Increase In Postprandial Energy Expenditure Research Articles

The effect of a high fat meal on heart rate variability and arterial stiffness in adolescents with or without type 1 diabetes

AimType 1 diabetes (T1D) is associated with increased arterial stiffness and cardiac autonomic neuropathy. We tested whether those variables are acutely affected by a high fat meal (HFM). MethodsResponses to a HFM were measured in adolescents with T1D (N = 14) or without T1D (Control, N = 21). Heart rate variability (HRV), arterial stiffness, blood pressure (BP), and energy expenditure (EE) were measured before (baseline) and four times over 180 min postprandially. ResultsT1D had higher blood glucose and insulin, but the suppression of fatty acids (~40%) and rise in triglycerides (~60%) were similar between groups. T1D had 9% higher EE, but postprandial increase in EE was similar to Controls. T1D had ~7 to 24% lower baseline HRV but a similar postprandial decline of ~8 to 25% as Controls. Both groups had a similar 2 to 5% increase in BP after the meal. Rate pressure product increased postprandially in both groups and was higher in T1D. Pulsewave velocity and augmentation index did not differ between groups or change postprandially. ConclusionAdolescents with T1D have evidence of cardiac autonomic dysfunction and increased EE, but those variables, along with arterial stiffness, are not acutely made worse by a HFM.

Metabolic Response to Daytime Dry Fasting in Bahá’í Volunteers—Results of a Preliminary Study

Each year in March, adherents of the Bahá’í faith abstain from eating and drinking from sunrise to sunset for 19 days. Thus, Bahá’í fasting (BF) can be considered as a form of daytime dry fasting. We investigated whether BF decreased energy expenditure after a meal and whether it improved anthropometric measures and systemic and tissue-level metabolic parameters. This was a self-controlled cohort study with 11 healthy men. We measured anthropometric parameters, metabolic markers in venous blood and pre- and postprandial energy metabolism at systemic (indirect calorimetry) and tissue (adipose tissue and skeletal muscle microdialysis) level, both before and during BF. During BF, we found reduced body weight, body mass index, body fat and blood glucose. Postprandial increase in energy expenditure was lower and diet-induced thermogenesis tended to be lower as well. In adipose tissue, perfusion, glucose supply and lipolysis were increased. In skeletal muscle, tissue perfusion did not change. Glucose supply and lipolysis were decreased. Glucose oxidation was increased, indicating improved insulin sensitivity. BF may be a promising approach to losing weight and improving metabolism and health. However, outside the context of religiously motivated fasting, skipping a meal in the evening (dinner cancelling) might be recommended, as metabolism appeared to be reduced in the evening.

Effect of High-Protein Diet on Postprandial Energy Expenditure in Children with Prader-Willi Syndrome: A Pilot and Feasibility Study.

The aim of this study was to explore the feasibility of measuring a postprandial increase in energy expenditure (ΔEE) using a state-of-the-art whole-body calorimetry unit (WBCU) in children and youth with Prader-Willi syndrome (PWS). Five participants (aged 10–25 y) received both a standard and a high-protein diet in a random order (crossover design). Resting energy expenditure, postprandial ΔEE 6 h after intake of a standard [15% of total energy (TE)] and a high-protein (30% TE) meal, and respiratory exchange ratio (RER) were measured in a WBCU. No differences were observed in ΔEE comparing the 2 meals. Mean RER was lower following the high-protein meal (0.80 ± 0.01) compared with the standard meal (0.87 ± 0.02) (P = 0.009). Despite the high participant burden, it was feasible to conduct this metabolic test in children and youth with PWS. This study paves the way for further studies targeting EE in this patient population.

