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

An obese patient with nephrotic syndrome was admitted to the hospital because of increasing edema in the legs. With 25 kg weight loss, proteinuria decreased from 15 g to 5 g/day. Renal biopsy revealed mesangial glomerulopathy. The serum IgE level was highly elevated, and the radioallergosorbent test (RAST) was strongly positive for many kinds of allergens. No significant change in proteinuria, compared with the highly right atrial pressure period, was observed after normalization in the right atrial pressure. In spite of a decrease in body weight (27 kg) (113 to 86 kg) in 140 days, no significant change in proteinuria was observed. After additional therapy with an anti-allergic drug, proteinuria was completely abolished. These results suggest that a combination of weight loss and treatment with an anti-allergic drug is very important therapy for massive obesity with nephrotic syndrome. Since RAST was strongly positive for many kinds of allergens, the pathophysiology in this nephrotic syndrome may be, at least partially, related to the immunologic abnormalities.
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PMID:Improvement of nephrotic syndrome in a massively obese patient after weight loss and treatment with an anti-allergic drug. 209 99

Enzyme-linked immunosorbent assay (ELISA) was used to study temporal development of murine autoantibodies against insulin and both type C and intracisternal type A retroviral antigens. The nonobese diabetic (NOD) mouse, a model for autoimmune, insulin-dependent diabetes, was compared with a related, but diabetes-resistant, strain, nonobese normal (NON). Similarly, C57BL/KsJ db/db mice (insulin-resistant model of insulin-dependent diabetes and obesity) were compared with diabetes-resistant C57BL/6 db/db mice. NOD mice developed much higher autoantibody titers than did NON mice. Whereas type C autoantibodies in NOD developed to peak titer shortly after mice were weaned, autoantibodies against insulin and p73 (group-specific antigen of the intracisternal type A particle) did not develop until shortly before, or concomitant with, the development of hyperglycemia. Two NOD mice not developing hyperglycemia during the 40-wk study period were distinguished from the mice developing diabetes by a delayed onset of insulin (but not p73) autoantibodies. Our findings suggest that in NOD mice, the appearance of insulin and p73 autoantibodies signifies that extensive underlying necrosis of beta-cells occurred. C57BL/KsJ db/db mice (with extensive beta-cell necrosis and early hyperglycemia) developed much higher autoantibody titers to insulin and p73 than did the diabetes-resistant C57BL/6 db/db mice. However, the presence of autoantibodies in normoglycemic C57BL/KsJ +/db controls demonstrated that elevated autoantibody titers alone were insufficient to produce diabetes in this model. Absorption studies indicated that autoantibodies against p73 recognized a common epitope on insulin and IgE-binding factor. The potential significance of this molecular mimicry is discussed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Molecular mimicry between insulin and retroviral antigen p73. Development of cross-reactive autoantibodies in sera of NOD and C57BL/KsJ db/db mice. 328 34

Hyper-IgE syndrome is basically characterized by recurrent infections, chronic eczematous lesions, specific IgE antibodies against Staphylococcus aureus and markedly high serum IgE values. We present the case of an 11-year-boy with no relevant personal or family history, who came to our Department with highly pruriginous papulovesicular skin lesions of 3 years' duration. He presented marked obesity (+4 SD) and micropapulovesicular lesions in the trunk and extension areas of the limbs. The rest of the physical exploration was normal. Complementary studies revealed peripheral eosinophilia, increase in globular sedimentation rate and IgE values of 20,000 IU/ml, a nonspecific reaction to skin tests, and a skin biopsy compatible with atopic dermatitis. Three months later, he presented eczematous lesions in the trunk and limbs, perforation of the nasal wall due to staphylococcal abscess (diagnosed by biopsy), bilateral maxillary sinusitis and IgE values of 59,238 IU/ml. The differential diagnoses are discussed, as well as new diagnostic-therapeutic possibilities.
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PMID:Perforation of the nasal wall and hyper-IgE syndrome. 828 56

