SARS-CoV-2 exposures among healthcare workers in New York City.

BACKGROUND: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has had a significant impact on hospitals, including the occupational health departments in charge of handling healthcare worker (HCW) staffing during high rates of exposure and infection of HCWs. HCWs who were exposed to a patient or community member infected with SARS-CoV-2 were required to isolate from work for a minimum of 14 days from the date of exposure. AIMS: This study was aimed to assess the relative risk of SARS-CoV-2 infection following different types of workplace and community exposures. METHODS: We analyzed the details of workplace and community exposures of HCWs to SARS-CoV-2 at Montefiore Medical Center in New York between 22 June 2020 and 22 November 2020. RESULTS: Of 562 HCW SARS-CoV-2 exposures analyzed, 218 were from the community and 345 were from the workplace. Twenty-nine per cent of community exposures resulted in infection, which was significantly greater than workplace exposure infection (2%). Household community exposures resulted in a larger frequency of infection than non-household community exposures. Of the seven infections after workplace exposures, five had qualifying exposures to a co-worker and two were exposed to an infected patient during a non-aerosolized procedure. CONCLUSIONS: HCW exposure to SARS-CoV-2 continues to present staffing challenges to healthcare systems. Even with deviations from standard personal protective equipment protocol, workplace exposures resulted in low frequencies of infection. In our study, the primary source of HCW infection was exposure in the community. Our findings support investing in efforts to educate around continued masking and social distancing in the community in addition to interventions targeted at addressing vaccine hesitancy.

Predictive value of early weight loss in obesity management with orlistat: an evidence-based assessment of prescribing guidelines.

OBJECTIVE: To assess the clinical usefulness of published guidelines for the use of orlistat, by studying whether weight loss >/=2.5 kg during a 4 week dietary lead-in period, and weight losses of >/=5% after 12 weeks and >/=10% after 6 months of drug therapy predict weight loss and risk factor changes after 2 years. DESIGN: A retrospective analysis of pooled data from 2 multicentre, randomised, placebo-controlled clinical trials with similar design. SETTING: Twenty-nine centres throughout Europe. PARTICIPANTS: Two hundred and twenty men and women (BMI 28-43 kg/m(2)) who completed 2 years of treatment. INTERVENTION: After a 4 week hypocaloric diet plus placebo, 2 years of treatment with orlistat 120 mg tid, plus a hypocaloric diet for the first year and a weight maintenance diet in year two. MAIN OUTCOME MEASURES: Weight loss and obesity-related risk factor changes. RESULTS: Weight loss >/=5% body weight after 12 weeks of diet plus orlistat therapy was a good indicator of 2 year weight loss, whereas weight loss of >/=2.5 kg during the 4 week lead-in and >/=10% after 6 months did not add significantly to the prediction of 2 year outcomes. Patients who lost >/=5% of their weight at 12 weeks (n=104, 47.3%) lost significantly more weight after 2 years than others: -11.9% (95% confidence interval (CI) -13.4% to -10.3%) vs -4.7% (-5.7% to -3.7%) (P=0.0001), and had significantly greater reductions in total cholesterol, LDL-cholesterol, triglycerides, glucose, insulin, and blood pressure. Among those who achieved >/=5% weight loss at 12 weeks, the overall health benefits were not significantly greater in patients who went on to lose >/=10% body weight at 6 months compared with those who did not achieve >/=10% weight loss by month 6. CONCLUSIONS: Of the criteria currently suggested for assessing response to orlistat treatment, weight loss of >/=5% at 12 weeks accurately predicts sustained improvements in weight and major risk factors at 2 years, while other suggested criteria are less useful.

Metabolic and hemodynamic responses to exercise in subcutaneous adipose tissue and skeletal muscle.