Abstract P471: Increased Salt Intake Reduces Diet-induced Thermogenesis in Healthy Men

Objective: High salt intake is a potential risk factor for obesity independent of energy intake, though underlying mechanisms remain unclear. Excessive body fat accumulation is caused by a positive energy balance over an extended period of time. Food intake causes a postprandial increase in energy expenditure. This postprandial effect represents approximately 10% of the total energy ingested over 24h. A decrease in diet-induced thermogenesis (DIT) contributes to a positive energy balance and weight gain over time. The present study investigated the effect of a 14-day high salt intake on DIT in healthy men. Methods: We enrolled eight healthy men (34 ± 7 years, BMI 24 ± 2 kg/m 2 ) in an exploratory, longitudinal study (Clincaltrials.gov identifier: NCT02509962). Probands received 6 g salt daily using sodium chloride tablets (Slow Sodium tablets, HK Pharma Ltd.) over 14 days on top of their habitual diet. Measurements were taken at baseline (V1), on day 3 (V2) and day 14 (V3) during and on day 9 (V4) after the salt challenge, respectively. At these time points, nocturnal ambulatory blood pressure monitoring, bioelectrical impedance analysis (BIA), food intake from 3-day food records, and resting and postprandial energy expenditure were obtained. Energy expenditure was measured by indirect calorimetry in a respiratory chamber after a 12h overnight fast and a standardized 440 kcal, high-protein meal. Results: Nocturnal systolic blood pressure increased after salt challenge (V1: 105.8 ± 8.5, V3: 111.2 ± 9.1 mmHg, P = 0.02). There was a trend towards higher energy intakes (V1: 2296 ± 752 kcal, V3: 2866 ± 831 kcal, P = 0.1). However, DIT was significantly decreased at all time points during and after salt challenge compared to baseline (V1: 17.3 ± 2.7%; V2: 11.3 ± 2.3%, P = 0.01; V3: 10.7 ± 3.6 %, P = 0.03; V4: 14.4 ± 2.5%, P = 0.04; all vs. V1). After 14 days of high salt, subjects expended 30 kcal less for metabolic processes after meal challenge. Assuming a total energy intake of 2300 kcal/d, this accounts for a 150 kcal positive energy balance. Conclusion: A moderate short-term increase of salt intake decreased the thermic effect of a high-protein meal. This could contribute to the observed weight gain in populations consuming a Western diet high in salt.

Postprandial Increase in Energy Expenditure Correlates with Body Weight Reduction in Patients with Type 2 Diabetes Receiving Diet Therapy.

Aim: The clinical significance of energy expenditure (EE) in the treatment of type 2 diabetes has not been fully elucidated. Here we analyzed the relationships between EE and clinical measurements in patients with type 2 diabetes receiving diet therapy.Methods: A total of 100 patients (34 women and 66 men) with type 2 diabetes admitted to our hospital for glycemic control were enrolled. The participants received an energy-restricted diet during their hospitalization (median, 15 days). EE was measured in the fasted (FEE) and postprandial (PPEE) states using indirect calorimetry. The postprandial increment of EE (ΔEE) was calculated from the FEE and PPEE (ΔEE=PPEE – FEE).Results: FEE, PPEE, and ΔEE were 0.997 ± 0.203, 1.104 ± 0.213, and 0.107 ± 0.134 kcal/min, respectively. Body weight decreased from 68.7 ± 16.6 to 66.8 ± 16.0 kg (p < 0.0001) during hospitalization. FEE and PPEE showed positive correlations with height, body weight, body mass index, and abdominal circumference at admission, but ΔEE was not correlated with these anthropometric measurements. On the other hand, ΔEE was inversely correlated with the body weight change. The association between ΔEE and the body weight change was independent of age, sex, and HbA1c.Conclusions: Postprandial increase in energy expenditure may be a determinant of individual differences in weight reduction in patients with type 2 diabetes on diet therapy. As a simple surrogate for diet-induced thermogenesis, ΔEE may serve as a useful predictive marker for the efficacy of diet therapy.

