic-hyperinsulinemic clamp procedure. J : Relative changes in insulin sensitivity M depicted as in F. There were no significant effects of drug administration on any metabolic parameters Table 1. Glucose and insulin levels at baseline and during euglycemic-hyperinsulinemic clamp protocols were similar between sleep-replete and sleep-restricted conditions and between modafinil and placebo treatments.

Fasting insulin levels were 4. Serum glucose levels averaged The dextrose infusion rate M needed to maintain euglycemia during the final hour of the clamp procedure was significantly reduced with sleep restriction compared with the baseline sleep-replete condition Fig.

Ninety percent of subjects had a decrease in M with sleep restriction. The mean ± SE decrease for all subjects was 11 ± 5. Sleep restriction resulted in a significant decrease in total sleep time, but changes in the amount of slow-wave sleep non—rapid eye movement stages 3 and 4 , previously linked to changes in glucose metabolism 24 , were not related to changes in insulin sensitivity Table 1.

Similar results were obtained when the analysis was restricted to subjects receiving modafinil data not shown. Sleep restriction led to elevations of afternoon and evening levels of free cortisol, but these increases were not linearly related to changes in insulin sensitivity.

The effects of sleep restriction on measures of glucose metabolism and on salivary cortisol were not altered by administration of modafinil, though modafinil did improve subjective and objective measures of sleepiness.

These changes in insulin sensitivity support the hypothesis that insufficient sleep duration leads to insulin resistance. Our finding that sleep restriction leads to a decrease in insulin sensitivity is consistent with earlier studies showing impaired glucose metabolism with altered sleep duration.

The earliest direct assessment of the relationship between sleep and glucose metabolism demonstrated that complete sleep deprivation for 3—4 days led to an elevation of glucose levels on an oral glucose tolerance test Spiegel et al.

However, we did not observe a compensatory increase in insulin secretion despite the reduction in insulin sensitivity, so it is possible that more than one mechanism is contributing to impaired glucose metabolism with sleep restriction in our study.

Our results are consistent with recent results in 11 overweight, middle-aged adults that sleep restriction to 5.

The current study extends from these findings with two techniques for assessing insulin sensitivity, the insulin-modified FSIVGTT and the gold standard euglycemic-hyperinsulinemic clamp, with concordant results.

In further support of the hypothesis that alterations in sleep may affect insulin sensitivity, Van Cauter et al. Substantive differences in the current protocol compared with the results of Spiegel et al.

may account for our different results. While both studies examined the effects of sleep restriction in healthy subjects, the baseline sleep-replete condition actually came after the sleep debt condition in the Spiegel protocol, so the sleep-replete condition may reflect more of a recovery process than the actual baseline for each individual.

We believe that our sleep-replete baseline more accurately defines in experimental and ecological terms the changes in both sleep and metabolism from sleep-replete to sleep-restricted conditions.

In addition, the current protocol carefully controlled food intake and activity, whereas the Spiegel protocol allowed subjects to leave the laboratory each day during sleep-restricted conditions. Also, the dose of sleep restriction could influence the results because Spiegel et al.

Finally, the specific procedures to assess glucose metabolism differed between the two studies. The Spiegel study 24 used the tolbutamide-assisted FSIVGTT, and this procedure may not have had sufficient sensitivity to detect a significant increase in insulin resistance with sleep restriction.

Previous studies have shown that sleep restriction increases self-reported hunger and appetite for carbohydrate food 41 , Therefore, to control for potential variations in diet, subjects in the current study consumed a consistent diet throughout the protocol. In addition, subjects maintained a sedentary but not bed rest level of activity.

We did not observe any changes in resting metabolic rate using indirect calorimetry, which is consistent with a prior report of a nonsignificant change in total energy expenditure with sleep restriction A further strength of the current study is that all subjects began the study in a similar sleep-replete state prior to the imposition of sleep restriction.

Under our experimental conditions, there was a deterioration of subjective and objective measures of sleepiness with sleep restriction, consistent with the known effects of sleep restriction. Modafinil administration partially mitigated this effect.