This study evaluated the effect of standardized bicycle exercise on metabolism and blood flow in abdominal ( aSAT) and femoral subcutaneous adipose tissue ( fSAT) and skeletal muscle in eleven women and nine men. Using microdialysis, the respective tissues were perfused with Ringer's solution (+ 50 mM ethanol) and dialysate [ethanol], [glycerol], [lactate] and [pyruvate] were measured in order to estimate blood flow (ethanol dilution technique), lipolysis and glycolysis, respectively. At rest, blood flow tended to be higher in the respective tissues of women when compared to men. During exercise, blood flow was increased significantly in fSAT and muscle, but not in aSAT. Dialysate [glycerol] was increased two- to three-fold in aSAT and fSAT, similarly in men and women. However, in muscle, dialysate [glycerol] was increased five-fold in women and four-fold in men without reaching a steady state in women. Corrected for blood flow, the increase in lipolysis was greater in muscle than in fSAT, and greater in fSAT than in aSAT, and in muscle the increase was greater for women compared with men. Dialysate [lactate] and [lactate]/[pyruvate] ratio were much more increased in muscle compared with aSAT and fSAT. It is concluded that lipids stored in muscle are rather used than lipids stored in adipose tissue for fueling the energy metabolism of muscle during exercise. During exercise, lipid mobilization is much greater in women than in men.

Effects of weight loss with orlistat on glucose tolerance and progression to type 2 diabetes in obese adults.

BACKGROUND: Orlistat is a gastrointestinal lipase inhibitor that reduces dietary fat absorption by approximately 30%, promotes weight loss, and may reduce the risk of developing impaired glucose tolerance and type 2 diabetes in obese subjects. OBJECTIVE: To test the hypothesis that orlistat combined with dietary intervention improves glucose tolerance status and prevents worsening of diabetes status more effectively than placebo. METHODS: We pooled data from 675 obese (body mass index, 30-43 kg/m2) adults at 39 US and European research centers in 3 randomized, double-blind, placebo-controlled multicenter clinical trials. Subjects received placebo plus a low-energy diet during a 4-week lead-in period. On study day 1, the diet was continued, and subjects were randomized to receive placebo 3 times a day (n=316) or treatment with orlistat, 120 mg 3 times a day (n=359), for 104 weeks. A standard 3-hour oral glucose tolerance test was performed on day 1 and at the end of treatment. MAIN OUTCOME MEASURES: The categorical assessment of glucose tolerance status (normal, impaired, diabetic) and changes in status from randomization to end of treatment were the primary efficacy measures. The secondary measures were fasting and postchallenge glucose and insulin levels. RESULTS: The mean length of follow-up was 582 days. Subjects who were treated with orlistat lost more weight (mean +/- SEM, 6.72 +/- 0.41 kg from initial weight) than subjects who received placebo (3.79+/-0.38 kg; P<.001). A smaller percentage of subjects with impaired glucose tolerance at baseline progressed to diabetic status in the orlistat (3.0%) vs placebo (7.6%) group. Conversely, among subjects with impaired glucose tolerance at baseline, glucose levels normalized in more subjects after orlistat treatment (71.6%) vs placebo (49.1%; P=.04). CONCLUSIONS: The addition of orlistat to a conventional weight loss regimen significantly improved oral glucose tolerance and diminished the rate of progression to the development of impaired glucose tolerance and type 2 diabetes.

Orlistat in the long-term treatment of obesity in primary care settings.