Increased plasma levels of glucose-dependent insulinotropic polypeptide are associated with decreased postprandial energy expenditure after modern Japanese meals

PurposeThe nutritional changes that have accompanied the modernization of Japanese dietary patterns have led to significant increases in the number of people who are overweight or obese. This study aimed to clarify the effects of these nutritional changes on postprandial energy expenditure and the release of metabolism-regulating hormones.MethodsThe total daily energy content (20 % breakfast, 40 % lunch, and 40 % dinner) and macronutrient composition (carbohydrate/fat/protein) was 8807.3 kJ and 364.3:30.1:66.4 (g) for the traditional test diet and 9217.6 kJ and 331.7:66.1:76.9 (g) for the modern test diet. In experiment 1, nine healthy Japanese men participated in a crossover study during which they ingested a test diet comprising three meals; postprandial blood parameters were measured after each meal. In experiment 2, another ten men participated in a crossover study during which they ingested 2 meals, after which metabolic responses and blood variables were evaluated.ResultsThe modern diet induced greater blood levels of glucose-dependent insulinotropic polypeptide (GIP) and ghrelin than did the traditional diet. The expected increase in postprandial energy expenditure (∆REE) tended to be dampened after the modern compared with the traditional diet. GIP was inversely correlated with ∆REE after lunch, and ghrelin was positively associated with ∆REE.ConclusionBoth GIP and ghrelin are robust indicators of postprandial energy expenditure. The nutritional changes accompanying the modernization of Japanese dietary patterns may increase the levels of the anabolic intestinal hormone GIP, which is associated with ∆REE, in the Japanese population. The contribution of an increased ghrelin concentration to the decreased ∆REE after the modern diet warrants further investigation.

Effect of breakfast skipping on diurnal variation of energy metabolism and blood glucose

Epidemiological studies suggest an association between breakfast skipping and body weight gain, insulin resistance or type 2 diabetes. Time when meal is consumed affects postprandial increase in energy expenditure and blood glucose, and breakfast skipping may reduce 24 h energy expenditure and elevate blood glucose level. The present study evaluated the effect of breakfast skipping on diurnal variation of energy metabolism and blood glucose. The skipped breakfast was compensated by following big meals at lunch and supper. In a randomized repeated-measure design with or without breakfast, eight males stayed twice in a room-size respiratory chamber. Blood glucose was recorded with a continuous glucose monitoring system. Breakfast skipping did not affect 24 h energy expenditure, fat oxidation and thermic effect of food, but increased overall 24 h average of blood glucose (83 ± 3 vs 89 ± 2 mg/dl, P < 0.05). Unlike 24 h glucose level, 24 h energy expenditure was robust when challenged by breakfast skipping. These observations suggest that changes in glucose homeostasis precede that of energy balance, in the potential sequence caused by breakfast skipping, if this dietary habit has any effect on energy balance.:

Energy expenditure in obese children with pseudohypoparathyroidism type 1a

ContextPatients with pseudohypoparathyroidism type 1a (PHP-1a) develop early-onset obesity. The abnormality in energy expenditure and/or energy intake responsible for this weight gain is unknown.ObjectiveThe aim of this study was to evaluate energy expenditure in children with PHP-1a compared with obese controls.PatientsWe studied 6 obese females with PHP-1a and 17 obese female controls. Patients were recruited from a single academic center.MeasurementsResting energy expenditure and thermogenic effect of a high fat meal were measured using whole room indirect calorimetry. Body composition was assessed using whole body dual energy x-ray absorptiometry. Fasting glucose, insulin and hemoglobin A1C were measured.ResultsChildren with PHP-1a had decreased resting energy expenditure compared with obese controls (P <0.01). After adjustment for fat free mass, the PHP-1a group’s resting energy expenditure was 346.4 kcals/day less than obese controls (95% CI [−585.5 to −106.9], P <0.01). The thermogenic effect of food, expressed as percent increase in postprandial energy expenditure over resting energy expenditure, was lower in PHP-1a patients than obese controls but did not reach statistical significance (absolute reduction of 5.9%, 95% CI [−12.2% to 0.3%], P = 0.06).ConclusionsOur data indicate that children with PHP-1a have decreased resting energy expenditure compared with obese controls and that may contribute to the development of obesity in these children. These patients may also have abnormal diet-induced thermogenesis in response to a high fat meal. Understanding the causes of obesity in PHP-1a may allow for targeted nutritional or pharmacologic treatments in the future.

