867 resultados para high fat meal
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Objective: to assess the between and within-device reproducibility, as well as within-day variability of body fat measurements. Methods: body fat percentage (%BF) was measured twice on seventeen female students aged between 18 and 20 with a body mass index of 21.9 22.6 kg/m2 (mean SD) using seven bipolar bioelectrical impedance devices (BF-306) according to the manufacturer's recommendations. Each student was also measured each hour between 7:00 and 22:00. Statistical analysis was conducted using a general linear model for repeated measurements. Results: the correlation between first and second measurements was very high (Pearson r between 0.985 and 1.000, p<0.001), as well as the correlation between devices (Pearson r between 0.986 and 0.999, all p<0.001). Repeated measurements analysis showed no differences were between devices (F test=0.83, p=0.59) or readings (first vs. second: F test=0.12, p=0.74). Conversely, significant differences were found between assessment periods throughout the day, measurements made in the morning being lower than those made in the afternoon. Assuming an overall daily average of 100 (based on all measurements), the values were 95.8 3.2 (mean SD) at 8:00 versus 101.3 3.0 at 20:00, corresponding to a mean change of 2.2 1.1 in %BF (F test for repeated values=6.58, p<0.001). Conclusions: the between and within-device reproducibility for measuring body fat is high, enabling the use of multiple devices in a single study. Conversely, small but significant changes in body fat measurements occur during the day, urging body fat measurements to be performed at fixed times.
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OBJECTIVE: Low and high body mass index (BMI) values have been shown to increase health risks and mortality and result in variations in fat-free mass (FFM) and body fat mass (BF). Currently, there are no published ranges for a fat-free mass index (FFMI; kg/m(2)), a body fat mass index (BFMI; kg/m(2)), and percentage of body fat (%BF). The purpose of this population study was to determine predicted FFMI and BFMI values in subjects with low, normal, overweight, and obese BMI. METHODS: FFM and BF were determined in 2986 healthy white men and 2649 white women, age 15 to 98 y, by a previously validated 50-kHz bioelectrical impedance analysis equation. FFMI, BFMI, and %BF were calculated. RESULTS: FFMI values were 16.7 to 19.8 kg/m(2) for men and 14.6 to 16.8 kg/m(2) for women within the normal BMI ranges. BFMI values were 1.8 to 5.2 kg/m(2) for men and 3.9 to 8.2 kg/m(2) for women within the normal BMI ranges. BFMI values were 8.3 and 11.8 kg/m(2) in men and women, respectively, for obese BMI (>30 kg/m(2)). Normal ranges for %BF were 13.4 to 21.7 and 24.6 to 33.2 for men and women, respectively. CONCLUSION: BMI alone cannot provide information about the respective contribution of FFM or fat mass to body weight. This study presents FFMI and BFMI values that correspond to low, normal, overweight, and obese BMIs. FFMI and BFMI provide information about body compartments, regardless of height.
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Resting metabolic rate (RMR) and the thermic effect of a meal (TEM) were measured in a group of 26 prepubertal children divided into three groups: (1) children with both parents obese (n = 8, group OB2); (2) children with no obese parents and without familial history of obesity (n = 8, OB0); and (3) normal body weight children (n = 10, C). Average RMR was similar in OB2 and OB0 children (4785 +/- 274 kJ/day vs 5091 +/- 543 kJ/day), but higher (P < 0.05) than in controls (4519 +/- 322 kJ/day). Adjusted for fat-free mass (FFM) mean RMRs were comparable in the three groups of children (4891 +/- 451 kJ/day vs 5031 +/- 451 kJ/day vs 4686 +/- 451 kJ/day in OB2, OB0, and C, respectively). The thermic response to the mixed meal was similar in OB2, OB0 and C groups. The TEM calculated as the percentage of RMR was lower (P < 0.05) in obese than in control children: 10.2% +/- 3.1% vs 10.9% +/- 4.3% vs 14.0% +/- 4.3% in OB2, OB0, and C, respectively. The similar RMR as absolute value as well as adjusted for FFM, and the comparable thermic effect of food in the obese children with or without familial history of obesity, failed to support the view that family history of obesity can greatly influence the RMR and the TEM of the obese child with obese parents.
