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Pilot study of sleep and meal timing effects, independent of sleep duration and food intake, on insulin sensitivity in healthy individuals.

ABSTRACT: 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/m2); 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>.35), acute insulin response to intravenous glucose (all P>.20), and disposition index (all P>.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.

SUBMITTER: Pizinger T

PROVIDER: S-EPMC5771427 | biostudies-literature | 2018 Feb

REPOSITORIES: biostudies-literature

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Pilot study of sleep and meal timing effects, independent of sleep duration and food intake, on insulin sensitivity in healthy individuals.

Pizinger Theresa T Kovtun Kyle K RoyChoudhury Arindam A Laferrère Blandine B Shechter Ari A St-Onge Marie-Pierre MP

Sleep health 20171120 1

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-modifi ...[more]

PMID: 29332677

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Project description:BACKGROUND:Recombinant leptin (metreleptin) ameliorates hyperphagia and metabolic abnormalities in leptin-deficient humans with lipodystrophy. We aimed to determine whether metreleptin improves glucose and lipid metabolism in humans when food intake is held constant. METHODS:Patients with lipodystrophy were hospitalized for 19 days, with food intake held constant by a controlled diet in an inpatient metabolic ward. In a nonrandomized, crossover design, patients previously treated with metreleptin (n = 8) were continued on metreleptin for 5 days and then taken off metreleptin for the next 14 days (withdrawal cohort). This order was reversed in metreleptin-naive patients (n = 14), who were reevaluated after 6 months of metreleptin treatment on an ad libitum diet (initiation cohort). Outcome measurements included insulin sensitivity by hyperinsulinemic-euglycemic clamp, fasting glucose and triglyceride levels, lipolysis measured using isotopic tracers, and liver fat by magnetic resonance spectroscopy. RESULTS:With food intake constant, peripheral insulin sensitivity decreased by 41% after stopping metreleptin for 14 days (withdrawal cohort) and increased by 32% after treatment with metreleptin for 14 days (initiation cohort). In the initiation cohort only, metreleptin decreased fasting glucose by 11% and triglycerides by 41% and increased hepatic insulin sensitivity. Liver fat decreased from 21.8% to 18.7%. In the initiation cohort, changes in lipolysis were not independent of food intake, but after 6 months of metreleptin treatment on an ad libitum diet, lipolysis decreased by 30% (palmitate turnover) to 35% (glycerol turnover). CONCLUSION:Using lipodystrophy as a human model of leptin deficiency and replacement, we show that metreleptin improves insulin sensitivity and decreases hepatic and circulating triglycerides and that these improvements are independent of its effects on food intake. TRIAL REGISTRATION:ClinicalTrials.gov NCT01778556FUNDING. This research was supported by the intramural research program of the NIDDK.

Project description:Background & aimsWhile environmental factors are presumed to be primary drivers of food timing, preliminary evidence suggests that genetics may be an additional determinant. The aim was to explore the relative contribution of genetics and environmental factors to variation in the timing of food intake in a Spanish twin population. Because chronotype, bedtime and wake time are related to food timing, covariance with food timing was further assessed.MethodsIn this observational study, 53 pairs of adult (mean (SD) = 52 (6.03) years) female twins (28 monozygotic; 25 dizygotic) were recruited from the Murcia Twin Register. Zygosity was determined by DNA-testing. Timing of the three main meals of the day was assessed via 7-day dietary records, and the midpoint of food intake was computed by calculating the midpoint between breakfast and dinner times. Chronotype, bedtime and wake time were self-reported. Heritability of food timing and related traits were estimated by comparing monozygotic and dizygotic twin correlations and fitting genetic structural equation models to measured variables.ResultsWe observed genetic influences for food timing, with highest heritability for the midpoint of food intake (64%) in an overweight/obese population (BMI = 26.01 ± 3.77). Genetic factors contributed to a higher degree to the timing of breakfast (56%) than the timing of lunch (38%) or dinner (n.s.). Similarly, heritability estimates were larger in related behavioral traits earlier on in the day (i.e. wake time, (55%)), than those later on in the day (i.e. bedtime, (38%)). Bivariate analyses revealed a significant genetic overlap between food timing and bedtime and chronotype (rG between 0.78 and 0.91).ConclusionsGenetic influences appear to account for a significant proportion of the variability in food timing, particularly breakfast. Thus, interventions related to food timing may be more effective when targeting afternoon/evening traits, such as lunch or dinner times. Furthermore, our data suggest shared genetic architecture underlying food timing and phenotypically related traits.Clinical trialNCT03059576. https://clinicaltrials.gov/ct2/show/NCT03059576.

Dataset Information

Pilot study of sleep and meal timing effects, independent of sleep duration and food intake, on insulin sensitivity in healthy individuals.

Publications

Pilot study of sleep and meal timing effects, independent of sleep duration and food intake, on insulin sensitivity in healthy individuals.

Similar Datasets

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