Therapeutic Application of Diacylglycerol Oil for Obesity: Serotonin Hypothesis

Characteristics for the serum lipid abnormalities in the obesity/metabolic syndrome are elevated fasting, postprandial triglyceride (TG), and decreased high-density lipoprotein-cholesterol (HDL-C). Diacylglycerol (DAG) oil ingestion has been reported to ameliorate postprandial hyperlipidemia and prevent obesity by increasing energy expenditure, due to the intestinal physiochemical dynamics that differ from triacylglycerol (TAG). Our study demonstrated that DAG suppresses postprandial increase in TG-rich lipoprotein, very low-density lipoprotein (VLDL), and insulin, as compared with TAG in young, healthy individuals. Interestingly, our study also presented that DAG significantly increases plasma serotonin, which is mostly present in the intestine, and mediates thermogenesis, proposing a possible mechanism for a postprandial increase in energy expenditure by DAG. Our other study demonstrated that DAG suppresses postprandial increase in TG, VLDL-C, and remnant-like particle-cholesterol, in comparison with TAG in an apolipoprotein C-II deficient subject, suggesting that DAG suppresses postprandial TG-rich lipoprotein independently of lipoprotein lipase. Further, to understand the molecular mechanisms for DAG-mediated increase in serotonin and energy expenditure, we studied the effects of 1-monoacylglycerol and 2-monoacylglycerol, distinct digestive products of DAG and TAG, respectively, on serotonin release from the Caco-2 cells, the human intestinal cell line. We also studied effects of 1- and 2-monoacylglycerol, and serotonin on the expression of mRNA associated with β-oxidation, fatty acids metabolism, and thermogenesis, in the Caco-2 cells. 1-monoacylglycerol significantly increased serotonin release from the Caco-2 cells, compared with 2-monoacylglycerol by approximately 40%. The expression of mRNA of acyl-CoA oxidase (ACO), fatty acid translocase (FAT), and uncoupling protein-2 (UCP-2), was significantly higher in 1-MOG-treated Caco-2 cells, than 2-MOG-treated cells. The expression of mRNA of ACO, medium-chain acyl-CoA dehydrogenase, FAT, and UCP-2, was significantly elevated in serotonin-treated Caco-2 cells, compared to cells incubated without serotonin. In conclusion, our clinical and in vitro studies suggested a possible therapeutic application of DAG for obesity, and obesity-related metabolic disorders.Key words: Diacylglycerol, intestine, obesity, serotonin, thermogenesis

Acute effect of late evening meal on diurnal variation of blood glucose and energy metabolism

The notion that late evening meal promotes weight gain is popular, and it may also elicit postprandial hyperglycemia, since glucose tolerance decreases during midnight. Diabetic patients with night-eating symptoms, compared with patients without night-eating behaviors, are more likely to be obese and to have elevated A1c. However, epidemiological analysis adjusted for difference in total energy intake did not identify nighttime eating as the risk of obesity. The present study evaluated the effect of a single loading of late evening meal on diurnal variation of blood glucose and 24-h energy expenditure. Ten young adults stayed twice in a room-size respiratory chamber for 24 h, in a randomized repeated-measures design. After the entrance to the chamber at 1700 h, the subjects took normal (1900 h) or late (2230 h) evening meal, breakfast and lunch, and remained in the chamber until 1700 h. Time course of blood glucose was measured by continuous glucose monitoring system. Late evening meal enhanced postprandial blood glucose response to the evening meal and the subsequent breakfast. Overall 24 h average blood glucose level was also elevated by late evening meal. Late evening meal shifted postprandial increase in energy expenditure toward late at night, but overall 24 h energy expenditure remained almost identical in the two dietary conditions. The present study under controlled sedentary condition supports the notion that a single loading of late evening meal enhances average blood glucose over 24 h, but does not support that late evening meal reduces 24 h energy expenditure.

