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

The effects of varying levels of exercise on oxygen uptake, CO2 production, blood pressure, arterial blood gasses, and arterial concentrations of glucose, insulin, and growth hormone were examined in ten normal weight and ten moderately overweight young men. At comparable external work loads with a bicycle ergometer, the lean men required less oxygen than the obese men. When oxygen uptakes were matched during exercise on a treadmill, the lean men were walking on a steeper grade or at a higher rate than the obese men. The efficiency of exercise as assessed by the relation between oxygen uptake and work did not differ between the two groups. Blood pressure rose more in the obese during exercise than in the lean. The fall in lactate and rise in bicarbonate was of greater magnitude during cycle ergometry than during treadmill exercise. Obese and lean men, however, showed similar changes. With each level of exercise, there was a fall in arterial insulin levels, but the concentrations in the blood of overweight men always remained significantly above that of the normal men. Growth hormones tended to be higher in the normal weight men, but the differences were usually not significant, and there was no significant rise with exercise in either group until the highest levels of work were achieved. Glucose concentrations tended to be higher in the obese men, but fell to constant levels in both groups during exercise. Blood pressure rose to a greater extent in the overweight men during exercise.
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PMID:Some respiratory and metabolic effects of exercise in moderately obese men. 1 81

Several characteristics of the binding of insulin and glucagon to human circulating mononuclear leukocytes have been studied. Functional analysis (latex bead ingestion) revealed that cell mixtures, as prepared according to Boyum and used generally in studies of insulin resistance in humans, consist of 20-29% phagocytic monocytes, with the remainder being lymphocytes. Partial separation of monocytes from lymphocytes on columns of Sephadex G-10, followed by correlation of insulin binding with cell type, confirms that the monocyte is the binding species. Insulin influenced neither glucose uptake nor the further conversion of glucose to lipids and CO2 by the leukocytes. The transport of alpha-aminoisobutyrate, a nonmetabolizable amino acid, into these cells was also unaffected by insulin. Monocyte/lymphocyte mixtures specifically bound glucagon and prostaglandin E1. At physiological concentrations of these hormones, steady states were reached in 15 min and 45 min, respectively. In contrast to the 8-10-fold increases in cellular cyclic AMP produced by prostaglandins, the effect of glucagon was very small but apparently real. Under appropriate preincubation conditions, sodium azide and iodoacetamide inhibited phagocytosis and insulin binding in parallel. The binding of glucagon was unaffected by these agents. Although both antimycin A and actinomycin D inhibited phagocytosis of the monocytes, only the former inhibited insulin binding; there was only a slight effect on glucagon binding. We would conclude that the binding of insulin to human circulating monocytes, although reflective of insulin resistance in diabetes mellitus and obesity, may not be to traditional receptors. In contrast, the binding of glucagon to lymphocyte/monocyte mixtures may be to function-linked receptors.
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PMID:Hormone receptors: VI. On the nature of the binding of glucagon and insulin to human circulating mononuclear leukocytes. 20 May 11

The deposition of edidymal and perirenal fat, serum insulin levels, and insulin sensitivity of epididymal fat, expressed as the insulin-stimulated production of CO2 from glucose, were determined in Wistar rats fed diets containing either 54% starch or sucrose ad libitum or pair-fed in meals. Regardless of the pattern of feeding, sucrose-fed rats deposited more adipose tissue per 100 g body weight and exhibited less insulin sensitivity than did starch-fed rats. Significant differences in adipose tissue weights were not always accompanied by significant differences in body weights. Meal-fed rats deposited less adipose tissue and showed a greater insulin sensitivity than did ad libitum rats fed the same carbohydrate. However, when changes in feeding pattern negated the difference in adipose weights there was no difference in the insulin sensitivity of the meal-fed and ad libitum-fed rats. Rats consuming the sucrose diet generally exhibited significantly higher fasting serum insulin levels than did rats consuming the starch diet. The serum insulin values tended to be higher in the ad libitum-fpididymal tissue from the meal-fed and starch-fed rats tended to be greater than that of the sucrose-fed or ad libitum-fed rats, respectively, suggesting differences in adipocyte composition. Since obesity, insulin insensitivity, and hyperinsulinism are associated with an impairment of glucose tolerance, the observed metabolic effects of dietary sucrose are considered to be undesirable.
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PMID:Insulin sensitivity and adipose tissue weight of rats fed starch or sucrose diets ad libitum or in meals. 83 76

Genetically obese Zucker rats, ob/ob mice and non-obese littermates were fed low carbohydrate (2%, 48%, and 50% of energy as carbohydrate, protein, and fat, respectively) and control (60%, 19%, and 21%, as carobhydrate, protein, and fat) diets. The oxidation of the energy components of these diets was measured by adding D-[U-14C]glucose, L-[U-14C]glutamic acid, and glyceryl tri-[1-14C]oleate to test meals given intragastrically and collecting respiratory CO2 for 4 hours. The animals responded to the low carbohydrate diet by oxidizing less glucose and more glutamic acid, but these amounts were proportional to dietary carbohydrate and protein composition, In contrast, the animals oxidized both higher amounts and percentages of glyceryl trioleate when fed the low carbohydrate diet. Obese Zucker rats oxidized less fat than non-obese rats when fed both diets, while obese mice oxidized fat to the same extent as non-obese mice. Feeding the low carbohydrate diet significantly increased body weight in the obese mice, but not in obese rats and non-obese mice and rats. The effect of obesity and the low carbohydrate diet on food intake, serum glucose and lipid values and CO2 production are also reported.
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PMID:Energy utilization of a low carbohydrate diet fed genetically obese rats and mice. 83 91

