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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Independent effects of obesity and insulin resistance on postprandial thermogenesis in men. 154 75

Female rats were assigned to dietary conditions as follows for 3.5 months: 1) Low-fat control (LFC); 2) Moderately high-fat control (HFC); 3) Alternation between restricted access to a low-fat diet and ad lib access to a very high fat diet (RA); 4) Unrestricted access to the same diets as RA (URA). Results indicate that: 1) HFC consumed the same energy as LFC, but showed a tendency to become heavier and fatter through greater food efficiency. 2) URA and LFC did not differ in body weight, food intake, body composition or energy efficiency. 3) Intake of the very high fat diet declined over time in the RA. 4) RA ate less total calories, weighed less than all other groups, and showed a tendency for decreased percentage body fat and increased percentage of weight gained due to FFM gained. Results provide no evidence that dieting and bingeing promote obesity or increased preference for dietary fat, and suggest that dietary restriction has greater impact on energy balance and body composition than does alternation of diet composition.
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PMID:Physiological effects of dieting and bingeing in rats. 174 42

The relationship of obesity and physical fitness (VO2max) to cardiopulmonary and metabolic function was examined in 132 healthy obese, nonsmoking men age 45-79. Obese men with higher VO2max had lower % body fat and waist-to-hip ratio (WHR) than obese men with low VO2max. The obese subjects with high WHR (upper body fat distribution) had higher systolic blood pressure, hyperinsulinemia and impaired glucose tolerance, lower high density lipoprotein cholesterol (HDL-C), and higher triglyceride (TG). VO2max (ml/kg FFM.min) was lower in the older men (r = -0.54, p less than .001), and 32% of the variation was accounted for by age and the one-second forced expiratory volume. Although pulmonary function was normal, 50% of the variability was predicted by age, height, and VO2max or WHR. Glucose tolerance and insulin correlated better with VO2max and indices of body composition than with age, while plasma TG and HDL-C correlated with body composition, not VO2max or age. Thus, while age affects the cardiopulmonary and metabolic function of obese older men, physical inactivity, obesity, and an abdominal body fat distribution (increased WHR) contributed significantly to their reductions in physiological function.
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PMID:Relationship of obesity and physical fitness to cardiopulmonary and metabolic function in healthy older men. 199 74

The immediate metabolic response to eating has been compared in a group of grossly obese subjects (W/H2 = 45) with that in lean controls (W/H2 = 22). Dietary intake of energy for obese subjects was based on their estimated basal energy expenditure for ideal body weight (given at an hourly rate of 3 X BMR over a 4-h period). Lean subjects were measured twice: control 1 with the same intake of energy as the obese in terms of ideal body weight and control 2 with the same energy intake in relation to each subject's measured resting energy expenditure (2.2 X REE). The changes in energy expenditure and nutrient disposal with the onset of eating have been assessed by a method of combined respiratory gas analysis and intravenous infusion of 13C-labelled leucine. Leucine kinetics were used to quantitate rapid changes in protein oxidation and to assess protein synthesis and degradation. 1) Total energy expenditure was 20-30 per cent greater in obese subjects than lean subjects in fasting and feeding. Energy expenditure expressed per kg fat-free mass, from D2O dilution, was similar in obese and lean subjects in both fasting (5.8 v. 5.5 kJ/kg FFM/h) and feeding [6.7 v. 6.3 (Control 2) kJ/kg FFM/h]. 2) The onset of eating was associated with increased carbohydrate and protein oxidation with decreased fat oxidation in both lean and obese individuals. In obese subjects, however, both the decrease in fat oxidation and the increase in protein oxidation were significantly smaller (P less than 0.05) than the corresponding increments in lean subjects (Control 2). 3) The rate of protein synthesis was significantly (P less than 0.05) higher in obese subjects both in the fasting state (99 v. 84 mumols leucine/kg FFM/h) and in the fed state [94 v. 67 (Control 2) mumols leucine/kg FFM/h]. The rate of protein degradation was also higher in obese individuals in fasting (117 +/- 6 v. 106 +/- 4 mumol leucine/kg FFM/h) and feeding [65 +/- 4 v. 54 +/- 6 (Control 2) mumol leucine/kg FFM/h] though these differences are not statistically significant (P greater than 0.05). 4) The observed differences between obese and lean individuals in protein and energy metabolism in the fasted state and in the immediate response to eating do not support a hypothesis of greater metabolic efficiency in obesity.
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PMID:Nutrient oxidation patterns and protein metabolism in lean and obese subjects. 222 98