OBJECTIVE: To evaluate the long-term efficacy and tolerability within primary care settings of orlistat, a gastrointestinal lipase inhibitor, for the treatment of obesity. DESIGN: Randomized, double-blind, placebo-controlled, multicenter study. PARTICIPANTS: A group of 796 obese patients (body mass index, 30-44 kg/m2), treated with placebo 3 times a day (TID), 60 mg of orlistat TID, or 120 mg of orlistat TID, in conjunction with a reduced-energy diet for the first year and a weight-maintenance diet during the second year. SETTING: Seventeen primary care centers in the United States. MAIN OUTCOME MEASURES: Changes in body weight and obesity-related disease risk factors. RESULTS: Patients treated with orlistat lost significantly more weight (7.08 +/- 0.54 and 7.94 +/- 0.57 kg for the 60-mg and 120-mg orlistat groups, respectively) than those treated with placebo (4.14 +/- 0.56 kg) in year 1 (P<.001) and sustained more of this weight loss during year 2 (P<.001). More patients treated with orlistat lost 5% or more of their initial weight in year 1 (48.8% and 50.5% of patients in the 60-mg and 120-mg groups, respectively) compared with placebo (30.7%; P<.001), and approximately 34% of patients in the orlistat groups sustained weight loss of 5% or greater over 2 years compared with 24% in the placebo group (P<.001). Orlistat produced greater improvements than placebo in serum lipid levels and blood pressure and was well tolerated, although treatment resulted in a higher incidence of gastrointestinal events. CONCLUSIONS: This long-term study indicates that orlistat is an effective adjunct to dietary intervention in the treatment of obesity in primary care settings.

Use of bioelectrical impedance analysis measurements as an evaluation for participating in sports.

Bioelectrical impedance analysis (BIA) has potential in the area of sports and exercise as a method for evaluating body composition in groups of athletes. BIA probably holds less promise for detecting small changes in percentage fat within an individual. Available data in athletes have indicated an urgent need to control for testing conditions such as hydration, temperature, glycogen stores, and preceding diet and exercise. There are almost no data available for female athletes, but acceptable results have been reported in males when conditions are well controlled. There is, however, a tendency for BIA to overestimate percentage body fat, and more so in African American athletes. BIA is also potentially useful for assessing the hydration status in wrestlers, but it is advisable to use untransformed BIA measurements rather than to convert resistance measurements to body fat because of the questionable hydration status in these athletes. Untransformed results are potentially useful in evaluating the clinical status of athletes at risk for abnormal hydration because of extreme dieting practices.

Relationship between insulin sensitivity and plasma leptin concentration in lean and obese men.

Alterations in the production of or the sensitivity to leptin, the protein encoded by the ob gene, cause obesity and diabetes in rodents. We evaluated the isolated relationship between leptin and insulin sensitivity in lean and obese humans. Three groups of subjects who were carefully matched for either insulin sensitivity (determined by the modified intravenous glucose tolerance test and minimal model analysis) or adiposity (determined by hydrodensitometry) were studied: 1) lean insulin-sensitive men (percentage body fat, 15 +/- 1%); 2) lean insulin-resistant men (percentage body fat, 16 +/- 1%), matched on percentage body fat and fat mass with the lean insulin-sensitive group; and 3) obese insulin-resistant men (percentage body fat, 31 +/- 3), matched on insulin sensitivity with the lean insulin-resistant group. Basal plasma leptin concentrations were significantly lower in the lean insulin-sensitive than in the lean insulin-resistant men (1.90 +/- 0.4 vs. 4.35 +/- 1.21 ng/ml, P < 0.05) despite identical body composition. Plasma leptin in the obese men (9.27 +/- 1.4 ng/ml) was significantly higher than values in the two lean groups (P < 0.01). Marked alterations in plasma glucose and insulin concentrations induced by glucose and tolbutamide injection did not cause any change in plasma leptin levels. These results demonstrate that insulin resistance is associated with elevated plasma leptin levels independent of body fat mass. However, plasma insulin itself does not acutely regulate leptin production.

Validity of a new portable indirect calorimeter: the AeroSport TEEM 100.

