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

The relationship between the resting response to CO2 rebreathing and the ventilatory response to CO2 production during exercise was examined in 20 healthy untrained male subjects and in six patients with obesity hypoventilation syndrome. Patients were chosen because of a severely reduced response to CO2 rebreathing. There was no correlation between the CO2 rebreathing response and the exercise ventilatory response in the normal subjects, the patients, or in the group considered as a whole. This lack of correlation could not be accounted for by differences in ventilatory and occlusion pressure responses nor by reporting responses as a function of a change in hydrogen ion concentration. The independence of the CO2 rebreathing response and the exercise ventilatory response suggests the CO2 rebreathing response does not measure the relevant parameters of ventilatory control during exercise.
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PMID:CO2 rebreathing and exercise ventilatory responses in humans. 642 45

30 women, aged between 21 and 52, with 2nd and 3rd grade obesity were investigated. Total lipids, total cholesterol, HDL cholesterol, tryglicerides and lipoprotein electrophoretic fractions from blood plasma were determined. The subjects were tested at a submaximal exercise intensity of a triangular type on the ergometric bicycle, starting from zero Watt to a progressive increasing load of 10 Watt/min., till the maximal optimal heart rate was reached. The heart rate, blood pressure, CO2 produced and O2 consumption were determined at rest, during exercise at each step, and in the recovery period, predicted the maximum oxygen consumption, evaluated by the Astrand method. The subjective sensation concerning the effort was taken into consideration, based on the modified Borg scale and adaptability to exercise was evaluated, expressed by the "adaptability coefficient" (AC). The index of correlation between the plasma lipid fractions and AC was also determined. Lipidograma showed modifications of 94.44 percent of which 27.77 percent belonged to type IV of H-LP. AC diminished to 50.2 percent as opposed to the ideal values; the maximum oxygen consumption was diminished as well, with an important functional aerobic impairment. There was not found a statistically significant correlation between plasma lipid fractions and AC.
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PMID:Lipidogram structure and the exercise capacity in obesity. 642 82

Obesity, because it alters the relationship between the lungs, chest wall, and diaphragm, has been expected to alter respiratory function. We studied 43 massively obese but otherwise normal, nonsmoking, young adults with spirometry, lung volume measurement by nitrogen washout, and single-breath diffusing capacity for carbon monoxide (DLCO). Changes in respiratory function were of two types, those that changed in proportion to degree of obesity--expiratory reserve volume (ERV) and DLCO--and those that changed only with extreme obesity--vital capacity, total lung capacity, and maximal voluntary ventilation. When compared with commonly used predicting equations, we found that mean values of subjects grouped by degree of obesity were very close to predicted values, except in those with extreme obesity in whom weight (kg)/height (cm) exceeded 1.0. In 29 subjects who lost a mean of 56 kg, significant increases in vital capacity, ERV, and maximal voluntary ventilation were found, along with a significant decrease in DLCO. Because most subjects fell within the generally accepted 95% confidence limits for the predicted values, we concluded that obesity does not usually preclude use of usual predictors. An abnormal pulmonary function test value should be considered as caused by intrinsic lung disease and not by obesity, except in those with extreme obesity.
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PMID:Effects of obesity on respiratory function. 661 44

Genetically lean and obese pigs of 27 kg body weight were individually fed at varying levels of intake. During the first 5 weeks (period 1) the pigs on the high plane nutrition (H) gained 19 kg, those on the medium plane (M) gained 7 kg and those on the low plane (L) lost 5 kg. During the second 5 weeks (period 2) the M pigs gained an additional 7 kg (MM), whereas the period 1 H pigs were fed to lose 5 kg (HL) and the period 1 L pigs were fed to gain 19 kg (LH). All pigs were targeted to weigh 41 kg at the end of 10 weeks. Subcutaneous adipose tissue samples were obtained by biopsy from each pig on day 28 and day 63 of the experiment, i.e., after 4 weeks of feeding a particular level of intake in each period. In vitro glucose metabolism to CO2, total lipids and glyceride fatty acids as well as basal and epinephrine-stimulated lipolytic rates were assessed. Obese pigs had greater cell size and lipogenic and lipolytic rates than lean pigs. During both periods the glucose metabolism rates paralleled the plane of nutrition, i.e., the low intake level yielded low rates and the high intake level yielded high rates. The lipolytic activities were refractory to the plane of nutrition. Finally the less muscular, obese and more muscular, lean pigs presented similar qualitative metabolic responses to their planes of nutrition, although the quantitative responses were divergent.
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PMID:Effect of plane of nutrition on adipose tissue lipid metabolism in genetically obese and lean pigs. 672 56

