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

A high fat (HF) diet is known to induce obesity, but susceptibility to obesity induced by a HF diet differs not only among different strains of rats but also within the same strain. The present study revealed that the Lee index (an index of obesity) positively correlated with insulin, and inversely correlated with both the mitochondrial oxygen consumption in interscapular brown adipose tissue (BAT) and the resting metabolic rate (RMR) in Sprague-Dawley rats. This suggests the contribution of BAT thermogenesis and RMR, in addition to hyperphagia, to the intrastrain variation in susceptibility to HF diet-induced obesity.
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PMID:Brown adipose tissue thermogenesis and metabolic rate contribute to the variation in obesity among rats fed a high fat diet. 147 84

Symptoms and signs in 12 patients with severe obstructive sleep apnea (OSA) syndrome have been presented. The most common symptoms were snoring , increased motor activity during sleep and excessive daytime somnolence. The factors predisposing to OSA syndrome were obesity and anatomic abnormalities of the upper airway structure. In some cases the signs of OSA syndrome included hypertension, right heart failure, chronic alveolar hypoventilation and polycythemia. Polysomnography showed sleep fragmentation and the prevalence of light sleep stages. Obstructive sleep apneas repeated 73 +/- 23 times per hour of sleep. The mean apnea duration was 19 +/- 8 s. The mean arterial oxygen saturation during apnea was 72 +/- 14%.
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PMID:[Diagnosis of obstructive sleep apnea syndrome]. 148 56

The mechanism behind the meal-induced increase in energy expenditure in humans and its reduction in obesity was examined in 15 normal-weight and seven obese subjects. The subjects were studied by indirect calorimetry in the basal state and during 2 hours after a mixed meal corresponding to 40% of the 24-hour basal energy requirement. Artificial thermal insulation was applied over the abdominal area before the study in seven of the normal-weight subjects. Thermistor catheters were inserted into a hepatic vein, the pulmonary artery, and a systemic artery for blood sampling and recording of blood temperatures. Basal hepatic venous drainage of heat in relation to the splanchnic oxygen uptake in the normal-weight subjects was low (12 +/- 1 J/mL O2) and became even lower after the meal (5 +/- 3 J/mL). In the obese individuals and the insulated subjects, blood-drained splanchnic heat amounted to 19 to 21 J/mL oxygen both before and after the meal. The postprandial increase in whole body energy expenditure was diminished both in the obese (12% +/- 1% above basal) and in the insulated subjects (15% +/- 1%) compared with the noninsulated controls (22% +/- 2%). In normal-weight subjects, there is a leakage of heat across the abdominal wall. Reduction or prevention of this leakage by artificial thermal insulation or by obesity is accompanied by a reduction of the postprandial increase in energy expenditure.
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PMID:Heat leakage across the abdominal wall and meal-induced thermogenesis in normal-weight and obese subjects. 153 91

In order to assess the complications of sleep apnea, we have reviewed a data base of 619 consecutive admissions to a university sleep disorders center. Although patients with obstructive sleep apnea (OSA) described more subjective sleepiness than patients with central sleep apnea (CSA) or primary snoring (PS), the multiple sleep latency test (MSLT) indicated similar levels of physiologic sleepiness in the two apneic groups, which was greater than among those with PS. There was no significant relationship between individual subjective estimates of habitual sleepiness and the MSLT values. Among the OSA patients the mean minimum arterial oxygen desaturation during REM sleep accounted for 65 percent of the variance of the mean sleep latency on the MSLT, with an additional, smaller, contribution of the disordered breathing rate per hour. Subjective reports of sleepiness were associated with sleep efficiency and the number of disordered breathing events in NREM sleep. Patients with OSA or CSA had similar diastolic blood pressures and frequencies of history of treatment for hypertension, which were significantly higher in OSA than in the PS group. In the OSA group the absolute minimum arterial oxygen desaturation during NREM sleep was the most significant contributor to waking diastolic blood pressure, with an additional small contribution by weight. A history of treatment for hypertension was most strongly associated with weight, without significant additional contributions by measures of disordered breathing events or oxygen desaturation; however, weight was highly intercorrelated with measures of the apnea/hypopnea index and minimum arterial oxygen desaturation. In summary, these data support recent findings which show a close relation of obesity to a history of hypertension in OSA, and extend to this group a previous observation that in regular heavy snorers, there may be a disparity between levels of physiologic and subjective sleepiness.
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PMID:Sleepiness and hypertension in obstructive sleep apnea. 155 54