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Introduction An impaired ability to oxidize fat may be a factor in the obesity's aetiology (3). Moreover, the exercise intensity (Fatmax) eliciting the maximal fat oxidation rate (MFO) was lower in obese (O) compared with lean (L) individuals (4). However, difference in fat oxidation rate (FOR) during exercise between O and L remains equivocal and little is known about FORs during high intensities (>60% ) in O compared with L. This study aimed to characterize fat oxidation kinetics over a large range of intensities in L and O. Methods 12 healthy L [body mass index (BMI): 22.8±0.4] and 16 healthy O men (BMI: 38.9±1.4) performed submaximal incremental test (Incr) to determine whole-body fat oxidation kinetics using indirect calorimetry. After a 15-min resting period (Rest) and 10-min warm-up at 20% of maximal power output (MPO, determined by a maximal incremental test), the power output was increased by 7.5% MPO every 6-min until respiratory exchange ratio reached 1.0. Venous lactate and glucose and plasma concentration of epinephrine (E), norepinephrine (NE), insulin and non-esterified fatty acid (NEFA) were assessed at each step. A mathematical model (SIN) (1), including three variables (dilatation, symmetry, translation), was used to characterize fat oxidation (normalized by fat-free mass) kinetics and to determine Fatmax and MFO. Results FOR at Rest and MFO were not significantly different between groups (p≥0.1). FORs were similar from 20-60% (p≥0.1) and significantly lower from 65-85% in O than in L (p≤0.04). Fatmax was significantly lower in O than in L (46.5±2.5 vs 56.7±1.9 % respectively; p=0.005). Fat oxidation kinetics was characterized by similar translation (p=0.2), significantly lower dilatation (p=0.001) and tended to a left-shift symmetry in O compared with L (p=0.09). Plasma E, insulin and NEFA were significantly higher in L compared to O (p≤0.04). There were no significant differences in glucose, lactate and plasma NE between groups (p≥0.2). Conclusion The study showed that O presented a lower Fatmax and a lower reliance on fat oxidation at high, but not at moderate, intensities. This may be linked to a: i) higher levels of insulin and lower E concentrations in O, which may induce blunted lipolysis; ii) higher percentage of type II and a lower percentage of type I fibres (5), and iii) decreased mitochondrial content (2), which may reduce FORs at high intensities and Fatmax. These findings may have implications for an appropriate exercise intensity prescription for optimize fat oxidation in O. References 1. Cheneviere et al. Med Sci Sports Exerc. 2009 2. Holloway et al. Am J Clin Nutr. 2009 3. Kelley et al. Am J Physiol. 1999 4. Perez-Martin et al. Diabetes Metab. 2001 5. Tanner et al. Am J Physiol Endocrinol Metab. 2002
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BACKGROUND: Hypertension, hypercholesterolemia, obesity and smoking are highly prevalent among patients with familial premature coronary artery disease (FP-CAD). Whether these risk factors equally affect other family members remains unknown. METHODS: We examined 222 FP-CAD patients, 158 unaffected sibs, 197 offspring and 94 spouses in 108 FP-CAD families (> or = 2 sibs having survived CAD diagnosed before age 51 (M)/56 (F)), and compared them to population controls. RESULTS: Unaffected sibs had a higher prevalence of hypertension (49% versus 24%, p<0.001), hypercholesterolemia (47% versus 34%, p=0.002), abdominal obesity (35% versus 24%, p=0.006) and smoking (39% versus 24%, p=0.001) than population controls. Offspring had a higher prevalence of hypertension (females), hypercholesterolemia and abdominal obesity than population controls. No difference was observed between spouses and controls. Compared to unaffected sibs, FP-CAD affected sibs had a similar risk factor profile, except for smoking, which was more prevalent (76% versus 39%, p=0.008). CONCLUSIONS: Hypertension, obesity and hypercholesterolemia are highly prevalent among first-degree relatives, but not spouses, of patients with FP-CAD. These persons deserve special medical attention due to their familial/genetic susceptibility to atherogenic metabolic abnormalities. In these families, smoking may be the trigger for FP-CAD.