The purpose of this study was to compare oxygen uptake (VO2) values collected with a new portable indirect calorimeter (AeroSport TEEM 100 Metabolic Analysis System) against a more traditional large calorimeter system that has been reported to be valid and reliable (SensorMedics 2900 Metabolic Measurement Cart). Minute ventilations ranging from rest up to heavy exercise were compared with simultaneous measurements from a 120-1 Tissot gasometer. Each of the three TEEM 100 pneumotachs were tested. Three hundred and sixty-one separate ventilation tests were performed using the low-flow, medium-flow, and high-flow heads of the portable calorimeter. For each of the pneumotachs, the correlation between the portable calorimeter values and the gasometer values exceeded r = 0.94. The standard error of estimate for the low-medium- and high-flow pneumotach were 5.96, 4.89 and 9.0%, respectively, expressed relative to the mean gasometer value. Simultaneous measurements of VO2 using the portable calorimeter and the SensorMedics 2900 unit were compared during rest and at work rates starting at zero watts, increasing by 25 W to 150 W. Each work rate was of 4 min duration. The average of data from minutes 3 and 4 were used in all analyses. There was very close agreement between the two metabolic measurement systems. Except at the 100-W work rate, where the VO2 difference was small (3.9%), yet statistically significant, all of the other differences in VO2 were small and non-significant. The scatter plot of VO2 for the SensorMedics versus the portable Aero-Sport calorimeter revealed close agreement; the correlation was r = 0.96, (SEE = 3.95%).(ABSTRACT TRUNCATED AT 250 WORDS)

Evidence for distinctive and intrinsic defects in insulin action in polycystic ovary syndrome.

Women with PCO have a unique but poorly characterized disorder of insulin action. Obese (n = 16) and nonobese (n = 14) PCO women and age- and weight-matched normal, nondiabetic ovulatory women (obese, n = 15; nonobese, n = 17) had insulin action determined in vivo with sequential multiple insulin dose euglycemic clamps and in isolated abdominal adipocytes to clarify the mechanisms of insulin resistance. PCO resulted in significant increases in the ED50 insulin for glucose utilization in vivo (P less than 0.001) and in adipocytes (P less than 0.01), without significant changes in adipocyte insulin-binding sites. PCO also resulted in significant decreases in maximal insulin-stimulated rates of glucose utilization in vivo (P less than 0.01) and in adipocytes (P less than 0.01). Obesity resulted in smaller decreases in insulin sensitivity than PCO (ED50 insulin, P less than 0.001 in vivo and P less than 0.05 in adipocytes), but greater decreases in insulin responsiveness (Vmax, P less than 0.001 in vivo and in adipocytes). The ED50 insulin for suppression of HGP was increased only in obese PCO women (P less than 0.001), and the interactions between PCO and obesity on this parameter were statistically significant. No significant correlations between androgen or estrogen levels and adipocyte insulin binding or action were found. Because insulin binding was not changed, we conclude that the major lesion causing insulin resistance in PCO is a striking decrease in insulin sensitivity secondary to a defect in the insulin receptor and/or postreceptor signal transduction. PCO also is associated with modest but significant decreases in glucose transport. These defects in insulin action appear to represent intrinsic abnormalities that are independent of obesity, metabolic derangements, body fat topography, and sex hormone levels. Conversely, changes in hepatic insulin sensitivity appear to be acquired with obesity.

Postprandial thermogenesis at rest and postexercise before and after physical training in lean, obese, and mildly diabetic men.

To determine the independent impact of physical training on postprandial thermogenesis at rest and after 1 hour of cycling at 100 W, 10 lean (15% +/- 1% body fat), 10 obese (33% +/- 2% fat), and six obese diet-controlled, type II diabetic men (34% +/- 4% fat) underwent 12 weeks of vigorous cycle ergometer training (4 h/wk at approximately 70% of maximum oxygen consumption [VO2max]) while maintaining body weight and composition. Body weight was held constant by refeeding the energy expended in each training session. Cardiorespiratory fitness increased by approximately 27%, but body weight and fat did not change. Before and at least 4 days after the last exercise session, energy expenditure was measured for 3 hours under four conditions: (1) rest, no meal; (2) rest, after a 720-kcal mixed meal; (3) postexercise after 1 hour cycling, no meal; and (4) postexercise, meal after exercise. The thermic effect of food was calculated as postprandial minus postabsorptive energy expenditure at rest and postexercise (kcal/3 h). Before and after training, the thermic effect of food during rest was lower in obese than in lean men, and lower in diabetic than in obese men (P less than .05). Thermogenesis was improved after short-term exercise in obese and diabetic men compared with that at rest, but was not normalized (P less than .05 for lean v obese, diabetic men). A significant effect of training on thermogenesis was due to a small but significant increase after training for diabetic men under the postexercise condition. Thus, while short-term exercise enhances but does not normalize thermogenesis in obese and diabetic men, long-term exercise training leading to increased cardiorespiratory fitness, in the absence of changes in body composition, leads to a small increase in thermogenesis in diabetic men, which manifests only after a short period of exercise.

