Effects of sleep manipulation on markers of insulin sensitivity: A systematic review and meta-analysis of randomized controlled trials.

Poor sleep habits are associated with increased risk of developing type 2 diabetes. In this review and meta-analysis, we aimed to investigate the effects of sleep manipulation on markers of insulin sensitivity from randomized, controlled trials. Sleep manipulation was defined as reduction in sleep duration, sleep quality, and circadian misalignment. A systematic literature search was conducted in three databases and resulted in 35 eligible articles. The studies included interventions on sleep restriction (26 studies), slow wave sleep suppression and rapid eye movement sleep disturbance (2 studies), sleep fragmentation (2 studies), and circadian misalignment (5 studies). The meta-analysis included 21 sleep restriction studies. Sleep restriction reduced insulin sensitivity assessed by oral or intravenous glucose tolerance test and homeostatic model assessment of insulin resistance. Whole-body insulin sensitivity was also reduced after short sleep when measured by the hyperinsulinemic euglycemic clamp, but peripheral insulin sensitivity was not affected. In addition, circadian misalignment and slow wave sleep suppression negatively affected insulin sensitivity, while rapid eye movement sleep disturbance and sleep fragmentation had no effect. In summary, the studies indicated that duration, quality, and timing of sleep are essential for metabolic function and risk of type 2 diabetes.

Salmon in Combination with High Glycemic Index Carbohydrates Increases Diet-Induced Thermogenesis Compared with Salmon with Low Glycemic Index Carbohydrates⁻An Acute Randomized Cross-Over Meal Test Study.

The study investigated the acute effects of meals containing either salmon or veal in combination with carbohydrates with high or low glycemic index (GI) on diet-induced thermogenesis (DIT) (primary endpoint), appetite sensations, and energy intake (EI). Twenty-five overweight men and women ingested four iso-caloric test meals: salmon with mashed potatoes (high GI) (SM), salmon with wholegrain pasta (low GI) (SP), veal with mashed potatoes (VM) and veal with wholegrain pasta (VP). Energy expenditure was measured in the fasting state and six times postprandially for 25 min with 5-min breaks between each measurement. Appetite sensations were measured every 30 min. Blood samples, from arterialized venous blood, were drawn every 20 min until an ad libitum buffet-style lunch was served 3.5 h later. DIT was 40% higher after the SM meal compared to the SP meal (p = 0.002). Prospective food consumption was lower after the SM meal compared with the VP meal (p = 0.01). There were no differences in satiety, hunger, fullness, or ad libitum EI between the test meals (all p > 0.05). In conclusion, salmon with high GI carbohydrates increased DIT compared to salmon with low GI carbohydrates. This indicates that DIT is sensitive to the GI of the carbohydrates after intake of salmon but not veal.

Meals based on cod or veal in combination with high or low glycemic index carbohydrates did not affect diet-induced thermogenesis, appetite sensations, or subsequent energy intake differently.

The objective of this study was to investigate the acute effects of meals containing protein from either cod or veal in combination with high or low glycemic index (GI) carbohydrates, on diet-induced thermogenesis (DIT) (primary endpoint), appetite, energy intake (EI), as well as postpranidal ghrelin, glucose, and insulin responses. Twenty-three overweight men and women (mean ±â€¯SD age: 30.0 ±â€¯7.6 y, BMI: 27.2 ±â€¯1.4 kg/m2) consumed 4 test meals: cod with mashed potatoes (high GI carbohydrate), cod with wholegrain pasta (low GI carbohydrate), veal with mashed potatoes, and veal with wholegrain pasta (∼2010 kJ, ∼25.5 E% protein, ∼41.0 E% carbohydrate, ∼33.5 E% fat). Energy expenditure was measured at baseline and six times postprandially, each lasting 25 min. Additionally, appetite sensations were measured every half hour. Arterialized venous blood samples were drawn every 20 min until an ad libitum buffet-style lunch was served 3.5 h later. DIT did not differ between test meals (P > 0.05), and there were no differences in appetite sensations or ad libitum EI (all, P > 0.05). Meal-time interactions were found for glucose and insulin (P = 0.04 and P < 0.001). Pairwise comparisons revealed that glucose and insulin peaks were higher after the meals with high GI carbohydrates. No differences were found between meals with cod or veal in combination with carbohydrates with low or high GI on DIT, appetite sensations, or EI in overweight men and women. However, as expected meals with high GI carbohydrates resulted in higher glucose and insulin responses compared to meals with low GI carbohydrates regardless of protein source.