Atrial Natriuretic Peptide Induces Postprandial Lipid Oxidation in Humans

OBJECTIVE—Atrial natriuretic peptide (ANP) regulates arterial blood pressure. In addition, ANP has recently been shown to promote human adipose tissue lipolysis through cGMP-mediated hormone-sensitive lipase activation. We hypothesized that ANP increases postprandial free fatty acid (FFA) availability and energy expenditure while decreasing arterial blood pressure.RESEARCH DESIGN AND METHODS—We infused human ANP (25 ng · kg−1 · min−1) in 12 men (age 32 ± 0.8 years, BMI 23.3 ± 0.4 kg/m2) before, during, and 2 h after ingestion of a standardized high-fat test meal in a randomized, double-blind, cross-over fashion. Cardiovascular changes were monitored by continuous electrocardiogram and beat-by-beat blood pressure recordings. Metabolism was monitored through venous blood sampling, intramuscular and subcutaneous abdominal adipose tissue microdialysis, and indirect calorimetry.RESULTS—ANP infusion decreased mean arterial blood pressure by 4 mmHg during the postprandial phase (P < 0.01 vs. placebo). At the same time, ANP induced lipolysis systemically (P < 0.05 vs. placebo) and locally in subcutaneous abdominal adipose tissue (P < 0.0001 vs. placebo), leading to a 50% increase in venous glycerol (P < 0.01) and FFA (P < 0.05) concentrations compared with placebo. The increase in FFA availability with ANP was paralleled by a 15% increase in lipid oxidation rates (P < 0.05 vs. placebo), driving a substantial increase in postprandial energy expenditure (P < 0.05 vs. placebo).CONCLUSIONS—Our data identify the ANP system as a novel pathway regulating postprandial lipid oxidation, energy expenditure, and concomitantly arterial blood pressure. The findings could have therapeutic implications.

Effects of Diacylglycerol on Glucose, Lipid Metabolism, and Plasma Serotonin Levels in Lean Japanese

Diacylglycerol (DAG)-rich oil has been suggested to suppress postprandial hyperlipidemia and promote negative caloric balance by increasing energy expenditure (EE), due to small intestine physiochemical dynamics that differ from triacylglycerol (TAG). We studied the effect of DAG on postprandial glucose/insulin metabolism by loading of carbohydrate with oil. Further, to reveal the mechanism for increased EE by DAG, we measured plasma serotonin, which is mostly present in the small intestine and mediates peripheral sympathetic thermogenesis. Randomized crossover study with 2-week wash-out interval between differing fat ingestion. Seven male, lean, Japanese students ingested DAG or TAG oil with 40 g of carbohydrate. Measurements of metabolic parameters were performed before and at 2, 4, and 6 h after fat ingestion. Plasma serotonin levels and cholesterol concentration in each lipoprotein were measured using high-performance liquid chromatography (HPLC). The substitution of DAG for TAG decreased very-low-density lipoprotein-cholesterol (VLDL-C) by 45.6% at 2 h, and decreased serum insulin by 41.3% at 4 h after ingestion. The incremental area under the curve (IAUC) for VLDL-C was positively correlated with the IAUC for insulin. Concurrently, DAG elevated plasma serotonin levels by 47.3% at 2 h, while TAG did not influence. This study indicates that the substitution of DAG for TAG suppresses the postprandial increase in serum VLDL-C and insulin. This study also demonstrates that DAG ingestion increases plasma serotonin, proposing a possible mechanism for a postprandial increase in EE by DAG.