Reliability of the measurement of postprandial thermogenesis in men of three levels of body fatness.

To determine the reliability of the measurement of postprandial thermogenesis by indirect calorimetry and to clarify further the relationship of obesity to thermogenesis in men, the thermic effect of a 720-kcal, mixed liquid meal was compared in 13 lean men (mean +/- SEM, 11.2% +/- 1.4% body fat), 10 average men (22.4% +/- 1.6% body fat), and 12 obese men (33.4% +/- 1.6% body fat) on two occasions. Resting metabolic rate (RMR) was measured for 3 hours: (1) in the fasted state, and (2) after a 720-kcal mixed liquid meal, on two occasions. The thermic effect of the meal, calculated as the postprandial energy expenditure minus the fasting RMR (kcal/3h), was greater for the lean and average men than for the obese men during both trials (P less than .001), but was only marginally different between the lean and average groups (P = .16). The mean values for the two trials were similar and the measurement of thermogenesis was highly reproducible with a reliability coefficient of r = .932 (P less than .001). Across all groups, thermogenesis correlated strongly with percent body fat (r = -.64, P less than .01), but within the average men, thermogenesis was uncorrelated with percent body fat (r = .09) but highly correlated with the glucose response to the meal (r = -.75, P less than .05). Thus, factors other than body fatness, such as insulin sensitivity, may determine thermogenesis within this heterogeneous middle group.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of exercise mode and intensity on postprandial thermogenesis in lean and obese men.

To characterize further the impact of exercise before a meal on thermogenesis, the effects of exercise intensity and mode and the duration of the effect of exercise on the thermic effect (TEF) of a 720-kcal mixed meal were compared in 10 lean and 10 obese men (16 +/- 1 vs. 34 +/- 2% fat). In study A, TEF (kcal/3 h) was significantly greater for the lean than the obese men during rest and immediately after 1 h of cycling at 50 and 100 W. TEF was significantly greater after both exercise intensities than during rest for the obese men, but exercise had no effect on TEF in the lean men. In study B, TEF was significantly greater for the lean than the obese men during rest and immediately after 1 h of leg cycling at an O2 consumption of 1.09 l/min but only marginally different after 1 h of arm exercise at the same O2 consumption (P = 0.15). For the obese men, TEF was greater after arm than leg cycling and greater after leg cycling than at rest (P less than 0.01), but TEF was not different among the three conditions for the lean men. In study C, TEF was compared at rest and immediately and 24 h after 1 h of cycling at 100 W. TEF was greater for the lean than the obese men under all conditions (P less than 0.05). For the obese but not the lean men, TEF was greater both immediately after and on the day after exercise than at rest (P less than 0.01). Thus, acute exercise improves but does not normalize the blunted TEF in obesity; a minimally intense bout of exercise is needed to improve TEF; exercise mode alters thermogenesis in the obese men, even at a fixed intensity; and TEF in the obese men is enhanced for as long as 24 h after exercise.

Independent effects of obesity and insulin resistance on postprandial thermogenesis in men.