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Introduction An impaired ability to oxidize fat may be a factor in the obesity's aetiology (3). Moreover, the exercise intensity (Fatmax) eliciting the maximal fat oxidation rate (MFO) was lower in obese (O) compared with lean (L) individuals (4). However, difference in fat oxidation rate (FOR) during exercise between O and L remains equivocal and little is known about FORs during high intensities (>60% ) in O compared with L. This study aimed to characterize fat oxidation kinetics over a large range of intensities in L and O. Methods 12 healthy L [body mass index (BMI): 22.8±0.4] and 16 healthy O men (BMI: 38.9±1.4) performed submaximal incremental test (Incr) to determine whole-body fat oxidation kinetics using indirect calorimetry. After a 15-min resting period (Rest) and 10-min warm-up at 20% of maximal power output (MPO, determined by a maximal incremental test), the power output was increased by 7.5% MPO every 6-min until respiratory exchange ratio reached 1.0. Venous lactate and glucose and plasma concentration of epinephrine (E), norepinephrine (NE), insulin and non-esterified fatty acid (NEFA) were assessed at each step. A mathematical model (SIN) (1), including three variables (dilatation, symmetry, translation), was used to characterize fat oxidation (normalized by fat-free mass) kinetics and to determine Fatmax and MFO. Results FOR at Rest and MFO were not significantly different between groups (p≥0.1). FORs were similar from 20-60% (p≥0.1) and significantly lower from 65-85% in O than in L (p≤0.04). Fatmax was significantly lower in O than in L (46.5±2.5 vs 56.7±1.9 % respectively; p=0.005). Fat oxidation kinetics was characterized by similar translation (p=0.2), significantly lower dilatation (p=0.001) and tended to a left-shift symmetry in O compared with L (p=0.09). Plasma E, insulin and NEFA were significantly higher in L compared to O (p≤0.04). There were no significant differences in glucose, lactate and plasma NE between groups (p≥0.2). Conclusion The study showed that O presented a lower Fatmax and a lower reliance on fat oxidation at high, but not at moderate, intensities. This may be linked to a: i) higher levels of insulin and lower E concentrations in O, which may induce blunted lipolysis; ii) higher percentage of type II and a lower percentage of type I fibres (5), and iii) decreased mitochondrial content (2), which may reduce FORs at high intensities and Fatmax. These findings may have implications for an appropriate exercise intensity prescription for optimize fat oxidation in O. References 1. Cheneviere et al. Med Sci Sports Exerc. 2009 2. Holloway et al. Am J Clin Nutr. 2009 3. Kelley et al. Am J Physiol. 1999 4. Perez-Martin et al. Diabetes Metab. 2001 5. Tanner et al. Am J Physiol Endocrinol Metab. 2002
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Body mass index (BMI) is related with cardiorespiratory fitness (CRF), but less is known regarding the combined relationships between BMI and body fat (BF) on CRF. Cross-sectional study included 2361 girls and 2328 boys aged 10–18 years living in the area of Lisbon, Portugal. BMI was calculated by measuring height and weight, and obesity was assessed by international criteria. BF was assessed by bioimpedance. CRF was assessed by the 20-m shuttle run and the participants were classified as normal-to-high or low-CRF level according to Fitness gram criterion-referenced standards. The prevalence of low CRF was 47 and 39% in girls and boys, respectively. The corresponding values for the prevalence of obesity were 4.8 and 5.6% (not significant) and of excess BF of 12.1 and 25.1% (P <0.001), respectively. In both sexes, BMI and BF were inversely related with CRF: r = – 0.53 and – 0.45 for BMI and % BF, respectively, in boys and the corresponding values in girls were – 0.50 and – 0.33 (all P <0.01). When compared with a participant with normal BMI and BF, the odds ratios (95% confidence interval) for low CRF were 1.94 (1.46–2.58) for a participant with normal BMI and high BF, and 6.19 (5.02–7.63) for a participant with high BMI and high BF. The prevalence of low-CRF levels is high in Portuguese youths. BF negatively influences CRF levels among children/adolescents with normal BMI.