The acute effects of different sources of dietary calcium on postprandial energy metabolism

Dairy Ca intake has been shown to be superior to elemental Ca in increasing the loss of body fat during energy restriction. We questioned whether the mechanisms involved an increase in postprandial energy expenditure, fat oxidation and/or a greater lipolysis. The acute effects of different sources of Ca were examined in eight subjects, aged 47-66 years and BMI 27.6-36.1 kg/m2, in a three-way cross-over study. Subjects were randomly provided breakfast meals either low in dairy Ca and vitamin D (LD; control), high in non-dairy Ca (calcium citrate) but low in vitamin D (HC) or high in dairy Ca and vitamin D (HD). Diet-induced thermogenesis, fat oxidation rates (FOR), carbohydrate oxidation rates (COR), insulin, glucose, NEFA and glycerol were measured hourly over a 6 h postprandial period. Postprandial data were calculated as a change (Delta) from the fasting value. Results showed that DeltaNEFA was significantly different between meals (LD -1.50 (sem 0.26), HC -1.22 (sem 0.32), HD -0.94 (sem 0.27) mmol/l x 6 h; P = 0.035), with a lesser suppression following both high-Ca meals. DeltaFOR was significantly higher following the two high-Ca meals (LD -6.5 (sem 2.2), HC 2.93 (sem 2.34), HD 3.3 (sem 2.5) g x 6 h; P = 0.005), while reciprocally DeltaCOR was significantly lower. DeltaGlycerol was less suppressed following the high-Ca meals but statistical significance was not achieved. No differences in diet-induced thermogenesis, insulin or glucose were observed. Regardless of source, Ca intake acutely stimulated postprandial fat oxidation; and there was a lesser suppression of NEFA following these meals.

Beneficial Postprandial Effect of a Small Amount of Alcohol on Diabetes and Cardiovascular Risk Factors: Modification by Insulin Resistance

Moderate alcohol consumption protects against type 2 diabetes and cardiovascular disease. Because humans spend most of their time in the postprandial state, we examined the effect of 15 g alcohol on postprandial metabolic factors in 20 postmenopausal women over 6 h. We measured 1) glucose, insulin, lipids, C-reactive protein, and adiponectin levels; 2) augmentation index by applanation tonometry; and 3) energy expenditure and substrate oxidation by indirect calorimetry. Subjects received low carbohydrate (LC; visits 1 and 2) and high carbohydrate (HC; visits 3 and 4) high fat meals with and without alcohol. Alcohol augmented the postprandial increment in insulin (P = 0.07) and reduced the postprandial increment in glucose (P = 0.04) after the LC meal only. Triglycerides were increased by alcohol after the LC (P = 0.002) and HC (P = 0.008) meals. Total and high-density lipoprotein cholesterol, fatty acids, and total adiponectin responses were unaffected. C-reactive protein levels decreased postprandially; reductions were enhanced by alcohol after the HC meal, but were attenuated after the LC meal. Postprandial reductions in the augmentation index were increased by alcohol after the LC meal only (P = 0.007). Alcohol enhanced the postprandial increase in energy expenditure 30-60 min after the LC meal (increase, 373 +/- 49 vs. 236 +/- 32 kcal/d; P = 0.02) and HC meal (increase, 362 +/- 36 vs. 205 +/- 34 kcal/d; P = 0.0009), but suppressed fat and carbohydrate oxidation. Some of our findings may be mechanisms for lower diabetes and cardiovascular risks in moderate drinkers.

Postprandial metabolism and aversive response in rats fed a threonine-devoid diet.

Lack of an indispensable amino acid in the diet induces a rapid reduction in food intake. In this study, we assessed whether the anorectic signal after ingestion of a meal lacking threonine originated from either direct perception of the decrease in plasma threonine or from an indirect effect related to increased postprandial amino acid catabolism and energy expenditure. We observed that 3 g of such a meal was sufficient to induce an aversive response to the diet within 2 h. Postprandial changes to plasma ammonia and urea, urinary urea, and energy metabolism did not differ from those measured after a control meal. In contrast, plasma threonine levels fell within 1 h after the meal. It is concluded that an increase in postprandial energy expenditure is not involved in the anorectic response to eating a threonine-devoid diet. The drop in plasma threonine levels may be a potential signal, but the fact that the decrease in food intake occurred 1 h after the decrease in plasma threonine questions a direct causal relationship.

