Sanne Pm Verhoef

Effects of oligofructose on appetite profile, glucagon-like peptide 1 and peptide YY3-36 concentrations and energy intake

In rats, oligofructose has been shown to stimulate satiety hormone secretion, reduce energy intake and promote weight loss. The present study aimed to examine the effect of oligofructose supplementation on appetite profiles, satiety hormone concentrations and energy intake in human subjects. A total of thirty-one healthy subjects (ten men and twenty-one women) aged 28 (SEM 3) years with a BMI of 24·8 (SEM 0·3) kg/m(2) were included in a randomised double-blind, cross-over study. The subjects received 10 g oligofructose, 16 g oligofructose or 16 g placebo (maltodextrin) daily for 13 d, with a 2-week washout period between treatments. Appetite profile, active glucagon-like peptide 1 (GLP-1) and peptide YY3-36 (PYY) concentrations and energy intake were assessed on days 0 and 13 of the treatment period. Time × treatment interaction revealed a trend of reduction in energy intake over days 0-13 by oligofructose (P = 0·068). Energy intake was significantly reduced (11 %) over time on day 13 compared with day 0 with 16 g/d oligofructose (2801 (SEM 301) v. 3217 (SEM 320) kJ, P < 0·05). Moreover, energy intake was significantly lower with 16 g/d oligofructose compared with 10 g/d oligofructose on day 13 (2801 (SEM 301) v. 3177 (SEM 276) kJ, P < 0·05). Area under the curve (AUC) for GLP-1 on day 13 was significantly higher with 16 g/d oligofructose compared with 10 g/d oligofructose (45 (SEM 4) v. 41 (SEM 3) pmol/l × h, P < 0·05). In the morning until lunch, AUC(0-230 min) for PYY on day 13 was significantly higher with 16 g/d oligofructose compared with 10 g/d oligofructose and placebo (409 (SEM 35) v. 222 (SEM 19) and 211 (SEM 20) pg/ml × h, P < 0·01). In conclusion, 16 g/d and not 10 g/d oligofructose may be an effective dose to reduce energy intake, possibly supported by higher GLP-1 and PYY concentrations.

Weight loss, weight maintenance, and adaptive thermogenesis

BACKGROUND Diet-induced weight loss is accompanied by adaptive thermogenesis, ie, a disproportional or greater than expected reduction of resting metabolic rate (RMR). OBJECTIVE The aim of this study was to investigate whether adaptive thermogenesis is sustained during weight maintenance after weight loss. DESIGN Subjects were 22 men and 69 women [mean ± SD age: 40 ± 9 y; body mass index (BMI; in kg/m(2)): 31.9 ± 3.0]. They followed a very-low-energy diet for 8 wk, followed by a 44-wk period of weight maintenance. Body composition was assessed with a 3-compartment model based on body weight, total body water (deuterium dilution), and body volume. RMR was measured (RMRm) with a ventilated hood. In addition, RMR was predicted (RMRp) on the basis of the measured body composition: RMRp (MJ/d) = 0.024 × fat mass (kg) + 0.102 × fat-free mass (kg) + 0.85. Measurements took place before the diet and 8, 20, and 52 wk after the start of the diet. RESULTS The ratio of RMRm to RMRp decreased from 1.004 ± 0.077 before the diet to 0.963 ± 0.073 after the diet (P < 0.001), and the decrease was sustained after 20 wk (0.983 ± 0.063; P < 0.01) and 52 wk (0.984 ± 0.068; P < 0.01). RMRm/RMRp was correlated with the weight loss after 8 wk (P < 0.01), 20 wk (P < 0.05), and 52 wk (P < 0.05). CONCLUSION Weight loss results in adaptive thermogenesis, and there is no indication for a change in adaptive thermogenesis up to 1 y, when weight loss is maintained. This trial was registered at clinicaltrials.gov as NCT01015508.

Sleep duration, sleep quality and body weight: parallel developments.