The putative blunted thermogenesis in obesity may be related to insulin resistance, but insulin sensitivity and obesity are potentially confounding factors. To determine the independent effects of obesity and insulin resistance on the thermic effect of food, at rest and after exercise, lean and obese men were matched at two levels of insulin sensitivity determined by insulin-stimulated glucose disposal (milligrams per kilogram fat-free mass [FFM] per minute) during the euglycemic, hyperinsulinemic (40 mU/m2.min) clamp: 5.4 mg/kg FFM for the lean and obese groups with low insulin sensitivity, and 8.1 mg/kg FFM for the groups with high insulin sensitivity. The two lean groups were matched for percent fat (approximately 15 +/- 1% fat), as were the two obese groups (approximately 33 +/- 2% fat). Energy expenditure was measured for 3 h in the fasting state and for 3 h after a 720-kcal mixed meal, each at rest and immediately after 1 h of cycling at 100 W. The thermic effect of food (TEF) was calculated as the postprandial minus fasting energy expenditure (kcal/3 h) during rest and after exercise. During rest, TEF was blunted by both obesity (24 +/- 5 and 34 +/- 6 kcal/3 h for obese groups with low and high insulin sensitivity vs. 56 +/- 6 and 74 +/- 6 kcal/3 h for the lean groups with low and high insulin sensitivity; P less than 0.01 lean vs. obese) and insulin resistance (insulin-resistant less than insulin-sensitive, at both levels of obesity; P less than 0.01). After exercise, TEF was also impaired in the obese (47 +/- 6 and 44 +/- 5 kcal/3 h for the insulin-resistant and -sensitive groups) and in the lean insulin-resistant (55 +/- 5 kcal/3 h), compared with the lean insulin-sensitive men (71 +/- 3 kcal/3 h), P less than 0.01. Compared with rest, TEF after exercise was improved, but not normalized, in both obese groups (P less than 0.05), but unchanged in the lean groups. These results suggest that both insulin resistance and obesity are independently associated with impaired TEF at rest, but the responsiveness of thermogenesis to exercise before a meal is related to the obese state and not independently to insulin resistance per se.

Effect of exercise training on insulin sensitivity and glucose metabolism in lean, obese, and diabetic men.

To clarify the impact of vigorous physical training on in vivo insulin action and glucose metabolism independent of the intervening effects of concomitant changes in body weight and composition and residual effects of an acute exercise session, 10 lean, 10 obese, and 6 diet-controlled type II diabetic men trained for 12 wk on a cycle ergometer 4 h/wk at approximately 70% of maximal O2 uptake (VO2max) while body composition and weight were maintained by refeeding the energy expended in each training session. Before and 4-5 days after the last training session, euglycemic hyperinsulinemic (40 mU.m2.min-1) clamps were performed at a plasma glucose of 90 mg/dl, combined with indirect calorimetry. Total insulin-stimulated glucose disposal (M) was corrected for residual hepatic glucose output. Body weight, fat, and fat-free mass (FFM) did not change with training, but cardiorespiratory fitness increased by 27% in all groups. Before and after training, M was lower for the obese (5.33 +/- 0.39 mg.kg FFM-1.min-1 pretraining; 5.33 +/- 0.46 posttraining) than for the lean men (9.07 +/- 0.49 and 8.91 +/- 0.60 mg.kg FFM-1.min-1 for pretraining and posttraining, respectively) and lower for the diabetic (3.86 +/- 0.44 and 3.49 +/- 0.21) than for the obese men (P less than 0.001). Insulin sensitivity was not significantly altered by training in any group, but basal hepatic glucose production was reduced by 22% in the diabetic men. Thus, when intervening effects of the last exercise bout or body composition changes were controlled, exercise training per se leading to increased cardiorespiratory fitness had no independent impact on insulin action and did not improve the insulin resistance in obese or diabetic men.

Physiologic responses to playing a video game.

The displacement of sports and other physical activities by television and video may contribute to the associations among television viewing, obesity, and reduced physical fitness. Because video games are widely played by children and adolescents, we assessed the metabolic and cardiovascular responses to video game playing. Heart rate, blood pressure, and oxygen consumption were measured serially over 30 minutes in 32 males and females aged 16 to 25 years (mean +/- SEM, 20 +/- 1 years) while they played the "Ms Pac-Man" video game under standard laboratory conditions and compared with measurements made in a standing but inactive position. Playing the video game significantly increased heart rate, systolic and diastolic blood pressure, and oxygen consumption. Energy expenditure increased from 6.08 +/- 0.24 kJ/min while the subjects stood inactive to 10.94 +/- 0.49 kJ/min while they played. The increase in metabolic rate and cardiovascular stimulation was similar in magnitude to mild-intensity exercise.