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ABSTRACT Fat oxidation kinetics: effect of exercise. During graded exercise, absolute whole body fat oxidation rates increase from low to moderate intensities, and then markedly decline at high intensities, implying an exercise intensity (Fatmax) at which the fat oxidation rate is maximal (MFO). The main aim of the present work was to examine the effect of exercise on whole body fat oxidation kinetics. For this purpose, a sinusoidal mathematical model (SIN) has been developped in the first study to provide an accurate description of the shape of fat oxidation kinetics during graded exercise, represented as a function of exercise intensity, and to determine Fatmax and MFO. The SIN model incorporates three independent variables (i.e., dilatation, symmetry, and translation) that correspond to main expected modulations of the basic fat oxidation curve because of factors such as mode of exercise or training status. The results of study 1 showed that the SIN model was a valuable tool to determine Fatmax and MFO, and to precisely characterize and quantify the different shape of fat oxidation kinetics through its three variables. The effectiveness of the SIN model to detect differences in fat oxidation kinetics induced by a specific factor was then confirmed in the second study, which quantitatively described and compared fat oxidation kinetics in two different popular modes of exercise: running and cycling. It was found that the mean fat oxidation kinetics during running was characterized by a greater dilatation and a rightward asymmetry compared with the symmetric parabolic curve in cycling. In the two subsequent studies, the effect of a prior endurance exercise of different intensities and durations on whole body fat oxidation kinetics was examined. Study 3 determined the impact of a 1-h continuous exercise bout at an exercise intensity corresponding to Fatmax on fat oxidation kinetics during a subsequent graded test, while study 4 investigated the effect of an exercise leading to a more pronounced muscle glycogen depletion. The results of these two latter studies showed that fat oxidation rates, MFO, and Fatmax were enhanced following endurance exercise, but were increased to a greater extent with a more severe mucle glycogen depletion, inducing therefore modifications in the postexercise fat oxidation kinetics (i.e., greater dilatation and rightward asymmetry). In perspective, further studies have been suggested 1) to assess physiological meaning of the three independent variables of the SIN model; and 2) to compare the effect of two different training programs on fat oxidation kinetics in obese subjects.
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Evidence is accumulating that total body mass and its relative composition influence the rate of fat utilization in man. This effect can be explained by two factors operating in concert: (i) the effect of the size of the tissue mass and (ii) the nature of the fuel mix oxidized, i.e. the proportion of energy derived from fat vs. carbohydrate. In a cross-sectional study of 307 women with increasing degrees of obesity, we observed that the respiratory quotient (RQ) in post-absorptive conditions became progressively lower with increased body fatness, indicating a shift in substrate utilization. However, the RQ is known to be also influenced by the diet commonly ingested by the subjects. A short-term mixed diet overfeeding in lean and obese women has also demonstrated the high sensitivity of RQ to changes in energy balance. Following a one-day overfeeding (2500 kcal/day in excess of the previous 24 h energy expenditure), the magnitude of increase in RQ was identical in lean and obese subjects and the net efficiency of substrate utilization and storage was not influenced by the state of obesity.
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Introduction An impaired ability to oxidize fat may be a factor in the obesity's aetiology (3). Moreover, the exercise intensity (Fatmax) eliciting the maximal fat oxidation rate (MFO) was lower in obese (O) compared with lean (L) individuals (4). However, difference in fat oxidation rate (FOR) during exercise between O and L remains equivocal and little is known about FORs during high intensities (>60% ) in O compared with L. This study aimed to characterize fat oxidation kinetics over a large range of intensities in L and O. Methods 12 healthy L [body mass index (BMI): 22.8±0.4] and 16 healthy O men (BMI: 38.9±1.4) performed submaximal incremental test (Incr) to determine whole-body fat oxidation kinetics using indirect calorimetry. After a 15-min resting period (Rest) and 10-min warm-up at 20% of maximal power output (MPO, determined by a maximal incremental test), the power output was increased by 7.5% MPO every 6-min until respiratory exchange ratio reached 1.0. Venous lactate and glucose and plasma concentration of epinephrine (E), norepinephrine (NE), insulin and non-esterified fatty acid (NEFA) were assessed at each step. A mathematical model (SIN) (1), including three variables (dilatation, symmetry, translation), was used to characterize fat oxidation (normalized by fat-free mass) kinetics and to determine Fatmax and MFO. Results FOR at Rest and MFO were not significantly different between groups (p≥0.1). FORs were similar from 20-60% (p≥0.1) and significantly lower from 65-85% in O than in L (p≤0.04). Fatmax was significantly lower in O than in L (46.5±2.5 vs 56.7±1.9 % respectively; p=0.005). Fat oxidation kinetics was characterized by similar translation (p=0.2), significantly lower dilatation (p=0.001) and tended to a left-shift symmetry in O compared with L (p=0.09). Plasma E, insulin and NEFA were significantly higher in L compared to O (p≤0.04). There were no significant differences in glucose, lactate and plasma NE between groups (p≥0.2). Conclusion The study showed that O presented a lower Fatmax and a lower reliance on fat oxidation at high, but not at moderate, intensities. This may be linked to a: i) higher levels of insulin and lower E concentrations in O, which may induce blunted lipolysis; ii) higher percentage of type II and a lower percentage of type I fibres (5), and iii) decreased mitochondrial content (2), which may reduce FORs at high intensities and Fatmax. These findings may have implications for an appropriate exercise intensity prescription for optimize fat oxidation in O. References 1. Cheneviere et al. Med Sci Sports Exerc. 2009 2. Holloway et al. Am J Clin Nutr. 2009 3. Kelley et al. Am J Physiol. 1999 4. Perez-Martin et al. Diabetes Metab. 2001 5. Tanner et al. Am J Physiol Endocrinol Metab. 2002
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Purpose: Recent studies showed that pericardial fat was independently correlated with the development of coronary artery disease (CAD). The mechanism remains unclear. We aimed at assessing a possible relationship between pericardial fat volume and endothelium-dependent coronary vasomotion, a surrogate of future cardiovascular events.Methods: Fifty healthy volunteers without known CAD or cardiovascular risk factors (CRF) were enrolled. They all underwent a dynamic Rb- 82 cardiac PET/CT to quantify myocardial blood flow (MBF) at rest, during MBF response to cold pressure test (CPT-MBF) and adenosine stress. Pericardial fat volume (PFV) was measured using a 3D volumetric CT method and common biological CRF (glucose and insulin levels, HOMA-IR, cholesterol, triglyceride, hs-CRP). Relationships between MBF response to CPT, PFV and other CRF were assessed using non-parametric Spearman correlation and multivariate regression analysis of variables with significant correlation on univariate analysis (Stata 11.0).Results: All of the 50 participants had normal MBF response to adenosine (2.7±0.6 mL/min/g; 95%CI: 2.6−2.9) and myocardial flow reserve (2.8±0.8; 95%CI: 2.6−3.0) excluding underlying CAD. Simple regression analysis revealed a significant correlation between absolute CPTMBF and triglyceride level (rho = −0.32, p = 0.024) fasting blood insulin (rho = −0.43, p = 0.0024), HOMA-IR (rho = −0.39, p = 0.007) and PFV (rho = −0.52, p = 0.0001). MBF response to adenosine was only correlated with PFV (rho = −0.32, p = 0.026). On multivariate regression analysis PFV emerged as the only significant predictor of MBF response to CPT (p = 0.002).Conclusion: PFV is significantly correlated with endothelium-dependent coronary vasomotion. High PF burden might negatively influence MBF response to CPT, as well as to adenosine stress, even in persons with normal hyperemic myocardial perfusion imaging, suggesting a link between PF and future cardiovascular events. While outside-to-inside adipokines secretion through the arterial wall has been described, our results might suggest an effect upon NO-dependent and -independent vasodilatation. Further studies are needed to elucidate this mechanism.
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The resting metabolic rate (RMR) and the thermic effect of a meal (TEM) were measured in a group of 16 prepubertal (8.8 +/- 0.3 y) obese children (43.6 +/- 9.2 kg) and compared with a group of 10 age-matched (8.6 +/- 0.4 y), normal-weight children (31.0 +/- 6.0 kg). The RMR was higher in the obese than in the control children (4971 +/- 485 vs 4519 +/- 326 kJ/d, P < 0.05); after the RMR was adjusted for the effect of fat-free mass (FFM) the values were not significantly different (4887 +/- 389 vs 4686 +/- 389 kJ/d). The thermic response to a liquid mixed meal, expressed as a percentage of the energy content of the meal, was significantly lower in obese than in control children (4.4 +/- 1.2% vs 5.9 +/- 1.7%, P < 0.05). The blunted TEM shown by the obese children could favor weight gain and suggests that the defect in thermogenesis reported in certain obese adults may have already originated early in life.
