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

Correction of some risk factors of atherosclerosis was tried in 247 patients with neurocirculatory dystonia who received dietary sea polyunsaturated fatty acids (PUFA) or balneotherapy (carbon dioxide arsenic mineral baths). As shown by assessment of clinico-functional characteristics, response of the microcirculatory bed, lipid metabolism, dietary PUFA and carbon dioxide arsenic mineral water have a positive effect on arterial hypertension, obesity and hyperlipidemia and thus can be used for primary prophylaxis of atherosclerosis.
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PMID:[Atherosclerosis: feasibility of non-pharmacological correction of some risk factors]. 1023 42

Obesity results when energy intake exceeds energy expenditure. Naturally occurring genetic mutations, as well as ablative lesions, have shown that the brain regulates both aspects of energy balance and that abnormalities in energy expenditure contribute to the development of obesity. Energy can be expended by performing work or producing heat (thermogenesis). Adaptive thermogenesis, or the regulated production of heat, is influenced by environmental temperature and diet. Mitochondria, the organelles that convert food to carbon dioxide, water and ATP, are fundamental in mediating effects on energy dissipation. Recently, there have been significant advances in understanding the molecular regulation of energy expenditure in mitochondria and the mechanisms of transcriptional control of mitochondrial genes. Here we explore these developments in relation to classical physiological views of adaptive thermogenesis.
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PMID:Towards a molecular understanding of adaptive thermogenesis. 1076 52

Chemical control of breathing in obstructive sleep apnoea (OSA) patients has been studied by many authors. The results of previous studies, especially those dealing with hypoxic drive, are discordant. Respiratory responses were studied during hypercapnic and hypoxic stimulation in a group of 37 normocapnic patients with OSA during wakefulness. The diagnosis of OSA was established by standard polysomnography. These patients had increased apnoea/hypopnoea index (AHI; 51 +/- 22 (mean +/- SD)), obesity (body mass index (BMI) 32.4 +/- 5.6 kg.m-2) and normal lung function tests. The control group consisted of 14 healthy obese subjects (BMI 31.2 +/- 3.3 kg.m-2). Respiratory responses (ventilatory and mouth occlusion pressure (P0.1)) during hypercapnic and hypoxic rebreathing tests were measured with the use of computerized equipment. Respiratory responses during hypercapnic stimulation were similar to those in the control group (change in (delta) minute ventilation (V'E)/delta carbon dioxide tension (PCO2) 23.5 +/- 14.8 versus 22.3 +/- 10.0 L.min-1.kPa-1, delta P0.1/delta PCO2 4.6 +/- 3.6 versus 4.2 +/- 2.6 cmH2O.kPa-1). During isocapnic hypoxic stimulation in OSA patients the mean ventilatory response was higher than in the control group (delta V'E/delta arterial oxygen saturation (Sa,O2) 2.6 +/- 1.7 versus 1.7 +/- 0.7 L.min-1.%-1) but this difference was not statistically significant. Nevertheless, it was found that 13 (35%) OSA patients had increased ventilatory responses. The mean P0.1 response in OSA patients was higher but did not differ significantly from those in the control group (delta P0.1/delta Sa,O2) 0.43 +/- 0.38 versus 0.35 +/- 0.12 cmH2O.%-1). The results demonstrated that respiratory responses to chemical stimulation in awake normocapnic patients with obstructive sleep apnoea were in the normal range, similar to those in control obese subjects. During hypoxic stimulation some of them had increased ventilatory (35%) and mouth occlusion pressure (16%) responses.
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PMID:Respiratory responses to chemical stimulation in patients with obstructive sleep apnoea. 1094 66

