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 mug/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

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 20-50y with a BMI of 27-38kg/m2 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

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/m2) 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 Baecke's questionnaire), and sleep (estimate 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 to /=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

A low glycaemic index diet incorporating isomaltulose is associated with lower glycaemic response and variability, and promotes fat oxidation in asians

10.3390/nu9050473Nutrients9547

Estimation of basal metabolic rate in Chinese: Are the current prediction equations applicable?

10.1186/s12937-016-0197-2Nutrition Journal15

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/m(2), 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