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OBJECTIVE: To assess the effects, on food intake, body weight and body composition, of compliance to advice aiming at increasing the carbohydrate to fat ratio of the everyday diet without imposing voluntary restriction on the amount of food consumed. DESIGN: Eight moderately overweight women (body mass index > 27 kg/m2, relative body fat mass > 30%) received dietary advice during a 2 month period. Additionally, each evening the subjects had to consume a meal artificially enriched with 13C-glucose in order to assess their compliance from the 13CO2 enrichment in expired air. MEASUREMENTS: Dietary intakes, body weight, body composition and individual compliance. RESULTS: The energy derived from fat decreased from 44 +/- 1% to 31 +/- 1% and the proportion of carbohydrate increased from 38 +/- 2% to 50 +/- 1%, whereas the absolute carbohydrate intake remained constant (182 +/- 18 g/d). Energy intake decreased by 1569 +/- 520 kJ/d. There was a net loss of fat mass (1.7 +/- 0.7 kg, P = 0.016) with fat free mass maintenance. Dietary compliance ranged from 20 to 93% (mean: 60 +/- 8%) and was positively correlated to the loss of body fat mass. CONCLUSION: Advice aiming at increasing diet's carbohydrate to fat ratio induces a loss of fat mass with fat-free mass maintenance.
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Aerobic exercise training performed at the intensity eliciting maximal fat oxidation (Fatmax) has been shown to improve the metabolic profile of obese patients. However, limited information is available on the reproducibility of Fatmax and related physiological measures. The aim of this study was to assess the intra-individual variability of: a) Fatmax measurements determined using three different data analysis approaches and b) fat and carbohydrate oxidation rates at rest and at each stage of an individualized graded test. Fifteen healthy males [body mass index 23.1±0.6 kg/m2, maximal oxygen consumption ([Formula: see text]) 52.0±2.0 ml/kg/min] completed a maximal test and two identical submaximal incremental tests on ergocycle (30-min rest followed by 5-min stages with increments of 7.5% of the maximal power output). Fat and carbohydrate oxidation rates were determined using indirect calorimetry. Fatmax was determined with three approaches: the sine model (SIN), measured values (MV) and 3rd polynomial curve (P3). Intra-individual coefficients of variation (CVs) and limits of agreement were calculated. CV for Fatmax determined with SIN was 16.4% and tended to be lower than with P3 and MV (18.6% and 20.8%, respectively). Limits of agreement for Fatmax were -2±27% of [Formula: see text] with SIN, -4±32 with P3 and -4±28 with MV. CVs of oxygen uptake, carbon dioxide production and respiratory exchange rate were <10% at rest and <5% during exercise. Conversely, CVs of fat oxidation rates (20% at rest and 24-49% during exercise) and carbohydrate oxidation rates (33.5% at rest, 8.5-12.9% during exercise) were higher. The intra-individual variability of Fatmax and fat oxidation rates was high (CV>15%), regardless of the data analysis approach employed. Further research on the determinants of the variability of Fatmax and fat oxidation rates is required.
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Energy expenditure (EE) was measured by indirect calorimetry in 20 subjects (10 men and 10 women) for 30 min before and 6 h after the ingestion of a mixed meal containing 20% protein, 33% fat, and either 75 g glucose or 75 g fructose as carbohydrate source (47%). Diet-induced thermogenesis (DIT) and the rate of carbohydrate oxidation were significantly greater with fructose (12.4 +/- 0.6% and 54.8 +/- 2.1 g/6 h, respectively) than with glucose (10.7 +/- 0.7%, p less than 0.01, and 48.3 +/- 2.4 g/6 h, p less than 0.01, respectively). The DIT of male (12.1 +/- 1% and 13.9 +/- 0.8% with glucose and fructose, respectively) was greater than that of female subjects (9.2 +/- 0.7%, p less than 0.05, and 11.0 +/- 0.7%, p less than 0.05, respectively). In contrast to the glucose meal, negligible changes in plasma levels of glucose and insulin were observed with the fructose meal but plasma levels of lactate increased more with fructose than with glucose (peak values: 3.3 +/- 0.6 vs 1.5 +/- 0.1 mmol/L, respectively). When fructose provides the only carbohydrate source of a mixed meal, it induces a larger increase in carbohydrate oxidation and thermogenesis than when glucose is the carbohydrate source.