To elucidate the role of serotonin in the maintenance of normal breathing and upper airway (UA) patency in obesity, we studied the effects of systemic administration of ritanserin, a serotonin (5-HT) 2A and 2C receptor antagonist, on ventilation (V E) during room air breathing and during hypoxic (10% O2) and hypercapnic (4% CO2) ventilatory challenges in awake young (6-8 wk) and older (7-8 mo) obese and lean Zucker (Z) rats. Older obese Z rats adopted a more rapid shallow breathing pattern compared with older lean rats. The administration of ritanserin (1 mg/kg intraperitoneally) to older obese rats resulted in a reduction in V E (439 +/- 35 [SD] to 386 +/- 41 ml/kg/min, p < 0.01), a decrease in respiratory rate, a prolongation of inspiratory time, and an increase in V O2 (16.4 +/- 1.7 to 18.2 +/- 1.9 ml/kg(0.75)/min, p < 0.05) during room air breathing. By comparison, it had little effect on ventilation in young lean and obese Z or older lean Z rats. Ritanserin also had no effect on ventilatory responses to either hypoxia or hypercapnia in young or older lean and obese Z rats. The collapsibility of the isolated UA was examined in older Z rats. The pharyngeal critical pressure (Pcrit) of older obese rats was significantly greater than that of lean rats (p < 0.05), indicating that obese rats have more collapsible UA than lean rats. The administration of ritanserin significantly increased Pcrit in older obese rats (-1.6 +/- 0.3 to -0.8 +/- 0.2 cm H2O, p < 0.01) and in lean rats (-3.1 +/- 1.0 to -2.4 +/- 0.6 cm H2O, p < 0.05). We suggest that the 5-HT(2A/2C) receptor subtype plays an important role in the maintenance of UA stability and normal breathing in obesity, and we speculate that older obese Z rats may have augmented serotonergic control of UA dilator muscles as a mechanism to prevent pharyngeal collapse.
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PMID:Serotonergic modulation of ventilation and upper airway stability in obese Zucker rats. 1131 30

The aim of this study was to assess the nature and magnitude of the differences in submaximal and maximal exercise capacity parameters between lean and obese women. A total of 225 healthy obese women 18-65 years (BMI> or=30 kg/m(2)) and 81 non-athletic lean women (BMI< or=26 kg/m(2)) were selected. Anthropometric measurements (weight and height), body composition assessment (bioelectrical impedance method) and a maximal exercise capacity test on a bicycle ergometer were performed. Oxygen uptake (VO(2)), carbon dioxide production (VCO(2)), expired ventilation (VE), respiratory quotient (RQ), breathing efficiency (VE/VO(2)), mechanical efficiency (ME) and anaerobic threshold (AT) were calculated. At a submaximal intensity load of 70 W, VO(2) (l/min) was larger in the obese women and was already 78% of their peak VO(2), whereas in the non-obese it was only 69% (P=0.0001). VE (l/min) was larger, VE/VO(2) did not differ and ME was lower in obese compared to the lean women. AT occurred at the same percentage of peak VO(2) in both lean and obese women. At peak effort, achieved load, terminal VO(2) (l min(-1) kg(-1)), VE, heart rate, RQ respiratory exchange ratio and perceived exertion were lower in obese subjects compared to the non-obese. Obese subjects mentioned significantly more musculoskeletal pain as a reason to end the test, whereas in lean subjects it was leg fatigue. Lean women recovered better as after 2 min they were already at 35% of the peak VO(2), whereas in the obese women it was 47% (P=0.0001). Our results confirm that exercise capacity is decreased in obesity, both at submaximal and peak intensity, and during recovery. Moreover, at peak effort musculoskeletal pain was an important reason to end the test and not true leg fatigue. These findings are important when designing exercise programs for obese subjects.
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PMID:Exercise capacity in lean versus obese women. 1169 16

A survey of our pulmonary service revealed little consensus as to the definition, work-up, and management of hypoventilation, more often encountered in the presence of obesity. If hypoventilation is defined by an arterial carbon dioxide level above 45mmHg, 22% of artrial blood gas samples over a 5-month period met this criterium, suggesting a high Oany-causeO prevalence. This article presents the rationale and explanation for a management protocol for obesity-hypoventilation that is currently being assessed in the VA Medical Center and Case Western Reserve University training program in Pulmonary and Critical Care Medicine.
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PMID:A Management Guideline for Obesity-Hypoventilation Syndromes. 1189 21

High pressure CO2-peritoneum for laparoscopic surgery is not indicated in patients with impairment of cardiorespiratory and renal function and in high risk patients and in obesity. On the other site the uncontrolled abdominal insufflation and the blind insertion of the first trocar in patients with extended intraperitoneal adhesions, often cause bleeding and the intestinal loops dislocation, and can determine visceral lesions. In these patients gasless technique with an abdominal laparolifter can be employed. We report an experience of 36 patients undergoing laparoscopic cholecystectomy by a subcutaneous planar retractor. It was observed a good operative exposure in 83.3%; the surgery was safely performed in 88.8%. Two suprafascial hematoma related to the insertion of the needles of the Laparo Tenser occurred. A regular post-operative discharge was observed in 84.4%. These good results supports the extension of the laparoscopic approach for the cholecystectomy to complicated or to high risk patients.
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PMID:[Use of abdominal wall retractor Laparo Tenser in gasless laparoscopic cholecystectomy]. 1219 87