Adipose tissue slices were prepared from middle subcutaneous or perirenal adipose tissue excised from pigs of different ages (and obesity) and incubated with [U-14C]glucose. After incubation, the slices were fixed with osmium tetroxide and separated into diameter ranges of 20--63, 63--102, and 102--153 microgram, respectively. Following determination of cell size and number, the fixed adipocytes were decolorized with H2O2 prior to quantification of glucose conversion to total lipid, glyceride fatty acids, glycerideglycerol, and CO2. Glucose conversion to total lipid or CO2 was unaffected by the presence of purified porcine insulin (0, 10, 100, 1000, and 100,000 microM/ml). Within animals, adipocytes of different sizes were not different with regard to insulin sensitivity. Within a weight (age) group, conversion of glucose to total lipid (insulin present) or to glyceride fatty acids and glyceride-glycerol (insulin absent) per cell was significantly greater in large adipocytes compared to small adipocytes, regardless of the group examined. With increasing weight or age, there was a markedly decreased conversion of glucose to total lipid and glyceride fatty acids among adipocytes of similar size within a cell-size fraction. The diminution in glucose metabolism was greater (as a percentage) in 20--63 microgram adipocytes than for 63--102 or 102--153 microgram adipocytes. However, for all cell-size fractions there was a marked decrease in glucose conversion to fatty acids. Glyceride-glycerol synthesis was impaired in adipocytes from older pigs, but the decrease was less than observed for glyceride fatty acid synthesis.
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PMID:Effects of cell size and animal age on glucose metabolism in pig adipose tissue. 678 14

Ketone body production and oxidation of 14C fatty acids to CO2 were measured in hepatocytes isolated from lean and obese Zucker rats. The oxidation of [1-14C]octanoate, [1-14C]palmitate and [1-14C]palmitoyl carnitine to 14CO2 was 50%--70% less in obese than in lean rats. Although ketone body production in hepatocytes from both lean and obese rats was increased by fasting, there was a significantly lower rate of ketone body production in hepatocytes from obese rats. Ketone body production was reduced to a comparable extent by increasing the glucose concentration in the incubation media of hepatocytes from both lean and obese rats. Glucagon and carnitine increased ketogenesis and the effect were additive and similar in lean and obese rats. These data suggest that beta-oxidation and ketogenesis are suppressed in the obese Zucker rat, and further that ketone bodies can be modulated similarly in hepatocytes from lean and obese rats by nutritional and hormonal intervention. It is postulated that the decreased beta-oxidation and ketone body production may play a role in the development or maintenance of obesity in the Zucker rat.
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PMID:Oxidation and ketogenesis in hepatocytes of lean and obese Zucker rats. 680 48

To define the roles of mechanical loading, respiratory neuromuscular control, and sleep apnea in the pathogenesis of obesity hypoventilation, respiratory muscle drive and output, assessed by diaphragmatic electromyogram (EMGdi) and mouth occlusion pressure (P 0.15), respectively, were determined during CO2 chemostimulation in nonobese volunteers who were subjected to abdominal mass loading, and in three groups of markedly obese patients: eucapnic obese without sleep apnea (O), eucapnic obese with sleep apnea (OSA), and hypercapnic obese with sleep apnea (OH). The P0.15 responses were decreased in OSA and OH, but the EMGdi responses were not significantly different from those in control subjects. In O patients EMGdi responses were significantly greater than those in control subjects as well as those in OSA and OH patients. EMGdi and P0.15 responses increased in all nonobese subjects when they were subjected to mass loading. We conclude that both OSA and OH patients were equally unable to develop the expected increase in respiratory muscle drive and output. The presence of sleep apnea, possibly by causing nocturnal hypoxemia and/or sleep fragmentation, may result in impaired mass load compensation and predispose obese patients to develop hypercapnia.
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PMID:Mass loading, sleep apnea, and the pathogenesis of obesity hypoventilation. 681 71