Reversible airway obstruction in childhood includes two major groups of patients: those with recurrent wheezing following bronchiolitis in early childhood, and those with allergic asthma, which represents an increasingly large proportion of cases through the school years. Over the last 40 years of the 20th century, allergic asthma has increased in many countries and in relation to several different allergens. Although this increase has differed in magnitude in different countries and also in the social groups most affected, it has had several features in common. The increase generally started between 1960 and 1970, has been progressive since then, and has continued into the 1990s without a defined peak. Among children 5-18 years of age, the increase has predominantly been among allergic individuals. Theories about the causes of the increase in asthma have focused on two scenarios: a) that changes in houses combined with increased time spent indoors have increased exposure to relevant allergens, or b) that changes in diet, antibiotic use, immunizations, and the pattern of infections in childhood have led to a change in immune responsiveness such that a larger section of the population makes T(H)2, rather than T(H)1 responses including IgE antibodies to inhalant allergens. There are, however, problems with each of these theories and, in particular, none of the proposed changes can explain the progressive nature of the increase over 40 years. The fact that the change in asthma has much in common with epidemic increase in diseases such as Type II diabetes or obesity suggests that similar factors could be involved. Several lines of evidence are reviewed that suggest that the decline in physical activity of children, particularly those living in poverty in the United States, could have contributed to the rise in asthma. The hypothesis would be that the progressive loss of a lung-specific protective effect against wheezing has allowed allergic children to develop symptomatic asthma. What is clear is that current theories do not provide either an adequate explanation of the increase or a practical approach to reversing the current trend.
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PMID:Specific and nonspecific obstructive lung disease in childhood: causes of changes in the prevalence of asthma. 1093 91

Some epidemiologic surveys have demonstrated that asthma is more prevalent in obese children and adults. However, the mechanism of association between obesity and asthma has not been fully clarified. This report investigates a murine model for antigen-induced asthma and diet-induced obesity from an immunologic perspective. For the induction of obesity, C57BL/6J mice were fed a high-fat diet supplemented with lard or soybean oil. Mice were then sensitized and challenged with ovalbumin (OVA) to induce allergic lung inflammation. OVA-specific serum immunoglobulin levels were lower in obese mice compared with non-obese control mice. The decline of OVA-specific IgE in the soybean oil group was found to be especially pronounced. However, obese mice with OVA-induced asthma showed a higher sensitivity of antigen-induced T-cell responses, and increased gamma interferon (IFN-gamma) production of splenocytes with phytohemagglutinin (PHA) stimulation. Furthermore, mast cell numbers in the tracheal mucosa were increased in obese mice upon sensitization by OVA. These results suggest that obesity-induced changes in T-cell function may be partly involved in the pathophysiology of asthma in human obesity, rather than Ig E-mediated allergic responses.
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PMID:Effect of diet-induced obesity on ovalbumin-specific immune response in a murine asthma model. 1237 Aug 41

Epidemiologic studies suggest increased asthma prevalence in obese subjects. However, the relation between obesity and airway inflammation remains unclear. This cross-sectional study aims to investigate the relation between obesity indices and exhaled nitric oxide (ENO) and leukotriene B(4) (LTB(4)) in children with asthma. Asthmatic patients aged 7-18 yr old were recruited. Weight-for-height Z score was calculated from anthropometry. ENO was measured by online single-breath method using a chemiluminescence analyzer, whereas LTB(4) concentrations in exhaled breath condensate (EBC) were quantified using competitive enzyme immunoassay. Ninety-two asthmatics and 23 controls were recruited. The mean ENO and LTB(4) concentrations in EBC were higher in asthmatic patients (87 p.p.b. and 40.5 pg/ml) than controls (25 p.p.b. and 18.7 pg/ml) (p < 0.0001 for both). Obesity, as defined by weight >120% median weight-for-height, was not associated with any alteration in ENO or LTB(4) concentrations in patients with asthma. Besides, these inflammatory markers did not differ between asthmatics in the highest and lowest quartiles of weight-for-height Z score. On multivariate analysis, ENO showed significant correlation with age (beta = 0.511, p < 0.0001), peripheral blood eosinophil count (beta = 0.222, p = 0.019), plasma total IgE concentration (beta = 0.187, p = 0.050) and forced expiratory volume in 1-s (FEV(1); beta = -0.221, p = 0.014). None of the factors was associated with LTB(4) concentration in EBC. In conclusion, ENO and LTB(4) concentration in EBC are increased in childhood asthma. However, these inflammatory markers did not differ between obese and non-obese children with asthma.
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PMID:The relation between obesity and asthmatic airway inflammation. 1530 44