The added risks of thromboembolic disease in pill users who also smoke cigarets are enumerated, then the physiological mechanisms explained. From retrospective studies it seems that heart attacks are more likely in women with oral contraception, smoking, obesity, hypertension, diabetes, and high cholesterol. With 1 of these factors the risk is 4-fold, with 2 factors 10-fold, and with 3 factors 78-fold, i.e., a synergic not additive effect. The progestagen in the pill is primarily responsible, acting by causing microthrombi. Strokes are more likely when headaches and hypertension, or oral contraception and smoking are present. Smoking is more often associated with hemorrhagic strokes, while hypertension increases risks of thrombotic and hemorrhagic strokes. The following effects of smoking are probably involved in thromboembolic disease: tachycardia, hypertension, peripheral vasoconstriction, carbon monoxide, inhibition of fibrinolysis, atherosclerosis, and increased blood viscosity.
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PMID:[Smoking and oral contraceptives]. 1233 82

Hepatic lipidosis, a hallmark lesion of lipid mobilization disorders in ruminants, was noted in four 3-year-old, pregnant bison (Bison bison) after periods of anorexia that progressed to recumbency and death. The affected bison were part of a herd at the National Animal Disease Center (NADC) that was used for brucellosis vaccine research. Microscopically, the liver contained swollen hepatocytes with numerous, variably sized, round, smoothly contoured vacuoles that displaced cytoplasmic structures. Hepatocytes in all zones of the lobule were affected equally. Hypoglycemia, decreased total carbon dioxide, elevated gamma-glutamyltransferase, elevated alkaline phosphatase, and increased nonesterified fatty acid levels were noted. As in the case of cattle, altered nutritional demands of late gestation combined with management factors such as obesity, nutrition, stress, and concomitant disease may be critical in the pathophysiology of lipid mobilization disorders in bison. Additionally, stressors unique to this research herd likely contributed to fatal hepatic lipidosis.
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PMID:Hepatic lipidosis in pregnant captive American bison (Bison bison). 1242 37

Four basic control mechanisms of breathing (brainstem respiratory centre, peripheral and central chemoreceptors, intero- and exteroceptive reflexes and suprapontine influences), as well as their sleep-related disorders are analysed. A decrease in central chemoreceptor sensitivity to CO2 and an increase in upper airway resistance during sleep result in hypoventilation and mild hypoxaemia already in physiological conditions. Compensatory increase in ventilatory effort with synchronous inhibition of pharyngeal dilators during sleep reduces the upper airway lumen manifesting with snoring, upper airway resistance syndrome, and OSA. The resulting hypoxaemia may cause marked cardiovascular, neuro-psychic, endocrine-metabolic and behavioural disorders. The augmented ventilatory effort and hypoxaemia evoke reflex dilation of airways and arousal from sleep, stimulating the sympatho-adrenal system, which provokes autoresuscitation by gasping preventing fatal asphyxia. Failure of this autoresuscitation mechanism seems to cause SIDS. Elimination of voluntary breathing by sleep either in Ondine's curse induced by lesions of respiratory centre, or in congenital central hypoventilation syndrome caused by insufficient central chemoreceptors result in respiratory failure and death. Nocturnal attacks of bronchial and cardiac asthma, lung oedema and other consequences of pulmonary congestion are also discussed. The pathomechanism of extreme daytime sleepiness, chronic fatigue, and disorders of memory, cognitive and other brain functions, are also analysed. Severe cardiovascular consequences of SAS may manifest acutely as angina pectoris, myocardial infarction. dysrhythmias, transient ischaemic attacks and even stroke or sudden cardiac death. OSAS may result also in development of hypertension, central obesity, diabetes mellitus, erectile dysfunction, depression, and various behavioural disorders.
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PMID:[Regulation of respiration and its sleep-related disorders]. 1244 39


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