The role of the sympathetic nervous system in free fatty acid (FFA) mobilization was assessed in this study. FFA turnover rate using 1-14C-palmitic acid and metabolic rate by using indirect calorimetry were measured in ten white and 12 Pima Indian males after an overnight fast and during propranolol infusion (120 micrograms/kg fat-free mass [FFM] bolus and 1.2 micrograms/kg FFM/min). Baseline FFA turnovers were similar in both racial groups and decreased similarly following propranolol infusion (-16% +/- 4%; P less than .001, n = 22). This decrease was greater in more obese subjects (decrease in FFA turnover v % body fat, r = -.59, P less than .01, n = 22). Propranolol also induced an increase in lipid oxidation, which was more marked in the subjects with a high ratio of abdomen to thigh circumference (A/T ratio) (r = .63, P less than .01, n = 22). On average the resting metabolic rate (RMR) was unchanged during propranolol infusion, but individuals with lower A/T ratio had greater decreases in RMR than subjects with higher A/T ratio (r = .48, P less than .05). Assuming that the change in FFA turnover following beta-blockade is proportional to the role that the catecholamines (and therefore the sympathetic nervous system) play in mobilization of FFA, the greater fall in FFA turnover after propranolol infusion in more obese subjects suggests that they have a higher basal sympathetic activity. Furthermore, the lack of decrease in metabolic rate in response to beta-blockade in persons with a high A/T ratio could be the reflection of an even greater SNS activity in individuals with central obesity.
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PMID:The effect of propranolol on free fatty acid mobilization and resting metabolic rate. 272 82

The purpose of this study was to validate the use of bioelectrical impedance in assessing human body composition and to explore the use of this technique in obesity. Eighty-seven adults varying widely in body composition (range: 8.8-59.0% body fat) underwent measurement of bioelectrical impedance and underwater weighing (density). Fat-free mass determined from density (FFMd) was compared with FFM estimated from bioelectric impedance according to previously published regression equations. Correlation coefficients were high at all levels of body fat (0.94-0.99) but impedance equations overestimated FFM compared with FFMd in subjects greater than 42% body fat. This effect was greatest in subjects greater than 48% body fat and a regression equation was derived for determination of FFM for these subjects. These data confirm the excellent agreement between body composition determined from bioelectrical impedance and density but suggest that caution should be used in applying existing regression equations to very obese subjects.
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PMID:Effect of obesity on bioelectrical impedance. 275 12

Metabolic and hemodynamic abnormalities have been separately described in obesity, and weight reduction is known to lead to some improvement in each. Our aim was to simultaneously assess metabolic and cardiovascular function in normotensive, normotolerant patients with moderate obesity (body mass index = 32.6 +/- 1.1 kg/m2) before and after weight loss. The obese were insulin resistant [37.4 +/- 4.8 mumol/min.kg FFM; P < 0.02 vs. 12 lean controls (50.6 +/- 2.6), on a euglycemic insulin clamp], secreted more insulin both in the fasting state and after oral glucose (70 +/- 10 vs. 48 +/- 6 nmol/mmol.L plasma glucose; P < 0.05), and had higher resting energy expenditure (4.62 +/- 0.18 vs. 4.00 +/- 0.23 kJ/min), systolic and mean blood pressure, stroke volume (87 +/- 8 vs. 67 +/- 4 mL/min; P = 0.05), and cardiac output. There was, however, no relationship between the metabolic and hemodynamic abnormalities. After a weight loss of 11 +/- 1 kg (approximately 15%), insulin sensitivity improved in proportion to the weight reduction, whereas insulin hypersecretion and high energy expenditure persisted. In contrast, all hemodynamic changes reverted to normal. We conclude that in moderate obesity, the metabolic and cardiovascular abnormalities are largely independent of one another; accordingly, weight loss affects them differentially. Partial weight normalization may provide sufficient cardiovascular protection.
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PMID:Metabolic and cardiovascular assessment in moderate obesity: effect of weight loss. 928 23