Protein from Meat or Vegetable Sources in Meals Matched for Fiber Content has Similar Effects on Subjective Appetite Sensations and Energy Intake-A Randomized Acute Cross-Over Meal Test Study.

Higher-protein meals decrease hunger and increase satiety compared to lower-protein meals. However, no consensus exists about the different effects of animal and vegetable proteins on appetite. We investigated how a meal based on vegetable protein (fava beans/split peas) affected ad libitum energy intake and appetite sensations, compared to macronutrient-balanced, iso-caloric meals based on animal protein (veal/pork or eggs). Thirty-five healthy men were enrolled in this acute cross-over study. On each test day, participants were presented with one of four test meals (~3550 kilojoules (kJ) 19% of energy from protein), based on fava beans/split peas (28.5 g fiber), pork/veal or eggs supplemented with pea fiber to control for fiber content (28.5 g fiber), or eggs without supplementation of fiber (6.0 g fiber). Subjective appetite sensations were recorded at baseline and every half hour until the ad libitum meal three hours later. There were no differences in ad libitum energy intake across test meals (p > 0.05). Further, no differences were found across meals for hunger, satiety, fullness, prospective food consumption, or composite appetite score (all p > 0.05). Iso-caloric, macronutrient-balanced, fiber-matched meals based on vegetable protein (fava beans/split peas) or animal protein (veal/pork or eggs) had similar effects on ad libitum energy intake and appetite sensations.

Acute Sleep Restriction Reduces Insulin Sensitivity in Adolescent Boys.

BACKGROUND: Short sleep duration has been linked to impaired glucose metabolism in many experimental studies. Moreover, studies have reported indications of an increased metabolic stress following sleep restriction. OBJECTIVE: We aimed to investigate the effects of partial sleep deprivation on markers of glucose metabolism. Additionally, we aimed to investigate if short sleep duration induces a state of endocrine stress. DESIGN: A randomized crossover design, with 2 experimental conditions: 3 consecutive nights of short sleep (SS, 4 h/night) and long sleep (LS, 9 h/night) duration. SUBJECTS AND MEASUREMENTS: In 21 healthy, normal-weight male adolescents (mean ± SD age: 16.8 ± 1.3 y) we measured pre- and post-prandial glucose, insulin, C-peptide, and glucagon concentrations. Furthermore, we measured fasting cortisol, 24-h catecholamines, and sympathovagal balance. RESULTS: Fasting insulin was 59% higher (P = 0.001) in the SS than the LS condition as was both fasting (24%, P < 0.001) and post-prandial (11%, P = 0.018) C-peptide. Pre- and post-prandial glucose and glucagon were unchanged between conditions. The homeostasis model assessment of insulin resistance (HOMA-IR) index was 65% higher (P = 0.002) and the Matsuda index was 28% lower (P = 0.007) in the SS condition compared to the LS condition. The awakening cortisol response and 24-h norepinephrine were not affected by sleep duration, whereas 24-h epinephrine was 24% lower (P = 0.013) in the SS condition. Neither daytime nor 24-h sympathovagal balance differed between sleep conditions. Short wave sleep was preserved in the SS condition. CONCLUSION: Short-term sleep restriction is associated with decreased insulin sensitivity in healthy normal-weight adolescent boys. There were no indications of endocrine stress beyond this. CITATION: Klingenberg L; Chaput JP; Holmbäck U; Visby T; Jennum P; Nikolic M; Astrup A; Sjödin A. Acute Sleep Restriction Reduces Insulin Sensitivity in Adolescent Boys. SLEEP 2013;36(7):1085-1090.

Sleep restriction is not associated with a positive energy balance in adolescent boys.