The increase in obesity, including childhood obesity, has developed over the same time period as the progressive decrease in self-reported sleep duration. Since epidemiological studies showed an inverse relationship between short or disturbed sleep and obesity, the question arose, how sleep duration and sleep quality are associated with the development of obesity. In this review, the current literature on these topics has been evaluated. During puberty, changes in body mass index (BMI) are inversely correlated to changes in sleep duration. During adulthood, this relationship remains and at the same time unfavorable metabolic and neuro-endocrinological changes develop, that promote a positive energy balance, coinciding with sleep disturbance. Furthermore, during excessive weight loss BMI and fat mass decrease, in parallel, and related with an increase in sleep duration. In order to shed light on the association between sleep duration, sleep quality and obesity, until now it only has been shown that diet-induced body-weight loss and successive body-weight maintenance contribute to sleep improvement. It remains to be demonstrated whether body-weight management and body composition improve during an intervention concomitantly with spontaneous sleep improvement compared with the same intervention without spontaneous sleep improvement.

Weight loss–induced reduction in physical activity recovers during weight maintenance

BACKGROUND Weight loss due to a negative energy balance is considered to be accompanied by a decrease in physical activity. OBJECTIVE The aim of this study was to investigate whether a decrease in physical activity is sustained during weight maintenance. DESIGN Subjects were 20 men and 31 women [mean (±SD) age: 42 ± 8 y; BMI (in kg/m(2)): 31.4 ± 2.8]. Weight loss was achieved by an 8-wk very-low-energy diet period, followed by 44 wk of weight maintenance. Physical activity measures were total energy expenditure expressed as a multiple of sleeping metabolic rate (PALSMR) and resting metabolic rate (PALRMR), activity-induced energy expenditure divided by body weight (AEE/kg), and activity counts measured by a triaxial accelerometer. Measurements took place at 0, 8, and 52 wk. RESULTS Body mass decreased significantly during the diet period (10.5 ± 3.8%, P < 0.001), and this reduction was sustained after 52 wk (6.0 ± 5.1%, P < 0.001). PALSMR and PALRMR decreased from 1.81 ± 0.23 and 1.70 ± 0.22, respectively, before the diet to 1.69 ± 0.20 and 1.55 ± 0.19 after the diet (P < 0.001) and increased again after weight maintenance to 1.85 ± 0.27 and 1.71 ± 0.23, respectively, compared with 8-wk measurements (P < 0.001). AEE/kg decreased from 0.043 ± 0.015 MJ/kg at baseline to 0.037 ± 0.014 MJ/kg after the diet (P < 0.001) and was higher after 52 wk (0.044 ± 0.17 MJ/kg) compared with after 8 wk (P < 0.001). Activity counts decreased from 1.64 ± 0.37 megacounts/d at baseline to 1.54 ± 0.35 megacounts/d after the diet (P < 0.05) and were higher after 52 wk (1.73 ± 0.49 megacounts/d) compared with 8 wk (P < 0.01). CONCLUSION A weight loss-induced reduction in physical activity returns to baseline values when weight loss is maintained. This trial was registered at clinicaltrials.gov as NCT01015508.

Concomitant changes in sleep duration and body weight and body composition during weight loss and 3-mo weight maintenance

BACKGROUND An inverse relation between sleep duration and body mass index (BMI) has been shown. OBJECTIVE We assessed the relation between changes in sleep duration and changes in body weight and body composition during weight loss. DESIGN A total of 98 healthy subjects (25 men), aged 20-50 y and with BMI (in kg/m(2)) from 28 to 35, followed a 2-mo very-low-energy diet that was followed by a 10-mo period of weight maintenance. Body weight, body composition (measured by using deuterium dilution and air-displacement plethysmography), eating behavior (measured by using a 3-factor eating questionnaire), physical activity (measured by using the validated Baeckes questionnaire), and sleep (estimated by using a questionnaire with the Epworth Sleepiness Scale) were assessed before and immediately after weight loss and 3- and 10-mo follow-ups. RESULTS The average weight loss was 10% after 2 mo of dieting and 9% and 6% after 3- and 10-mo follow-ups, respectively. Daytime sleepiness and time to fall asleep decreased during weight loss. Short (≤7 h) and average (>7 to <9 h) sleepers increased their sleep duration, whereas sleep duration in long sleepers (≥9 h) did not change significantly during weight loss. This change in sleep duration was concomitantly negatively correlated with the change in BMI during weight loss and after the 3-mo follow-up and with the change in fat mass after the 3-mo follow-up. CONCLUSIONS Sleep duration benefits from weight loss or vice versa. Successful weight loss, loss of body fat, and 3-mo weight maintenance in short and average sleepers are underscored by an increase in sleep duration or vice versa. This trial was registered at clinicaltrials.gov as NCT01015508.

