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

Fatty masses of the heart usually arise in the interatrial septum and are uncommon. The autopsy files from LAC-USC Medical Center contain 15 such cases from 1952 through 1972. Although these masses are yellow and attain a large size, most are considered to represent lipomatous infiltrations rather than true lipomas since they usually lack encapsulation and do contain cardiac muscle in varying amounts. The lesion is most often associated with obesity. Surprisingly, even the large masses produce few clinical symptoms and none was suspected clinically, each being an incidental finding at necropsy. However, these masses do infiltrate the conduction system and can cause arrhythmias and sudden death. Echocardiography or other noninvasive techniques may bring attention to a lipomatous mass that may or may not be asymptomatic. This can result in a clinical dilemma in differential diagnosis and treatment since myxomas, rhabdomyomas, and sarcomas also arise in the interatrial septum.
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PMID:Lipomatous infiltrates of the heart. 57 67

The effects of variations in the volume conductor properties of the torso on the electrocardiogram were studied by means of a theoretical eccentric spheres model. The model includes a blood cavity, cardiac muscle layer, pericardium, lung region, skeletal muscle layer, and subcutaneous fat. The source of the field is a double-layer spherical cap located within the myocardium. The following effects regarding the electrocardiogram (ECG) potentials were determined: (1) blood augments the potential, but less than predicted by simpler published models; (2) in anemia, high potentials are expected, whereas in polycythemia, voltages are reduced; (3) abnormally low lung conductivity (emphysema) causes low surface potentials whose magnitude is controlled by the low conductivity skeletal muscle layer; (4) low voltages result both from low and high pericardial conductivities; (5) the surface potential increases with increasing myocardial conductivity; (6) low skeletal muscle conductivity (Pompe's disease) causes high surface potentials; (7) obesity lowers the potential only slightly; (8) a thick myocardium, protruding into the lung region, slightly augments the potential; (9) an increase in the thickness of the myocardium at the expense of the blood cavity causes a decrease in potential; (10) the potential increases with increasing heart size; and (11) the location of the heart within the torso has a very significant effect on the surface potential distribution.
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PMID:The effects of variations in conductivity and geometrical parameters on the electrocardiogram, using an eccentric spheres model. 75 26

Obesity is the presence of excess body fat and is associated with a variety of medical conditions which increase morbidity and mortality. Millions of individuals participate in weight-reduction programmes which include reduced calorie diets and may also include exercise. Very low calorie diets (VLCD) of 400 to 800 kcal/day appear attractive as they generally show an increase in weight loss from 0.2 to 0.5 kg/week found with the traditional diet to 1.5 to 2.0 kg/week. Early use of very low calorie diets with poor quality protein and loose medical supervision resulted in about 60 deaths, many of which were attributed to loss of lean body mass and in particular, cardiac muscle atrophy. Although current very low calorie diets are presumed safe, concern regarding preservation of lean body mass (LBM) remains. Investigators have used exercise to slow the depletion of lean body mass during very low calorie diets; however, the results are not conclusive. A host of different methodologies and questionable documentation and design of exercise protocols precludes a definitive statement for the benefits of exercise during very low calorie diets for the purpose of LBM retention.
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PMID:Diet and body composition. Effect of very low calorie diets and exercise. 178 76

A 61-year-old woman with low grade obesity index complained of general fatigue. Cardiomegaly had been present since the age of 45. According to a roentgenogram on admission, her cardia-thoracic ratio was 61%. Pericardial effusion was strongly suspected because of extra echo spaces on both posterior and anterior walls, and unsynchronized echocardiograph waves of epicardium and pericardium. However, values of dynamic CT measured at areas equivalent to the extra echo spaces were -120. On admission, T1-emphasized MRI image showed a high signal density in those areas. After significant weight reduction, the abnormal values and signs of the clinical examinations, as well as the patient's complaints were attenuated or disappeared. Together with these results, cardiomegaly of the patient was diagnosed to be due to excessive fat deposit between the epicardium and cardiac muscle. Dissociation between mildness of obesity index and excessive deposition of fat in the pericardium was discussed from the point of view of body mass index and time course of fat deposition.
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PMID:[A case of mild obesity accompanied by epicardial fat deposition]. 214 82