Insulin resistance and insulin hypersecretion are established features of obesity. Their prevalence, however, has only been inferred from plasma insulin concentrations. We measured insulin sensitivity (as the whole-body insulin-mediated glucose uptake) and fasting posthepatic insulin delivery rate (IDR) with the use of the euglycemic insulin clamp technique in a large group of obese subjects in the database of the European Group for the Study of Insulin Resistance (1,146 nondiabetic, normotensive Caucasian men and women aged 18-85 yr, with a body mass index (BMI) ranging from 15 to 55 kg.m-2). Insulin resistance, defined as the lowest decile of insulin sensitivity in the lean subgroup (608 subjects with a mean BMI of 29 kg.m-2). Insulin sensitivity declined linearly with BMI at an age- and sex-adjusted rate of 1.2 micromol.min-1.kg FFM-1 per BMI unit (95% confidence intervals = 1.0-1.4). Insulin hypersecretion, defined as the upper decile of IDR, was significantly (P<0.0001) more prevalent (38%) than insulin resistance in the obese group. In the whole dataset, IDR rose as a function of both BMI and insulin resistance in a nonlinear fashion. Neither the waist circumference nor the waist-to-hip ratio, indices of body fat distribution, was related to insulin sensitivity after adjustment for age, gender, and BMI; both, however, were positively associated (P<0.001) with insulin hypersecretion, particularly in women. In nondiabetic, normotensive obese subjects, the prevalence of insulin resistance is relatively low, and is exceeded by the prevalence of insulin hypersecretion, particularly in women with central obesity. In the obese with preserved insulin sensitivity, risk for diabetes, cardiovascular risk, and response to treatment may be different than in insulin resistant obesity.
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PMID:Insulin resistance and hypersecretion in obesity. European Group for the Study of Insulin Resistance (EGIR). 930 23

Childhood obesity represents an increasing dysmetabolic condition. The aim of our study was to evaluate the influence of Fat Mass (FM%) on Resting Metabolic Rate (RMR) and Respiratory Quotient (RQ) as indicator of substrate oxidation. FFM and FM were estimated by bioelectrical impedance analysis (BIA), using the Kushner equation. Resting metabolic rate was determined by open-circuit indirect calorimetry. The mean (SD) of RMR 1517.6 (236.8) was found to be different from predicted RMR 1470.6 (190) calculated using the Fleisch equations. The best predictors of RMR were weight (p = 0.000) and FFM (p = 0.000); whereas correlation between RMR and fat mass (FM%) was not significant. Therefore low RMR cannot be responsible of fat mass degree, in fact, it is not reduced in obese children. Different values of RQ were found suggesting different metabolic behaviours to oxidate substrates. These data indicate that genetics may play a significant role in the development of many types of obesity.
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PMID:[Basal metabolism and respiratory quotient in obese children]. 1033 39

Metabolically obese, normal-weight (MONW) individuals are a hypothesized subgroup of the general population. These normal-weight individuals potentially display a cluster of obesity-related features, although this has not been systematically tested in young women. We hypothesized that MONW young women would display higher levels of total and visceral fat and lower levels of physical activity than normal women. In a cohort of 71 healthy nonobese women (21-35 years old), we identified MONW women based on cut points for insulin sensitivity (normal = glucose disposal >8 mg x min(-1) x kg(-1) of fat-free mass [FFM], n = 58; impaired = glucose disposal <8 ml x min(-1) x kg(-1) of FFM, n = 13). Thereafter, we measured body composition (dual energy X-ray absorptiometry) and body fat distribution (computed tomography), cardiorespiratory fitness (VO2max on a treadmill), physical activity energy expenditure (doubly labeled water and indirect calorimetry), glucose tolerance (oral glucose tolerance test), serum lipid profile, and dietary intake. We found a higher body fat percentage (32 +/- 6 vs. 27 +/- 6%, P = 0.01) and higher subcutaneous (213 +/- 61 vs. 160 +/- 78 cm2, P = 0.03) and visceral (44 +/- 16 vs. 35 +/- 14 cm2, P < 0.05) abdominal adiposity in the MONW group versus the normal group. The MONW group showed a lower physical activity energy expenditure (2.66 +/- 0.92 vs. 4.39 +/- 1.50 MJ/day, P = 0.01), but no difference in cardiorespiratory fitness was noted between groups. In conclusion, despite a normal body weight, a subset of young, apparently healthy women displayed a cluster of risky phenotypic characteristics that, if left untreated, may eventually predispose them to type 2 diabetes and cardiovascular disease.
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PMID:Phenotypic characteristics associated with insulin resistance in metabolically obese but normal-weight young women. 1053 56


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