The aim of the investigation was to see whether a defect in energy expenditure could be found in the Zucker rat at the onset of obesity. Obese (fa/fa) and lean (Fa/fa) 7-day-old pups were studied at three ambient temperatures. At 33 degrees C fa/fa pups showed a reduction in oxygen consumption, respiratory CO2 production, in vivo oxidation of injected [1-14C]palmitic acid, as well as in core temperature. When the pups were kept at 28 degrees C, the difference between genotypes was considerably accentuated, thus indicating a subnormal thermogenic response of the fa/fa pups to a mildly cold environment. At 20 degrees C, however, the metabolic rates dropped to the same low level, and the core temperature equilibrated with ambient temperature in both genotypes. The results demonstrate that the 1-wk-old fa/fa pup has a defect in thermoregulatory thermogenesis. The magnitude of the deficit in energy expenditure was more than adequate to account for the 50% greater fat content of 7-day-old fa/fa pups.
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PMID:Evidence of a defect in energy expenditure in 7-day-old Zucker rat (fa/fa). 688 26

The normoxic ventilatory drive contributes to the normal level of ventilation, and the hypoxic ventilatory drive contributes to the maintenance of adequate gas exchange in the presence of ventilation/blood flow maldistribution and increased mechanical load to breathing. This respiratory drive arises principally from stimuli at the carotid chemoreceptors. The reflex cardiovascular responses to hypoxia also contribute to the delivery of O2 to vital organs, and their efficacy depends on the integrity of the respiratory response and the autonomic nervous system as well as the function of the vascular system. Prolonged exposure to hypoxemia from altitude, cyanotic congenital heart disease, and chronic pulmonary disease impair the ventilatory response to hypoxia. In addition, the respiratory and cardiovascular responses to hypoxemia are impaired by familial or acquired abnormalities of the autonomic effector system. There is growing evidence that impaired respiratory response to hypoxemia is a major factor in recurrent respiratory failure in obesity, obstructive pulmonary disease, idiopathic or familial "hypoventilation," and contributes to disturbances in oxygenation during sleep [152, 189, 192, 202]. Although the ventilatory response to hypoxemia was traditionally thought to be resistant to the effects of inhalational anesthetics, barbiturates, and narcotics, there is abundant evidence that in fact the ventilatory response to hypoxia is more sensitive to depression by drugs than the ventilatory response to CO2. In addition, the hemodynamic responses to hypoxia are modified by anesthesia and anesthetic techniques. The clinical implications of these observations are wide. The ventilatory and cardiovascular response to hypoxemia will be altered, and usually depressed by age, disease processes, premedicant and anesthetic drugs, and autonomic blocking drugs. The cardiovascular responses will be modified indirectly by altered ventilatory control due to neuromuscular blocking drugs and controlled ventilation. Thus, not only will the responses to hypoxemia be depressed by anesthesia but the early clinical hemodynamic signs will be modified or absent, or indeed the cardiovascular response will further impair oxygen delivery. Furthermore, it is not only anesthetic doses that impair the reflex respiratory responses, but also subanesthetic doses of inhalational anesthetics and premedicant doses of barbiturates and narcotics. Hence the patient in the perioperative period continues to have impaired respiratory response to hypoxemia. As anesthetic and surgical care extends to older patients, patients with systemic disease, and recipients of cardiovascular peripheral and central drugs, the clinical implications of the impairment of ventilatory and cardiovascular responses to hypoxia, and the maintenance of organ and system function, escalate. Only a few hesitant steps have been taken into this vast arena of clinical and experimental research.
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PMID:Respiratory and cardiovascular responses to hypoxemia and the effects of anesthesia. 702 55

A mixture of [U-14C]amino acids was injected intraperitoneally into fed obese and non-obese Zucker rats that were either growing (8 weeks of age) or at maintenance (17 weeks of age). The metabolic fate of the dietary amino acid pool was determined from the distribution of 14C into carcass lean tissue, carcass lipid, CO2 and urine. In a second experiment, urinary and skeletal muscle 3-methylhistidine content was used to compare the rate of muscle protein breakdown between phenotypes at 8 weeks of age. The obese rat deposited a smaller proportion of its dietary amino acid pool in lean tissue compared with its non-obese control during growth and at maintenance. Obese rats incorporated a greater proportion of dietary amino acids into body lipid at both ages and metabolized a greater proportion of dietary amino acid carbon to CO2 during growth. At 8 weeks of age, the obese rat had a higher fractional rate of muscle protein breakdown and was less efficient at retaining amino acids that had been incorporated into muscle. These latter differences were major factors in producing the variation in dietary amino acid utilization and protein accretion between growing obese and non-obese rats. At maintenance, the variation in dietary amino acid utilization between phenotypes was due principally to the smaller body protein mass of the obese animals.
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PMID:Comparative amino acid and protein metabolism in obese and non-obese Zucker rats. 741 Dec 43


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