An experimental model for investigating the disparate effects of obesity and hypertension on the heart was developed by ligation of the aorta of male Sprague-Dawley rats made obese through ad libitum feeding. Experimental obesity was associated with an increased body fat and cardiac muscle mass, yet a normotensive systemic arterial pressure. Aortic ligation produced an elevated mean arterial pressure and resting heart rate, whereas body weight was similar to that of normotensive lean control rats. Obesity and hypertension together were associated with a significantly increased percent body fat, mean arterial pressure, and left ventricular mass compared with lean controls, whereas pressure and left ventricular weight were greater than those observed in rats with only obesity or hypertension. Cardiac adaptations corrected for body weight indicated that left ventricular weight increased as a function of body weight and body fat, but hypertension produced left ventricular adaptations independent of these variables. These initial studies indicate an additional contribution of hypertension to the left ventricular adaptations of obesity, and this model could therefore be used in future investigations concerning the cardiovascular effects of the simultaneous occurrence of these separate diseases.
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PMID:Development of an animal model for investigating disparate myocardial effects of obesity and hypertension. 296 92

Pyruvate dehydrogenase complex activity is the major determinant of glucose oxidation in animal cells. Tissue glucose oxidation is reduced in obesity and states of insulin resistance and alternate fuels are utilized for energy and pyruvate dehydrogenase activity is reduced in cardiac muscle in obesity. The effect of four different diets (standard laboratory chow, high-carbohydrate, high-protein and high-fat) on weight gain, cardiac pyruvate dehydrogenase activity (PDHa) and serum insulin, glucose and free fatty acids was studied in the gold thioglucose obese mouse. All four diets produced significant weight gain in the gold thioglucose injected animal. Cardiac PDHa was influenced by both obesity and diet composition. The obese chow-fed animals had significantly reduced PDHa. On high-carbohydrate and high-protein feeding lean controls had a significant decrease in cardiac PDHa compared to chow-fed controls, but only in high-carbohydrate-fed animals was this further reduced by obesity. High-fat feeding produced a rapid and almost complete suppression of PDHa in both lean and obese animals. Serum insulin, glucose and free fatty acids were also affected by diet as well as obesity. The highest serum insulins were found in chow-fed obese animals whereas the highest serum glucoses were in high-carbohydrate-fed obese animals. Hyperinsulinaemia did not develop in the high-fat-fed obese animal, but the highest serum free fatty acids were found in high-fat feeding. It is concluded that both diet composition and obesity affect cardiac PDHa and therefore glucose utilization in this tissue. Insulin resistance in the acute stages of obesity development is also affected by diet composition.
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PMID:The effect of diet composition on weight gain and pyruvate dehydrogenase activity in heart muscle in the gold thioglucose obese mouse. 312 9

Isolated cardiac myocytes from lean and genetically obese (fa/fa) Zucker rats were used to study cellular alterations related to the obesity syndrome in this tissue. Scatchard analysis of insulin binding data suggested a reduction in the number of low affinity sites in cells from obese rats; in contrast, an unaltered high affinity segment with Kd values of 5.7 +/- 0.6 and 4.5 +/- 0.7 X 10(-10) mol/liter (n = 4) in lean and obese rats, respectively, has been observed. Insulin internalization, as estimated from the amount of increased cell-associated radioactivity in chloroquine-treated cells, was decreased by 70% from 12.8 fmol insulin/10(6) cells X 120 min in lean rats to 3.8 fmol/10(6) cells X 120 min in obese rats. Determinations of initial velocities of 3-O-methylglucose influx were used for assessing glucose transport activity. Basal activity of the glucose transport system was reduced in cells from obese animals. This was found to be due to a decreased maximum velocity of the carrier with corresponding values of 69.8 +/- 5.2 and 38.3 +/- 3.2 nmol/10 sec X 10(6) cells (n = 3) in cardiocytes from lean and obese rats, respectively. Glucose transport exhibited an unaltered sensitivity toward stimulation by insulin, but an impaired responsiveness in cardiocytes from obese rats. The data suggest involvement of both receptor and postreceptor defects in the development of an insulin-resistant state in cardiac muscle.
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PMID:Insulin resistance in the heart: studies on isolated cardiocytes of genetically obese Zucker rats. 388 13