Estimation of extracellular and total body water by multiple-frequency bioelectrical-impedance measurement.

This study evaluated a new technology of bioelectrical-impedance (BI) measurement that makes use of multiple frequencies (5, 50, and 100 kHz) for estimation of extracellular and total body water. In 36 healthy males, resistance and reactance at three frequencies were compared with extra-cellular water (ECW) and total body water (TBW) determined by isotope dilution. ECW was best predicted by resistance measured at 5 kHz, corrected for height and weight (R = 0.930, SEE = 1.94 L) whereas TBW was best predicted by resistance at 100 kHZ and weight (R = 0.947, SEE = 2.64 L). Cross-validation analysis on two randomly selected subsets (n = 18 each) indicated that the prediction equations were reproducible and valid. Thus, BI at dual frequencies is valid for determination of body-water compartments and may be useful in the nutritional assessment of patients in whom body water and hydration is of clinical concern.

Thermic effect of a meal over 3 and 6 hours in lean and obese men.

Controversy regarding defective postprandial thermogenesis in obesity may partly be due to methodological factors such as duration of measurement. To clarify further the role of blunted thermogenesis in obesity, the thermic effect of food was compared in seven lean (mean +/- SEM, 15.7% +/- 1.5% body fat, by densitometry) and seven obese men (37.3% +/- 3% fat) over 3 and 6 hours. The groups were matched for age (35 +/- 2 and 33 +/- 2 years for the lean and obese groups; range, 25 to 39 years), fat-free mass (FFM), and aerobic fitness. Resting metabolic rate (RMR) was measured by indirect calorimetry for 6 hours on two mornings, in randomized order: (1) after a 720-kcal liquid mixed meal, which was 24% protein, 21% fat, and 55% carbohydrate; and (2) in the postabsorptive state. The thermic effect of food, calculated as postprandial minus postabsorptive RMR, was significantly greater for the lean than obese men for the first 3 hours of measurement (67 +/- 6 v 49 +/- 3 kcal/3 hours; P less than .01). During the second 3 hours, the thermic effect of food was marginally, but not significantly, greater for the lean than obese men (34 +/- 8 v 20 +/- 4 kcal/3 hours; P = .10, NS). Over the entire 6 hours, the thermic effect of food was significantly greater for the lean than obese men (100 +/- 12 v 69 +/- 5 kcal/6 hours; P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Resting metabolic rate and postprandial thermogenesis in polycystic ovarian syndrome.

To determine whether the high frequency of obesity in women with polycystic ovary syndrome (PCO) is related to a defect in energy expenditure, resting metabolic rate (RMR) and the thermic response to a standard meal were compared in 10 obese PCO women, nine obese but otherwise normal women, and 11 lean women. All groups were matched with respect to age and fat-free mass and the two obese groups were matched for degree of obesity. RMR was measured by indirect calorimetry for 3 h on two days: (1) in the postabsorptive state; and (2) after a 720 kcal (3014 kJ) liquid mixed meal. The thermic effect of food, calculated as 3 h postprandial minus fasting RMR, was significantly greater for the lean [52.9 +/- 5.5 kcal/3 h (221 +/- 23 kJ/3 h)] than the obese [17.2 +/- 5.1 kcal/3 h (72 +/- 21 kJ/3 h)] and the PCO women [22.8 +/- 5.2 kcal/3 h (95 +/- 22 kJ/3)], P less than 0.001). The thermic effect of food was negatively related to percent body fat (r = -0.694, P less than 0.001). Resting metabolic rate did not differ significantly among the three groups, and was strongly related to fat-free mass (r = 0.687, P less than 0.001). These results confirm previous reports of blunted thermogenesis in obese individuals, but provide no evidence of altered resting metabolic rate or postprandial thermogenesis in women with PCO compared with normal women of similar degree of obesity.