Explore the vast range of titles available.

The human circadian system regulates hunger independently of behavioral factors, resulting in a trough in the biological morning and a peak in the biological evening. However, the role of the only known orexigenic hormone, ghrelin, in this circadian rhythm is unknown. Furthermore, although shift work is an obesity risk factor, the separate effects of the endogenous circadian system, the behavioral cycle, and circadian misalignment on ghrelin has not been systematically studied. Here we show—by using two 8-day laboratory protocols—that circulating active (acylated) ghrelin levels are significantly impacted by endogenous circadian phase in healthy adults. Active ghrelin levels were higher in the biological evening than the biological morning (fasting +15.1%, P = 0.0001; postprandial +10.4%, P = 0.0002), consistent with the circadian variation in hunger (P = 0.028). Moreover, circadian misalignment itself (12-h behavioral cycle inversion) increased postprandial active ghrelin levels (+5.4%; P = 0.04). While not significantly influencing hunger (P > 0.08), circadian misalignment increased appetite for energy-dense foods (all P < 0.05). Our results provide possible mechanisms for the endogenous circadian rhythm in hunger, as well as for the increased risk of obesity among shift workers.

Abstract Background The question of whether there is daytime time variation in diet-induced thermogenesis (DIT) has not been clearly answered. Moreover, it is unclear whether a potential diurnal variation in DIT is preserved during hypocaloric nutrition. Objective We hypothesized that DIT varies depending on the time of day and explored whether this physiological regulation is preserved after low-calorie compared with high-calorie intake. Design Under blinded conditions, 16 normal-weight men twice underwent a 3-day in-laboratory, randomized, crossover study. Volunteers consumed a predetermined low-calorie breakfast (11% of individual daily kilocalorie requirement) and high-calorie dinner (69%) in one condition and vice versa in the other. DIT was measured by indirect calorimetry, parameters of glucose metabolism were determined, and hunger and appetite for sweets were rated on a scale. Results Identical calorie consumption led to a 2.5-times higher DIT increase in the morning than in the evening after high-calorie and low-calorie meals (P < .001). The food-induced increase of blood glucose and insulin concentrations was diminished after breakfast compared with dinner (P < .001). Low-calorie breakfast increased feelings of hunger (P < .001), specifically appetite for sweets (P = .007), in the course of the day. Conclusions DIT is clearly higher in the morning than in the evening, irrespective of the consumed calorie amount; that is, this physiological rhythmicity is preserved during hypocaloric nutrition. Extensive breakfasting should therefore be preferred over large dinner meals to prevent obesity and high blood glucose peaks even under conditions of a hypocaloric diet.

Circadian (daily) regulation of metabolic pathways implies that food may be metabolized differentially over the daily cycle. To test that hypothesis, we monitored the metabolism of older subjects in a whole-room respiratory chamber over two separate 56-h sessions in a random crossover design. In one session, one of the 3 daily meals was presented as breakfast, whereas in the other session, a nutritionally equivalent meal was presented as a late-evening snack. The duration of the overnight fast was the same for both sessions. Whereas the two sessions did not differ in overall energy expenditure, the respiratory exchange ratio (RER) was different during sleep between the two sessions. Unexpectedly, this difference in RER due to daily meal timing was not due to daily differences in physical activity, sleep disruption, or core body temperature (CBT). Rather, we found that the daily timing of nutrient availability coupled with daily/circadian control of metabolism drives a switch in substrate preference such that the late-evening Snack Session resulted in significantly lower lipid oxidation (LO) compared to the Breakfast Session. Therefore, the timing of meals during the day/night cycle affects how ingested food is oxidized or stored in humans, with important implications for optimal eating habits.