From a conceptual standpoint, the tests of pulmonary function can be divided into those that assess the ventilatory function of the lungs and those concerned with gas exchange. Tests of ventilatory function reflect alterations of the elastic resistance and flow resistance of the respiratory apparatus. The elastic properties of the lungs are assessed by determining the position and shape of the curve representing the relationship between the pressure across the lungs and absolute lung volume. When there is reduced distensibility of either the lungs or the chest wall, the volume-pressure curve is shifted down and to the right. The slope of the curve is reduced in the patient with pulmonary fibrosis, while it is normal in the patient with obesity. In asthma (or chronic bronchitis) and emphysema, the volume-pressure curve is shifted up and to the left. In emphysema, the slope of the curve is increased, while it is normal in patients with asthma or bronchitis. In practice, lung volume is used as an index of alterations of the volume-pressure characteristics of the lungs and/or chest wall. The vital capacity is often used as a surrogate for the TLC but it is lower than expected in both restrictive and obstructive disorders. The FEV1.0 reflects the degree of expiratory flow limitation. In a restrictive disorder, lung volume and the FEV1.0 are reduced, but the FEV1.0/FVC ratio is normal. In airflow limitation, lung volume, the FEV1.0, and the FEV1.0/FVC ratio are lower than expected. In airflow limitation, the reversibility with inhaled bronchodilator should be determined. Tests of airway responsiveness are indicated when evaluating patients with unexplained chronic cough, chest tightness, or wheezing, particularly if other lung function tests are normal. The adequacy of gas exchange is assessed by determining the arterial blood gas tensions--PaO2 and PaCO2--and the alveoloarterial pO2 gradient--P(A-a)O2. A lower-than-expected PaO2 can result from several different physiologic disturbances. When alveolar hypoventilation is the sole disturbance, the oxygen in the alveoli and in the blood perfusing them virtually comes into equilibrium, so that the P(A-a)O2 is normal. An elevated P(A-a)O2 is caused by either mismatching of ventilation and perfusion, true venous admixture, a diffusion abnormality, or a combination of these disturbances. Because dyspnea on exertion is a cardinal symptom of respiratory disease, exercise tolerance should be assessed. A reduced exercise tolerance may result from ventilatory limitation, impaired gas exchange, cardiac impairment, impaired delivery of the oxygen to the working muscles, or an inability to use the energy.
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PMID:Evaluation of respiratory function in health and disease. 160 91

Levels of R proteins, immunoglobulins A, M, and G, natural anti-sheep erythrocyte antibodies, active oxygen (superoxide) were measured in the neutrophilic leukocytes in pregnant females at a risk for late gestosis. The examinees were found to have high levels of R proteins, IgA, IgM, natural anti-sheep erythrocyte antibodies, neutrophils capable to restore NST, and low levels of IgG. Teen-agers, old-year primiparas, pregnant females with a history of pyelonephritis, obesity, neuropathy in the prior labour, and hypertensive vegetovascular dystonia constituted a gestosis-risk group. The R-protein test should be considered to be the most informative indicator of a gestosis risk.
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PMID:[Immunity indices in the diagnosis of pretoxicosis in women with an increased risk for the development of late toxicosis]. 165 May 37

Elevated arterial pressure in patients with obesity-hypertension is associated with an increased cardiac output and total peripheral resistance. The elevated output is related to expanded intravascular volume that increases cardiopulmonary volume, venous return, and left ventricular preload; the elevated pressure and total peripheral resistance increase afterload. This dual ventricular overload promotes a dimorphic, concentric, and eccentric hypertrophy in response to the volume and pressure overload. Increased myocardial oxygen demand results from the elevated tension in the left ventricular wall, reflecting its increased diameter and pressure, and provides physiologic rationale for the greater potential of coronary arterial insufficiency and cardiac failure. There are greater renal blood flow and lower renal vascular resistance in patients with obesity-hypertension at any level of arterial pressure. This may be offset by an increased renal filtration fraction that may favor protein deposition and glomerulosclerosis, and predisposition of obese patients for diabetes may aggravate this problem. With weight reduction, these hemodynamic derangements may be reversed: intravascular volume contracts, cardiac output decreases, and arterial pressure falls.
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PMID:Obesity and hypertension. Hemodynamic aspects. 166 10