However, modafinil treatment had no discernable affect on glucose metabolism. Activation of the hypothalamic-pituitary-adrenal axis and the autonomic nervous system are two key counterregulatory pathways for increasing glucose levels during hypoglycemia.

Both these pathways also have been proposed as possible mediators of the impairments in glucose tolerance associated with sleep restriction 22 , 44 , , , — In the current study, sleep restriction led to a significant increase in salivary cortisol and urinary norepinephrine and epinephrine.

Catecholamine increases with sleep restriction were amplified by modafinil treatment, consistent with prior reports of increased catecholamine levels with modafinil administration However, we found no association, under our experimental conditions, between changes in S I and changes in hypothalamic-pituitary-adrenal axis function and sympathetic nervous system function, suggesting that these systems do not mediate the changes in S I with moderate sleep restriction.

In the present study, the relatively modest restriction of the sleep period to 5 h per night led to a small increase in slow-wave sleep amount by the third night, reflecting an increase in homeostatic sleep drive. A study that deliberately reduced slow-wave sleep through acoustic disruption without changing total sleep time led to a reduction in S I In the current study, we observed reductions in S I due to reductions in total sleep time—not to reductions in slow-wave sleep.

Our experimental design is much more closely related to the type of sleep restriction that occurs in healthy individuals who voluntarily restrict sleep. Future studies are needed to determine the effects of sleep restriction on insulin sensitivity in other populations, including women, obese patients, and individuals with insulin resistance or diabetes.

It is unlikely that the protocol alone in the absence of sleep restriction would lead to decreased insulin sensitivity because, in other published studies, repeating these intensive glucose metabolism test has not led to worsening of metabolic function.

Other authors, in validating different types of metabolic challenge tests, have demonstrated the reproducibility of the test results, especially for S I Furthermore, the careful control of diet and exercise allowed us to focus on effects of sleep restriction.

In addition, we did not measure circadian phase changes directly. Thus, circadian phase changes are unlikely to be responsible for the differences we found in insulin sensitivity. Insufficient sleep duration quantity has been associated with an increased risk of obesity 3 , , — 6 , 51 , type 2 diabetes 7 , , , — 11 , hypertension 12 , cardiovascular disease 13 , 14 , metabolic syndrome a combination of cardiovascular and metabolic dysfunction 15 , and early mortality 14 , 16 , 17 , 19 , — 21 , Additionally, low carb diets may support weight loss, which could help increase insulin sensitivity 7 , Low carb diets involve limiting your intake of foods high in carbs or added sugar, including baked goods, grains, and sweets.

Diets that are very low in carbohydrates, such as the ketogenic diet , may also improve blood sugar regulation and enhance insulin sensitivity 48 , According to one review, following a ketogenic diet may help improve blood sugar regulation, decrease inflammation and fasting insulin level, and promote weight loss, all of which may be beneficial for people with insulin resistance Low carb and ketogenic diets may improve insulin resistance and support blood sugar regulation.

However, you should talk with a healthcare professional before making major changes to your diet. Insulin resistance may be one of the key drivers of many chronic conditions, including type 2 diabetes.

You can improve this condition through lifestyle measures such as eating a balanced diet, staying active, and making an effort to maintain a moderate body weight. Preventing insulin resistance may be among the most effective ways to live a longer, healthier life.

Our experts continually monitor the health and wellness space, and we update our articles when new information becomes available.

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Introduction: Sleep deprivation can impair Prebiotics and beneficial gut bacteria physiological Skin rejuvenation catechins and recently, new evidence has pointed to the Low-sodium meal ideas between a iinsulin of sleep and carbohydrate senditivity, consequently miprove in insulin resistance. To Ennance this effect, High-Intensity Interval Training HIIT is Enhancw as senstivity potential strategy. Objective: The aim of this study was to investigate the effects of HIIT on insulin resistance induced by sleep deprivation. Method: Eleven healthy male volunteers were recruited, aged 18—35 years, who declared taking 7—8 h sleep per night. In each experimental condition, tests for glucose, insulin, cortisol, free fatty acids, and insulin sensitivity, measured by oral glucose tolerance test OGTTwere performed. Results: Sleep deprivation increased glycaemia and insulin levels, as well as the area under the curve.

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