BACKGROUND: A short sleep (SS) duration has been linked to obesity in observational studies. However, experimental evidence of the potential mechanisms of sleep restriction on energy balance is conflicting and, to our knowledge, nonexistent in adolescents. OBJECTIVE: We investigated the effects of 3 consecutive nights of partial sleep deprivation on components of energy balance. DESIGN: In a randomized, crossover design, 21 healthy, normal-weight male adolescents (mean ± SD age: 16.8 ± 1.3 y) completed the following 2 experimental conditions, each for 3 consecutive nights: an SS (4 h/night) and a long sleep (LS; 9 h/night) duration. Endpoints were 24-h energy expenditure (EE), spontaneous physical activity (SPA), postintervention diet-induced thermogenesis (DIT), appetite sensations, ad libitum energy intake (EI), and profiles of plasma ghrelin and leptin. RESULTS: The 24-h EE on day 3 was 370 ± 496 kJ higher in the SS condition than in the LS condition (P = 0.003). This difference in EE was explained by prolonged wakefulness in the SS condition and a 19% higher SPA (P = 0.003). In a postintervention breakfast-meal challenge, there was a 0.19-kJ/min smaller incremental AUC in DIT over 4 h in the SS condition than in the LS condition (P = 0.012) with no time × condition effect (P = 0.29). Subjects consumed 13% less energy in the ad libitum meal in the SS condition (P = 0.031), with a concomitant decreased motivation to eat. Concentrations of ghrelin and leptin remained unchanged with sleep restriction. CONCLUSION: Short-term sleep restriction in male adolescents is associated with a small negative energy balance driven by increased EE from prolonged wakefulness and a concomitant decreased EI and motivation to eat. This trial was registered at clinicaltrials.gov as NCT01198431.

Video game playing increases food intake in adolescents: a randomized crossover study.

BACKGROUND: Video game playing has been linked to obesity in many observational studies. However, the influence of this sedentary activity on food intake is unknown. OBJECTIVE: The objective was to examine the acute effects of sedentary video game play on various components of energy balance. DESIGN: With the use of a randomized crossover design, 22 healthy, normal-weight, male adolescents (mean ± SD age: 16.7 ± 1.1 y) completed two 1-h experimental conditions, namely video game play and rest in a sitting position, followed by an ad libitum lunch. The endpoints were spontaneous food intake, energy expenditure, stress markers, appetite sensations, and profiles of appetite-related hormones. RESULTS: Heart rate, systolic and diastolic blood pressures, sympathetic tone, and mental workload were significantly higher during the video game play condition than during the resting condition (P < 0.05). Although energy expenditure was significantly higher during video game play than during rest (mean increase over resting: 89 kJ; P < 0.01), ad libitum energy intake after video game play exceeded that measured after rest by 335 kJ (P < 0.05). A daily energy surplus of 682 kJ (163 kcal) over resting (P < 0.01) was observed in the video game play condition. The increase in food intake associated with video game play was observed without increased sensations of hunger and was not compensated for during the rest of the day. Finally, the profiles of glucose, insulin, cortisol, and ghrelin did not suggest an up-regulation of appetite during the video game play condition. CONCLUSION: A single session of video game play in healthy male adolescents is associated with an increased food intake, regardless of appetite sensations. The trial was registered at clinicaltrials.gov as NCT01013246.

Physical activity plays an important role in body weight regulation.

Emerging literature highlights the need to incorporate physical activity into every strategy intended to prevent weight gain as well as to maintain weight loss over time. Furthermore, physical activity should be part of any plan to lose weight. The stimulus of exercise provides valuable metabolic adaptations that improve energy and macronutrient balance regulation. A tight coupling between energy intake and energy expenditure has been documented at high levels of physical exercise, suggesting that exercise may improve appetite control. The regular practice of physical activity has also been reported to reduce the risk of stress-induced weight gain. A more personalized approach is recommended when planning exercise programs in a clinical weight loss setting in order to limit the compensatory changes associated to exercise-induced weight loss. With modern environment promoting overeating and sedentary behavior, there is an urgent need for a concerted action including legislative measures to promote healthy active living in order to curb the current epidemic of chronic diseases.

Do all sedentary activities lead to weight gain: sleep does not.

PURPOSE OF REVIEW: To discuss the benefits of having a good night's sleep for body weight stability. RECENT FINDINGS: Experimental studies have shown that short-term partial sleep restriction decreases glucose tolerance, increases sympathetic tone, elevates cortisol concentrations, decreases the satiety hormone leptin, increases the appetite-stimulating hormone ghrelin, and increases hunger and appetite. Short sleep duration might increase the risk of becoming obese, because it does not allow the recovery of a hormonal profile facilitating appetite control. Lack of sleep could also lead to weight gain and obesity by increasing the time available for eating and by making the maintenance of a healthy lifestyle more difficult. Furthermore, the increased fatigue and tiredness associated with sleeping too little could lessen one's resolve to follow exercise regimens. SUMMARY: Short sleep duration appears to be a novel and independent risk factor for obesity. With the growing prevalence of chronic sleep restriction, any causal association between reduced sleep and obesity would have substantial importance from a public health standpoint. Future research is needed to determine whether sleep extension in sleep-deprived obese individuals will influence appetite control and/or reduce the amount of body fat.