We measured hypoxic and hypercapnic ventilatory drive in a 64 year old woman with acute respiratory failure, congestive heart failure and obesity when she was in remission. She had a ventilatory response to carbon dioxide (CO2) comparable to that in six obese women without hypoventilation but no ventilatory response to hypoxia or to vital capacity breaths of 15 per cent CO2 in N2. Following weight loss, her ventilatory response to CO2 increased but hypoxic ventilatory response to CO2 increased but hypoxic ventilatory drive remained absent. These findings indicate that attenuation of hypoxic ventilatory drive caused by loss of peripheral chemoreceptor function can be a predisposing factor in the development of acute respiratory failure associated with obesity.
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PMID:Acute respiratory failure and obesity with normal ventilatory response to carbon dioxide and absent hypoxic ventilatory drive. 86 Jul 28

A 3-year-old girl with a history of excessive weight gain from birth presented with obesity, somnolence, and cyanosis, characteristic of the Pickwickian syndrome. Obesity was familial and exogenous without endocrine or neurologic anomaly. Respiratory center sensitivity to carbon dioxide was normal. Excessive somnolence was due to the obesity, which during sleep caused airway obstruction, apnea, and awakening, finally resulting in sleep deprivation. The sleep apneas and the daytime somnolence disappeared with weight reduction, showing that obesity alone had been responsible for the disorder.
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PMID:Sleep apnea in a child with the pickwickian syndrome. 89 58

Abnormalities of the respiratory function are a common finding in adult obesity. In order to investigate the occurrence of similar facts in pediatric age, a group of 39 obese children (20 girls and 19 boys, aged from 7 to 15 years) whose weight excess for their height ranged from 25 to 105 p. 100 was studied and compared to a control group of normal children of similar ages. Lung volumes, blood gases, transfer factor of the lung for CO, dynamic lung compliance, total lung resistance and ventilatory response to CO2 have been studied. In these obese children by contrast to obese adults, the vital capacity and the residual volume were normal. The blood gases, the transfer factor for CO, the dynamic lung compliance and the total resistances of the lung were similar to those of the normal group. The respiratory patterns were normal in all children but one who had during a short time a periodic ventilation with short periods of breath-holding. The ventilatory response to CO2 of the obese children was decreased and a highly significant correlation was found between the individual values of the respiratory response to CO2 and the percentage of weight excess. Different hypotheses are discussed to explain these results.
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PMID:[Respiratory function at rest in obese children (author's transl)]. 90 64

A 29-year-old obese man had marked tonsillar hypertrophy, somnolence, hypoxemia, and hypercapnia. Endotracheal intubation followed by tracheostomy relieved the hypoventilation. Weight loss improved the arterial blood gas levels. Sequential upright and supine flow-volume loops were compatible with a fixed upper-airway obstruction (such as would occur) with enlarged tonsils) prior to tonsillectomy. Following surgery, the expiratory flow-volume curve was abnormal in the supine position, consistent with the additional diagnosis of posterior pharyngeal hypotonia. Thus, in this patient the unique combination of tonsillar hypertrophy, posterior pharyngeal hypotonia, obesity, and a depressed respiratory center led to retention of carbon dioxide.
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PMID:Tonsillar hypertrophy in an adult with obesity-hypoventilation syndrome. The use of the flow-volume loop. 97 91

A formula is derived for maintaining normocapnia during controlled ventilation using a circle system without carbon dioxide absorption. In a series of 70 patients, unselected in terms of age, sex, obesity, ASA status, body position during operation, type of anaesthetic administered or type of circle system used, it was found that a total fresh gas flow of 50 ml/kg body weight/min and a minute ventilation of 120 to 150 ml/kg body weight at a rate of 10 to 12/min achieved normocapnia. For moderate hypocapnia a total fresh gas flow of 60 ml/kg body weight/min and a minute ventilation of 120 ml/kg at a rate of 10-12/min is suggested.
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PMID:Normocapnic ventilation using the circle system. 99 Sep 83

Weanling male Sprague-Dawley rats received bilateral electrolytic lesions in the dorsomedial hypothalamic area by means of a direct cathodal current. Sham-operated rats served as controls. Ponderal and linear growth, obesity index, food intake, and several indices of intermediary metabolism of adipose tissue and muscle were measured. Cathodal lesions, as did anodal lesions reported on previously resulted in retardation of body weight, length, and food intake, while the obesity index remained in the normal range. Similarly, the metabolic data in adipose tissue and muscle are comparable to those from experiments in which dorsomedial lesions were placed by anodal current: incorporation of glucose into CO2 lipid, and glycogen of muscle tissue (diaphragm) were similar in DMN-lesioned rats and controls. The difference between anodal and cathodal lesions in this hypothalamic syndrome is a delay in the onset of hypophagia until about 30 days after the hypothalamic operation. The data support the concept that lesions in the hypothalamus, in general, exert their effect by destruction of neuronal assemblies, i.e., nerve cells and/or fiber tracts passing through the lesioned area.
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PMID:Production of the weanling rat dorsomedial hypothalamic syndrome by cathodal electrolytic lesion current. 101 1


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