The coexistence of the syndromes of essential hypertension and coronary artery disease (CAD) poses a major but common therapeutic challenge. High blood pressure is one of the most potent risk factors for the early development of CAD. Conversely, the presence of CAD significantly worsens the predictive prognosis associated with high blood pressure. Moreover, metabolic risk factors for the acceleration of both syndromes are similar, particularly with regard to abnormalities of the blood lipid profile, carbohydrate intolerance, and obesity. It is clinically crucial, therefore, to direct drug therapy not only at the immediate alleviation of the symptoms and signs of each syndrome but also to control the cardiac and vascular risk factors common to both syndromes. Carvedilol is a third-generation vasodilating beta-adrenoceptor antagonist with advantageous ancillary pharmacologic properties for the treatment of the patient with high blood pressure complicated by CAD. The immediate advantages of the drug in the treatment of both syndromes are distinct. In the patient with high blood pressure, carvedilol controls the pressure throughout the 24 h of the day and suppresses the increase associated with exercise. In the patient with CAD, the drug is efficacious in relieving anginal pain and electrocardiographic signs of myocardial ischemia. By reducing blood pressure and heart rate and retarding their increases during exercise, the drug exhibits a potent ability to reduce left ventricular work, wall stress, myocardial oxygen consumption, and left ventricular myocardial ischemia. In the patient in whom both syndromes coexist, carvedilol affords a remedy for both.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypertension and coronary artery disease: a therapeutic challenge. 172 78

Left ventricular hypertrophy (LVH), an increase in the muscle mass of the left ventricle, has been identified as a powerful risk factor for future cardiovascular morbidity and mortality. The risk of acute myocardial infarction, congestive heart failure, sudden death, and other cardiovascular events increases six- to eightfold with the presence of LVH. The increase in myocardial mass lowers coronary reserve and enhances cardiac oxygen requirements, gives rise to ventricular ectopy, and impairs left ventricular filling and contractility. Hypertension, obesity, advanced age, valvular heart disease, and other disorders that cause an increase in the hemodynamic burden can lead to LVH. Left ventricular hypertrophy and its sequelae can be reduced by specific antihypertensive therapy but, despite these promising findings, future epidemiological studies are necessary to document the clinical benefits of a reduction of LVH.
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PMID:Left ventricular hypertrophy: an independent risk factor. 172 10

Respiratory function undergoes sleep-associated changes which in normal subjects leave it unaffected. However in some cases they may be more marked than usual or may be superimposed on a pre-existing disease, thus giving rise to sleep-related ventilation disorders. These include obstructive sleep apnea syndrome (OSAS), nocturnal desaturation events of chronic obstructive pulmonary disease (COPD) and restrictive syndromes, as well as nocturnal asthmatic attacks. OSAS is a condition characterized by the frequent recurrence of interruptions of oronasal flow (greater than 10 s.) due to upper airway occlusion induced by a reduction in pharyngeal muscle tone. This phenomenon, particularly prominent in REM sleep, results in oxyhemoglobin desaturation and marked cardiovascular consequences (arrhythmias, increases in pulmonary and systemic arterial pressure), as well as symptoms (loud intermittent snoring, daytime sleepiness, intellectual deterioration etc.). Obesity is often associated with OSAS or may lead to a sleep-related hypoventilation syndrome. Treatment is based on weight loss, surgery of upper airway abnormalities, if present, and on splinting of the upper airway by the application of nasal continuous positive airway pressure. In COPD and restrictive disorders, nocturnal hypoxemia is mainly due to REM-associated loss of respiratory muscle tone, as well as in the sleep-related exaggeration of functional defects due to COPD (low chemoreceptor sensitivity, high closing volume etc.). Treatment is based on oxygen administration, provided that possible side-effects are carefully monitored. Nocturnal asthma is due to circadian changes in hormonal secretion (catecholamines, cortisol), as well as supine posture, reduced muco-ciliary clearance, gastro-esophageal reflux etc. Sleep itself plays some role through a depressed arousal reaction in slow wave sleep, resulting in more marked and prolonged attacks in this stage. Slow-release theophylline or beta-mimetic medications, as well as new chromones and antimuscarinic drugs are therapeutic alternatives.
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PMID:Cardio-respiratory function during sleep. 174 49


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