Genetic predisposition, dietary restraint and disinhibition in relation to short and long-term weight loss

BACKGROUND Interindividual differences in response to weight loss and maintenance thereafter are ascribed to genetic predisposition and behavioral changes. OBJECTIVE To examine whether body weight and short and long-term body weight loss were affected by candidate single nucleotide polymorphisms (SNPs) and changes in eating behavior or by an interaction between these genetic and behavioral factors. METHODS 150 healthy subjects (39 males, 111 females) aged 20-50 y with a BMI of 27-38 kg/m(2) followed a very low energy diet for 8-weeks, followed by a 3-month weight maintenance period. SNPs were selected from six candidate genes: ADRB2, FTO, MC4R, PPARG, PPARD, and PPARGC1A. Changes in eating behavior were determined with the Three Factor Eating Questionnaire. RESULTS A high genetic predisposition score was associated with a high body weight at baseline and more short-term weight loss. From the six selected obesity-related SNPs, FTO was associated with increased body weight at baseline, and the effect allele of PPARGC1A was positively associated with short-term weight loss, when assessed for each SNP separately. Long-term weight loss was associated with a larger increase in dietary restraint and larger decrease in disinhibition. CONCLUSION During long-term weight loss, genetic effects are dominated by changes in eating behavior.

Validating measures of free-living physical activity in overweight and obese subjects using an accelerometer

Background:Free-living physical activity can be assessed with an accelerometer to estimate energy expenditure but its validity in overweight and obese subjects remains unknown.Objective:Here, we validated published prediction equations derived in a lean population with the TracmorD accelerometer (DirectLife, Philips Consumer Lifestyle) in a population of overweight and obese. We also explored possible improvements of new equations specifically developed in overweight and obese subjects.Design:Subjects were 11 men and 25 women (age: 41±7 years; body mass index: 31.0±2.5 kg m−2). Physical activity was monitored under free-living conditions with TracmorD, whereas total energy expenditure was measured simultaneously with doubly-labeled water. Physical activity level (PAL) and activity energy expenditure (AEE) were calculated from total energy expenditure and sleeping metabolic rate.Results:The published prediction equation explained 47% of the variance of the measured PAL (P<0.001). PAL estimates were unbiased (errors (bias±95% confidence interval): −0.02±0.28). Measured and predicted AEE/body weight were highly correlated (r2=58%, P<0.001); however, the prediction model showed a significant bias of 8 kJ kg−1 per day or 17.4% of the average AEE/body weight. The new prediction equation of AEE/body weight developed in the obese group showed no bias.Conclusions:In conclusion, equations derived with the TracmorD allow valid assessment of PAL and AEE/body weight in overweight and obese subjects. There is evidence that estimates of AEE/body weight could be affected by gender. Equations specifically developed in overweight and obese can improve the accuracy of predictions of AEE/body weight.

Leptin and energy restriction induced adaptation in energy expenditure

BACKGROUND Diet-induced weight loss is accompanied by adaptive thermogenesis, i.e. a disproportional reduction of resting energy expenditure (REE) a decrease in physical activity and increased movement economy. OBJECTIVE To determine if energy restriction induced adaptive thermogenesis and adaptations in physical activity are related to changes in leptin concentrations. METHODS Eighty-two healthy subjects (23 men, 59 women), mean ± SD age 41 ± 8 years and BMI 31.9 ± 3.0 kg/m(2), followed a very low energy diet for 8 weeks with measurements before and after the diet. Leptin concentrations were determined from fasting blood plasma. Body composition was assessed with a three-compartment model based on body weight, total body water (deuterium dilution) and body volume (BodPod). REE was measured (REEm) with a ventilated hood and predicted (REEp) from measured body composition. Adaptive thermogenesis was calculated as REEm/REEp. Parameters for the amount of physical activity were total energy expenditure expressed as a multiple of REEm (PAL), activity-induced energy expenditure divided by body weight (AEE/kg) and activity counts measured by a tri-axial accelerometer. Movement economy was calculated as AEE/kg (MJ/kg/d) divided by activity counts (Mcounts/d). RESULTS Subjects lost on average 10.7 ± 4.1% body weight (P<0.001). Leptin decreased from 26.9 ± 14.3 before to 13.9 ± 11.3 μg/l after the diet (P<0.001). REEm/REEp after the diet (0.963 ± 0.08) was related to changes in leptin levels (R(2)=0.06; P<0.05). There was no significant correlation between changes in leptin concentrations and changes in amount of physical activity. Movement economy changed from 0.036 ± 0.011 J/kg/count to 0.028 ± 0.010 J/kg/count and was correlated to the changes in leptin concentrations (R(2)=0.07; P<0.05). CONCLUSION During energy restriction, the decrease in leptin explains part of the variation in adaptive thermogenesis. Changes in leptin are not related to the amount of physical activity but could partly explain the increased movement economy.