Abstract Context Consuming calories later in the day is associated with obesity and metabolic syndrome. We hypothesized that eating a late dinner alters substrate metabolism during sleep in a manner that promotes obesity. Objective The objective of this work is to examine the impact of late dinner on nocturnal metabolism in healthy volunteers. Design and Setting This is a randomized crossover trial of late dinner (LD, 22:00) vs routine dinner (RD, 18:00), with a fixed sleep period (23:00-07:00) in a laboratory setting. Participants Participants comprised 20 healthy volunteers (10 male, 10 female), age 26.0 ± 0.6 years, body mass index 23.2 ± 0.7 kg/m2, accustomed to a bedtime between 22:00 and 01:00. Interventions An isocaloric macronutrient diet was administered on both visits. Dinner (35% daily kcal, 50% carbohydrate, 35% fat) with an oral lipid tracer ([2H31] palmitate, 15 mg/kg) was given at 18:00 with RD and 22:00 with LD. Main Outcome Measures Measurements included nocturnal and next-morning hourly plasma glucose, insulin, triglycerides, free fatty acids (FFAs), cortisol, dietary fatty acid oxidation, and overnight polysomnography. Results LD caused a 4-hour shift in the postprandial period, overlapping with the sleep phase. Independent of this shift, the postprandial period following LD was characterized by higher glucose, a triglyceride peak delay, and lower FFA and dietary fatty acid oxidation. LD did not affect sleep architecture, but increased plasma cortisol. These metabolic changes were most pronounced in habitual earlier sleepers determined by actigraphy monitoring. Conclusion LD induces nocturnal glucose intolerance, and reduces fatty acid oxidation and mobilization, particularly in earlier sleepers. These effects might promote obesity if they recur chronically.

We determined the effects of time-restricted feeding (TRF; 8 h/d) versus extended feeding (EXF; 15 h/d) on 24-h and postprandial metabolism and subjective opinions of TRF in men with overweight/obesity. In a randomized crossover design, 11 sedentary males (age 38 ± 5 y; BMI: 32.2 ± 2.0 kg/m2) completed two isoenergetic diet protocols for 5 days, consuming meals at 1000, 1300 and 1700 h (TRF) or 0700, 1400 and 2100 h (EXF). On Day 5, participants remained in the laboratory for 24 h, and blood samples were collected at hourly (0700–2300 h) then 2-hourly (2300–0700 h) intervals for concentrations of glucose, insulin and appetite/incretin hormones. Structured qualitative interviews were conducted following completion of both dietary conditions and investigated thematically. Total 24-h area under the curve (AUCtotal) [glucose] tended to be lower for TRF versus EXF (−5.5 ± 9.0 mmol/L/h, p = 0.09). Nocturnal glucose AUC was lower in TRF (−4.2 ± 5.8 mmol/L/h, p = 0.04), with no difference in waking glucose AUC or AUCtotal for [insulin]. Attitudes towards TRF were positive with improved feelings of well-being. Barriers to TRF were work schedules, family commitments and social events. Compared to extended feeding, short-term TRF improved nocturnal glycemic control and was positively perceived in men with overweight/obesity.