Hyperinsulinemia and regulation of energy balance

Recent data suggest that hyperinsulinemia with euglycemia may favor the restoration of energy balance when one gains body weight. To test the validity of this concept in humans, the data of 24 young men who had been exposed to a 353-MJ overfeeding protocol for 100 d and who were remeasured after a 4-mo follow-up were analyzed. The sample was subdivided in two groups on the basis of the overfeeding-induced change in postprandial plasma insulin. The increase in postprandial energy expenditure induced by overfeeding was significantly greater in high than in low postprandial insulin responders (P < 0.05) but not after body fat gain was controlled for. After the overfeeding protocol, the loss of subcutaneous adiposity was greater in high than in low postprandial insulin responders. However, this difference was no more significant after the gain in fat mass was controlled for. There was no difference between the two groups in post-overfeeding loss of body weight, fat mass, or fat-free mass. These results partly agree with the idea that hyperinsulinemia resulting from a long-term positive energy balance and its associated fat gain exert a regulatory role promoting the restoration of energy balance.

Heat leakage across the abdominal wall and meal-induced thermogenesis in normal-weight and obese subjects

The mechanism behind the meal-induced increase in energy expenditure in humans and its reduction in obesity was examined in 15 normal-weight and seven obese subjects. The subjects were studied by indirect calorimetry in the basal state and during 2 hours after a mixed meal corresponding to 40% of the 24-hour basal energy requirement. Artificial thermal insulation was applied over the abdominal area before the study in seven of the normal-weight subjects. Thermistor catheters were inserted into a hepatic vein, the pulmonary artery, and a systemic artery for blood sampling and recording of blood temperatures. Basal hepatic venous drainage of heat in relation to the splanchnic oxygen uptake in the normal-weight subjects was low (12 ± 1 J/mL O 2) and became even lower after the meal (5 ± 3 J/mL). In the obese individuals and the insulated subjects, blood-drained splanchnic heat amounted to 19 to 21 J/mL oxygen both before and after the meal. The postprandial increase in whole body energy expenditure was diminished both in the obese (12% ± 1% above basal) and in the insulated subjects (15% ± 1%) compared with the noninsulated controls (22% ± 2%). In normal-weight subjects, there is a leakage of heat across the abdominal wall. Reduction or prevention of this leakage by artificial thermal insulation or by obesity is accompanied by a reduction of the postprandial increase in energy expenditure.

Postprandial energy expenditure and respiratory quotient during early and late pregnancy

Rates of energy expenditure after a 750-kcal meal were determined by open circuit, indirect calorimetry for four women in late pregnancy (30 to 40 wk gestation), six women in early pregnancy (10 to 20 wk gestation), and six nonpregnant women. Preprandial resting metabolic rates, expressed in kcal min−1, were 22.5% higher (p < 0.05) in the late pregnancy group compared to the early pregnancy, and 15.9% higher (p < 0.05) in the early pregnancy compared to the nonpregnant women. No differences in preprandial energy expenditure rates were seen between groups when expressed as kcal kg−1 h−1. Rates of energy expenditure increased above preprandial levels in all groups by 15 min postprandially and remained significantly elevated for the next 175 min. The total increase in postprandial energy expenditure above preprandial levels did not differ significantly due to stage of gestation. Respiratory quotient, the ratio of VCO2:VO2, increased significantly in all groups (p < 0.05) above preprandial levels by 15 min after the meal. Respiratory quotient values began decreasing after 95 min and returned, in all groups, to preprandial levels by 175 min. The results from this study demonstrate that the increase in the rates of energy expenditure after a mixed meal was not altered by gestation.