Physiological Response of Adipocytes to Weight Loss and Maintenance

Background Metabolic processes in adipose tissue are dysregulated in obese subjects and, in response to weight loss, either normalize or change in favor of weight regain. Objective To determine changes in adipocyte glucose and fatty acid metabolism in relation to changes in adipocyte size during weight loss and maintenance. Methods Twenty-eight healthy subjects (12 males), age 20–50 y, and BMI 28–35 kg/m2, followed a very low energy diet for 2 months, followed by a 10-month period of weight maintenance. Body weight, body composition (deuterium dilution and BodPod), protein levels (Western blot) and adipocyte size were assessed prior to and after weight loss and after the 10-month follow-up. Results A 10% weight loss resulted in a 16% decrease in adipocyte size. A marker for glycolysis decreased (AldoC) during weight loss in association with adipocyte shrinking, and remained decreased during follow-up in association with weight maintenance. A marker for fatty acid transport increased (FABP4) during weight loss and remained increased during follow-up. Markers for mitochondrial beta-oxidation (HADHsc) and lipolysis (ATGL) were only increased after the 10-month follow-up. During weight loss HADHsc and ATGL were coordinately regulated, which became weaker during follow-up due to adipocyte size-related changes in HADHsc expression. AldoC was the major denominator of adipocyte size and body weight, whereas changes in ATGL during weight loss contributed to body weight during follow-up. Upregulation of ATGL and HADHsc occured in the absence of a negative energy balance and was triggered by adipocyte shrinkage or indicated preadipocyte differentiation. Conclusion Markers for adipocyte glucose and fatty acid metabolism are changed in response to weight loss in line with normalization from a dysregulated obese status to an improved metabolic status. Trial Registration ClinicalTrials.gov NCT01015508

No effects of Korean pine nut triacylglycerol on satiety and energy intake

BackgroundTriacylglycerols (TAG) have been shown to have potential appetite suppressing effects. This study examined the effects of 3 g and 6 g Korean pine nut triacylglycerols (PinnoThin) on appetite and energy intake.Methods130 g Isoenergetic yogurt containing either placebo (milk fat) or PinnoThin TAG was consumed as a breakfast, after an overnight fast, in a double blind randomized crossover design. Appetite profile ratings were determined by visual analogue scale at regular intervals for a period of 4 h after the breakfast. In phase I, 6 g PinnoThin TAG and placebo was tested in thirty-three healthy women (mean ± SD, BMI 26.4 ± 3.8 kg/m2; age 28 ± 10 y) to determine the appetite suppressing effect in time. In phase II, an additional dose of 3 g PinnoThin TAG, as well as 6 g PinnoThin TAG and placebo, was tested in thirty-four women (BMI 25.8 ± 2.9 kg/m2; age 25 ± 9 y) to determine energy intake from an ad libitum lunch offered at 210 min after the breakfast, at which maximal differences in appetite profile ratings were present in phase I.ResultsArea under the curve of appetite profile ratings was not significantly different between the conditions. Energy intake was 9.5% lower after 6 g PinnoThin TAG compared with 3 g PinnoThin TAG, but there was no significant difference with the placebo.ConclusionA dosage of 6 g PinnoThin TAG is not sufficient to suppress appetite and energy intake.Trial registrationClinical Trials NCT01034605