Aims/hypothesis Investigation of dietary therapy for diabetes has focused on meal size and composition; examination of the effects of meal sequence on postprandial glucose management is limited. The effects of fish or meat before rice on postprandial glucose excursion, gastric emptying and incretin secretions were investigated. Methods The experiment was a single centre, randomised controlled crossover, exploratory trial conducted in an outpatient ward of a private hospital in Osaka, Japan. Patients with type 2 diabetes ( n  = 12) and healthy volunteers ( n  = 10), with age 30–75 years, HbA 1c 9.0% (75 mmol/mol) or less, and BMI 35 kg/m 2 or less, were randomised evenly to two groups by use of stratified randomisation, and subjected to meal sequence tests on three separate mornings; days 1 and 2, rice before fish (RF) or fish before rice (FR) in a crossover fashion; and day 3, meat before rice (MR). Pre- and postprandial levels of glucose, insulin, C-peptide and glucagon as well as glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide were evaluated. Gastric emptying rate was determined by 13 C-acetate breath test involving measurement of 13 CO 2 in breath samples collected before and after ingestion of rice steamed with 13 C-labelled sodium acetate. Participants, people doing measurements or examinations, and people assessing the outcomes were not blinded to group assignment. Results FR and MR in comparison with RF ameliorated postprandial glucose excursion (AUC −15–240 min -glucose: type 2 diabetes, FR 2,326.6 ± 114.7 mmol/l × min, MR 2,257.0 ± 82.3 mmol/l × min, RF 2,475.6 ± 87.2 mmol/l × min [ p  < 0.05 for FR vs RF and MR vs RF]; healthy, FR 1,419.8 ± 72.3 mmol/l × min, MR 1,389.7 ± 69.4 mmol/l × min, RF 1,483.9 ± 72.8 mmol/l × min) and glucose variability (SD −15–240 min -glucose: type 2 diabetes, FR 1.94 ± 0.22 mmol/l, MR 1.68 ± 0.18 mmol/l, RF 2.77 ± 0.24 mmol/l [ p  < 0.05 for FR vs RF and MR vs RF]; healthy, FR 0.95 ± 0.21 mmol/l, MR 0.83 ± 0.16 mmol/l, RF 1.18 ± 0.27 mmol/l). FR and MR also enhanced GLP-1 secretion, MR more strongly than FR or RF (AUC −15–240 min -GLP-1: type 2 diabetes, FR 7,123.4 ± 376.3 pmol/l × min, MR 7,743.6 ± 801.4 pmol/l × min, RF 6,189.9 ± 581.3 pmol/l × min [ p  < 0.05 for FR vs RF and MR vs RF]; healthy, FR 3,977.3 ± 324.6 pmol/l × min, MR 4,897.7 ± 330.7 pmol/l × min, RF 3,747.5 ± 572.6 pmol/l × min [ p  < 0.05 for MR vs RF and MR vs FR]). FR and MR delayed gastric emptying (Time 50% : type 2 diabetes, FR 83.2 ± 7.2 min, MR 82.3 ± 6.4 min, RF 29.8 ± 3.9 min [ p  < 0.05 for FR vs RF and MR vs RF]; healthy, FR 66.3 ± 5.5 min, MR 74.4 ± 7.6 min, RF 32.4 ± 4.5 min [ p  < 0.05 for FR vs RF and MR vs RF]), which is associated with amelioration of postprandial glucose excursion (AUC −15–120 min -glucose: type 2 diabetes, r  = −0.746, p  < 0.05; healthy, r  = −0.433, p  < 0.05) and glucose variability (SD −15–240 min -glucose: type 2 diabetes, r  = −0.578, p  < 0.05; healthy, r  = −0.526, p  < 0.05), as well as with increasing GLP-1 (AUC −15–120 min -GLP-1: type 2 diabetes, r  = 0.437, p  < 0.05; healthy, r  = 0.300, p  = 0.107) and glucagon (AUC −15–120 min -glucagon: type 2 diabetes, r  = 0.399, p  < 0.05; healthy, r  = 0.471, p  < 0.05). The measured outcomes were comparable between the two randomised groups. Conclusions/interpretation Meal sequence can play a role in postprandial glucose control through both delayed gastric emptying and enhanced incretin secretion. Our findings provide clues for medical nutrition therapy to better prevent and manage type 2 diabetes. Trial registration: UMIN Clinical Trials Registry UMIN000017434. Funding: Japan Society for Promotion of Science, Japan Association for Diabetes Education and Care, and Japan Vascular Disease Research Foundation.

Breakfast omission is associated with obesity and CVD/diabetes, but the acute effects of extended morning fasting upon subsequent energy intake and metabolic/hormonal responses have received less attention. In a randomised cross-over design, thirty-five lean men ( n 14) and women ( n 21) extended their overnight fast or ingested a typical carbohydrate-rich breakfast in quantities relative to RMR (i.e. 1963 ( sd 238) kJ), before an ad libitum lunch 3 h later. Blood samples were obtained hourly throughout the day until 3 h post-lunch, with subjective appetite measures assessed. Lunch intake was greater following extended fasting (640 ( sd 1042) kJ, P < 0·01) but incompletely compensated for the omitted breakfast, with total intake lower than the breakfast trial (3887 ( sd 1326) v. 5213 ( sd 1590) kJ, P < 0·001). Systemic concentrations of peptide tyrosine–tyrosine and leptin were greater during the afternoon following breakfast (both P < 0·05) but neither acylated/total ghrelin concentrations were suppressed by the ad libitum lunch in the breakfast trial, remaining greater than the morning fasting trial throughout the afternoon (all P < 0·05). Insulin concentrations were greater during the afternoon in the morning fasting trial (all P < 0·01). There were no differences between trials in subjective appetite during the afternoon. In conclusion, morning fasting caused incomplete energy compensation at an ad libitum lunch. Breakfast increased some anorectic hormones during the afternoon but paradoxically abolished ghrelin suppression by the second meal. Extending morning fasting until lunch altered subsequent metabolic and hormonal responses but without greater appetite during the afternoon. The present study clarifies the impact of acute breakfast omission and adds novel insights into second-meal metabolism.