Adult male Sprague-Dawley rats (> or = 180 days old) develop an obesity-exacerbated insulin resistance in contrast with female animals of the same strain. Given the fact the maintenance of muscle mass requires an adequate supply of insulin and active insulin receptors, we postulated that gender differences might exist in both protein content and metabolic properties of skeletal and cardiac muscle in adult Sprague-Dawley rats. Therefore, to test this hypothesis, we examined activities of bioenergetic enzymes and total protein content in the diaphragm, the heart and the plantaris muscle in 12-month-old male and female animals. Mean (+/- SD) body weights of male animals were significantly (P < 0.05) greater than female animals (598 +/- 8 vs. 362 +/- 19 g) and the diaphragm weight/body weight ratio was significantly lower in males compared to females (2.36 +/- 0.05 vs. 3.02 +/- 0.13 mg/g). The activities of isocitrate dehydrogenase (NADP-specific) and succinate dehydrogenase were significantly lower (P < 0.05) in male animals compared to females in both the crural and costal regions of the diaphragm, the heart, and the plantaris muscle. In contrast, no gender differences (P > 0.05) existed in lactate dehydrogenase activity in any of the muscles studied. Finally, muscle protein concentration was significantly higher in female animals when compared to males (P < 0.05) in all muscles studied except the heart. These data support the hypothesis that gender differences exist for adult Sprague-Dawley rats in general and specific protein content of the diaphragm, locomotor muscles, and the heart.
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PMID:Gender differences in diaphragmatic metabolic properties of the adult Sprague-Dawley rat. 797 31

We report the cloning of a 3656-bp cDNA encoding a putative human very low density lipoprotein (VLDL)/apolipoprotein E (ApoE) receptor. The gene encoding this protein was mapped to chromosome 9pter-p23. Northern analysis of human RNA identified cognate mRNAs of 6.0 and 3.8 kb with most abundant expression in heart and skeletal muscle, followed by kidney, placenta, pancreas, and brain. The pattern of expression generally paralleled that of lipoprotein lipase mRNA but differed from that of the low density lipoprotein (LDL) receptor and the low density lipoprotein receptor-related protein/alpha 2-macroglobulin receptor (LRP), which are members of the same gene family. VLDL/ApoE receptor message was not detected in liver, whereas mRNAs for both LDL receptor and LRP were found in hepatic tissue. In mouse 3T3-L1 cells, VLDL/ApoE receptor mRNA was induced during the transformation of the cells into adipocytes. Expression was also detected in human choriocarcinoma cells, suggesting that at least part of the expression observed in placenta may be in trophoblasts, cells which would be exposed to maternal blood. Expression in brain may be related to high levels of ApoE expression in that organ, an observation of potential relevance to the recently hypothesized role for ApoE in late onset Alzheimer disease. Our results suggest that the putative VLDL/ApoE receptor could play a role in the uptake of triglyceride-rich lipoprotein particles by specific organs including striated and cardiac muscle and adipose tissue and in the transport of maternal lipids across the placenta. The findings presented here, together with recent observations from other laboratories, bring up the possibility that a single gene, the VLDL/ApoE receptor, may play a role in the pathogenesis of certain forms of atherosclerosis, Alzheimer disease, and obesity.
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PMID:Cloning of a cDNA encoding a putative human very low density lipoprotein/apolipoprotein E receptor and assignment of the gene to chromosome 9pter-p23. 812 15

Although various factors, such as myocardial infarction, pressure overload and volume overload, result in the development of congestive heart failure (CHF), the pathogenesis of contractile dysfunction in this situation is poorly understood. Loss of cardiac muscle due to myocardial infarction appears to activate several humoral and hormonal pathways, including the renin-angiotensin and sympathetic systems which serve as adaptive mechanisms to maintain cardiovascular performance at early stages of failure. However, under chronic conditions, an altered hormonal profile produces deleterious effects and permits transition from the compensated heart to the failing heart. Since several risk factors--such as hypertension, hypercholesteremia, stress, diabetes, smoking, ageing, obesity and lack of exercise--precipitate ischemic heart disease, it is possible that development of CHF due to myocardial infarction may vary according to the nature of these pathogenetic entities. While a great deal of research work remains in this area of investigation, it is becoming evident that cardiac dysfunction is intimately associated with calcium handling abnormalities of cardiac cells. In view of the role of sarcolemma, sarcoplasmic reticulum and mitochondria in regulating the intracellular concentration of Ca2+ and the importance of myofibrillar interaction with Ca2+, it appears that Ca2+ handling and Ca2+ interaction abnormalities in the failing heart are due to remodelling of different subcellular organelles. Such a remodelling of the subcellular organelles may be due to changes in gene expression for different protein components or the interactions of proteins with phospholipids. Accordingly, it is proposed that new interventions, which could prevent the remodelling of subcellular organelles, be developed for improving the therapy of CHF.
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PMID:Pathophysiology of cardiac dysfunction in congestive heart failure. 828 76


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