Asthma is a severe problem among inner city children, and recent evidence suggests that both allergen exposure and lifestyle can impact the disease early in childhood. This study was designed to investigate the association between physical activity and wheezing among a population of inner city children enrolling in Head Start. The parents of children aged 3-5 years responded to a questionnaire (N = 144) to determine the presence and severity of wheezing and asthma. Information was also gathered regarding home environment, food frequency, and presence of other allergic diseases. Serum was obtained to measure total IgE and specific IgE levels to common allergens. Height and weight for body mass index were recorded. Lastly, motion sensor wristwatches (Actiwatch) were worn continuously by a subset of these children (n = 54) for 6 or 7 days. Physical activity measured with the motion sensor was decreased among children with a history of wheezing. The significant differences involved those measures of activity relating to prolonged or sustained physical activity. The correlates of asthma associated with decreased levels of physical activity included: 1) a history of wheezing in the last 12 months, 2) the diagnosis of asthma, and 3) presentation to the emergency room in the last 12 months for wheezing or asthma. In a preschool-age population, decreased physical activity was observed among children with a history of asthma or wheezing. Decreased physical activity could contribute to persistence of asthma or put children at higher risk for obesity and other chronic diseases.
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PMID:Decreased physical activity among Head Start children with a history of wheezing: use of an accelerometer to measure activity. 1585 99

We investigated IgE-mediated allergic responses in a metabolic syndrome model rat strain, SHRSP.Z, which develops obesity and hypertension to cast light on the relationship between metabolic disturbances and allergic responses. IgE-mediated cutaneous anaphylactic responses were severely attenuated in this strain regardless of the presence of fa/fa mutation, compared with the parental WKY/Izm strain. Furthermore, in the peritoneal mast cells of both the SHRSP.Z and SHRSP/Izm strains, IgE-mediated activation, such as degranulation and protein tyrosine phosphorylation, was severely impaired whereas no significant differences were found in morphology and number of peritoneal mast cells. Immunoblot analyses revealed that phosphorylation levels of Syk upon IgE-mediated antigen stimulation were significantly decreased and basal expression of linker for activation of T cells (LAT) was down-regulated in peritoneal mast cells of the SHRSP strains. These results suggest that attenuated cutaneous allergic responses in the SHRSP.Z strain might be attributed to impaired FcvarepsilonRI-mediated signal transduction in mast cells.
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PMID:Impaired activation of mast cells upon IgE-mediated antigen stimulation in a stroke-prone spontaneously hypertensive rat strain, SHRSP.Z. 1994

Recently the prevalence of both asthma and obesity have increased substantially in many countries. The aim of this study was to evaluate the role of retinol-binding protein (RBP) 4 in childhood asthma and its association with atopy markers, pulmonary function, and bronchial hyperresponsiveness in relation to obesity. We studied 160 children between the ages 6 to 10 yr, including 122 asthmatics and 38 controls. The body mass index, pulmonary function tests, and methacholine challenge tests were measured on the same day. Total eosinophil count, serum total IgE, serum eosinophil cationic protein, and serum RBP4 were measured in all subjects. There was no difference in serum RBP4 levels between the asthmatics and the control group. In all subjects or subgroups, serum RBP4 was not associated with total eosinophil count, serum total IgE, serum eosinophil cationic protein, or PC(20). There was no relationship between serum RBP4 and pulmonary function in female asthmatics. Forced expiratory volume in 1 second/forced vital capacity (FVC) and forced expiratory flow between 25% and 75% of FVC contributed to serum RBP4 in male asthmatics. Our findings show an association between RBP4 and pulmonary function in prepubertal male asthmatics. This relationship may indirectly affect the high prevalence of childhood asthma in males.
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PMID:Clinical implications of serum retinol-binding protein 4 in asthmatic children. 1994 53

Few reports show whether a high-fat (HF) dietary environment in the fetal period affects immune function or the development of lifestyle-related disease at maturity. We examined the influence of an HF dietary environment in the fetal period on postnatal metabolic and immune function. A total of 16 pregnant mice were given control (CON) diet and 16 were given HF diet in the gestational period, from mating to delivery. After delivery lactating mice were given either CON or HF diet, resulting in four groups. After weaning, the offspring mice were given the same diet that their mothers received during lactation. HF dietary intake in the postnatal period increased fat pad weights, serum glucose, and leptin levels. An HF diet in the fetal period resulted in fewer splenic lymphocytes, a thinner thymic cortex, and impaired antigen-specific immune reactions. Furthermore, tumor necrosis factor (TNF)-alpha production and serum triglyceride levels were elevated in the fetal HF group. In addition, the HF-HF group showed a consistent decrease in ovalbumin (OVA)-specific IgG and elevation of IgE, associated with advanced fatty changes in the liver. Results from this study suggest that HF environment during the fetal period induces epigenetic propensity toward obesity and immunological burden in part due to increased adipose tissue mass, significant reduction in the number of immune cells and decreased activities of immune cells.
Obesity (Silver Spring) 2010 Sep
PMID:The influence of a high-fat dietary environment in the fetal period on postnatal metabolic and immune function. 2011 Oct 14


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