The aim of the current study was to investigate the effect of the glycemic index of post-exercise meals on sleep quality and quantity, and assess whether those changes could affect the next day’s exercise performance. Following a baseline/familiarization phase, 10 recreationally trained male volunteers (23.2 ± 1.8 years) underwent two double-blinded, randomized, counterbalanced crossover trials. In both trials, participants performed sprint interval training (SIT) in the evening. Post-exercise, participants consumed a meal with a high (HGI) or low (LGI) glycemic index. Sleep parameters were assessed by a full night polysomnography (PSG). The following morning, exercise performance was evaluated by the countermovement jump (CMJ) test, a visual reaction time (VRT) test and a 5-km cycling time trial (TT). Total sleep time (TST) and sleep efficiency were greater in the HGI trial compared to the LGI trial (p < 0.05), while sleep onset latency was shortened by four-fold (p < 0.05) and VRT decreased by 8.9% (p < 0.05) in the HGI trial compared to the LGI trial. The performance in both 5-km TT and CMJ did not differ between trials. A moderate to strong correlation was found between the difference in TST and the VRT between the two trials (p < 0.05). In conclusion, this is the first study to show that a high glycemic index meal, following a single spring interval training session, can improve both sleep duration and sleep efficiency, while reducing in parallel sleep onset latency. Those improvements in sleep did not affect jumping ability and aerobic endurance performance. In contrast, the visual reaction time performance increased proportionally to sleep improvements.

Background There is considerable uncertainty regarding the impact of tableware size on food consumption. Most existing studies have used small and unrepresentative samples and have not followed recommended procedures for randomised controlled trials, leading to increased risk of bias. In the first pre-registered study to date, we examined the impact on consumption of using larger versus smaller plates for self-served food. We also assessed impact on the underlying meal micro-structure, such as number of servings and eating rate, which has not previously been studied. Methods The setting was a purpose-built naturalistic eating behaviour laboratory. A general population sample of 134 adult participants (aged 18–61 years) was randomly allocated to one of two groups varying in the size of plate used for self-serving lunch: large or small. The primary outcome was amount of food energy (kcal) consumed during a meal. Additionally, we assessed impact on meal micro-structure, and examined potential modifying effects of executive function, socio-economic position, and sensitivity to perceptual cues. Results There was no clear evidence of a difference in consumption between the two groups: Cohen’s d  = 0.07 (95% CI [− 0.27, 0.41]), with participants in the large plate group consuming on average 19.2 (95% CI [− 76.5, 115.0]) more calories (3%) compared to the small plate group (large: mean ( SD ) = 644.1 (265.0) kcal, versus small: 624.9 (292.3) kcal). The difference between the groups was not modified by individual characteristics. There was no evidence of impact on meal micro-structure, with the exception of more food being left on the plate when larger plates were used. Conclusions This study suggests that previous meta-analyses of a low-quality body of evidence may have considerably overestimated the effects of plate size on consumption. However, the possibility of a clinically significant effect – in either direction – cannot be excluded. Well-conducted trials of tableware size in real-world field settings are now needed to determine whether changing the size of tableware has potential to contribute to efforts to reduce consumption at population-level. Trial registration The study protocol ( https://osf.io/e3dfh/ ) and data analysis plan ( https://osf.io/sh5u7/ ) were pre-registered on the Open Science Framework.

Background Smaller portions may help to reduce energy intake. However, there may be a limit to the magnitude of the portion size reduction that can be made before consumers respond by increasing intake of other food immediately or at later meals. We tested the theoretical prediction that reductions to portion size would result in a significant reduction to daily energy intake when the resulting portion was visually perceived as ‘normal’ in size, but that a reduction resulting in a ‘smaller than normal’ portion size would cause immediate or later additional eating. Methods Over three 5-day periods, daily energy intake was measured in a controlled laboratory study using a randomized crossover design ( N  = 30). The served portion size of the main meal component of lunch and dinner was manipulated in three conditions: ‘large-normal’ (747 kcal), ‘small-normal’ (543 kcal), and ‘smaller than normal’ (339 kcal). Perceived ‘normality’ of portion sizes was determined by two pilot studies. Ad libitum daily energy intake from all meals and snacks was measured. Results Daily energy intake in the ‘large-normal’ condition was 2543 kcals. Daily energy intake was significantly lower in the ‘small-normal’ portion size condition ( mean difference − 95 kcal/d, 95% CI [− 184, − 6], p =  .04); and was also significantly lower in the ‘smaller than normal’ than the ‘small-normal’ condition ( mean difference − 210 kcal/d, 95% CI [− 309, − 111], p  < .001). Contrary to predictions, there was no evidence that the degree of additional food consumption observed was greater when portions were reduced past the point of appearing normal in size. Conclusions Reductions to the portion size of main-meal foods resulted in significant decreases in daily energy intake. Additional food consumption did not offset this effect, even when portions were reduced to the point that they were no longer perceived as being normal in size. Trial registration Prospectively registered protocol and analysis plan: https://osf.io/natws/ ; retrospectively registered: https://clinicaltrials.gov/ct2/show/NCT03811210 .