Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma levels of beta-thromboglobulin (BTG) and platelet count were studied in 69 control subjects, 19 patients with operable abdominal malignancy, and 9 patients with acute bacterial infection. In control subjects there was a significant rise in BTG and fall in platelet count with age, and a negative correlation of BTG with obesity. BTG and platelet count were normal in patients with operable malignancy, but significantly increased in patients with acute bacterial infection. These effects must be considered in studies of BTG and thrombosis.
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PMID:Beta-thromboglobulin and platelet counts - effect of malignancy, infection, age and obesity. 618 Apr 99

Surgery for obesity has developed continuously since it was introduced in 1956. The early idea of small intestinal bypass has been refined to the point that the majority of surgeons agree that about 45 cm of small bowel should be left in continuity, 30 cm of jejunum and 15 cm of ileum. Providing care is taken to given dietary supplements plus a high protein, low fat, low oxalate and high calcium diet, together with a ready response to severe liver damage by treatment of bacterial infection in the bypassed loop, this operation or one of its variants appears to be reasonably safe. But it is nevertheless followed by significant and undesirable side effects. Wiring the jaw is effective in producing weight loss and has the advantage of simplicity and cheapness. Unfortunately when the suffer is released weight is gained in all cases. Gastric operations designed to reduce the size of the proximal stomach to a paltry 50 ml are of two types--gastric bypass in which the small and otherwise closed pouch is drained into the small bowel and gastroplasty in which a 9 mm stoma drains the pouch into the distal stomach. There is much to commend gastroplasty and reports so far do not indicate such a large number of late complications as with jejuno-ileal bypass. This surely is where the future of surgery in this condition lies.
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PMID:The surgical treatment of obesity. 651 51

Periodontal diseases now is a chronic inflammatory disease caused by Gram negative bacterial infection. Recently, it is of interest to evaluate risk factors that modulate initiation and development of this disease. A recent study have suggested that obesity is one of the risk factors. In this regard, most recently, we found that leptin, a regulator of food intake and whole-body energy metabolism, acts as a negative regulator of LPS-induced expression of inflammatory cytokines of macrophages via inhibition of NF-kB.
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PMID:[Risk factors that modulate periodontal diseases]. 1577 25

Obesity is associated with an impaired immune response, an increased susceptibility to bacterial infection, and a chronic increase in proinflammatory cytokines such as IL-6 and TNFalpha. However, few studies have examined the effect of obesity on the immune response to viral infections. Because infection with influenza is a leading cause of morbidity and mortality worldwide, we investigated the effect of obesity on early immune responses to influenza virus exposure. Diet-induced obese and lean control C57BL/6 mice were infected with influenza A/PR8/34, and lung pathology and immune responses were examined at d 0 (uninfected), 3, and 6, postinfection. Following infection, diet-induced obese mice had a significantly higher mortality rate than the lean controls and elevated lung pathology. Antiviral and proinflammatory cytokine mRNA production in the lungs of the infected mice was markedly different between obese and lean mice. IFNalpha and beta were only minimally expressed in the infected lungs of obese mice and there was a notable delay in expression of the proinflammatory cytokines IL-6 and TNFalpha. Additionally, obese mice had a substantial reduction in NK cell cytotoxicity. These data indicate that obesity inhibits the ability of the immune system to appropriately respond to influenza infection and suggests that obesity may lead to increased morbidity and mortality from viral infections.
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PMID:Diet-induced obese mice have increased mortality and altered immune responses when infected with influenza virus. 1744 87

Obesity has been suggested to be associated with an increased susceptibility to bacterial infection. However, few studies have examined the effect of obesity on the immune response to bacterial infections. In the present study, we investigated the effect of obesity on innate immune responses to Porphyromonas gingivalis infection, an infection strongly associated with periodontitis. Mice with diet-induced obesity (DIO) and lean control C57BL/6 mice were infected orally or systemically with P. gingivalis, and periodontal pathology and systemic immune responses were examined postinfection. After oral infection with P. gingivalis, mice with DIO had a significantly higher level of alveolar bone loss than the lean controls. Oral microbial sampling disclosed higher levels of P. gingivalis in mice with DIO vs. lean mice during and after infection. Furthermore, animals with DIO exposed to oral infection or systemic inoculation of live P. gingivalis developed a blunted inflammatory response with reduced expression of TNF-alpha, IL-6, and serum amyloid A (SAA) at all time points compared with lean mice. Finally, peritoneal macrophages harvested from mice with DIO and exposed to P. gingivalis exhibited reduced levels of proinflammatory cytokines compared with lean mice and when exposed to P. gingivalis LPS treatment had a significantly reduced recruitment of NF-kappaB to both TNF-alpha and IL-10 promoters 30 min after exposure. These data indicate that obesity interferes with the ability of the immune system to appropriately respond to P. gingivalis infection and suggest that this immune dysregulation participates in the increased alveolar bone loss after bacterial infection observed in mice with DIO.
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PMID:Diet-induced obesity in mice causes changes in immune responses and bone loss manifested by bacterial challenge. 1807 29

TNFalpha is a proinflammatory cytokine secreted by macrophages in response to bacterial infection. Recently new evidence has emerged suggesting that stressed or injured myocytes produce TNFalpha that then acts as an autocrine and/or paracrine mediator. TNFalpha receptors types 1 and 2 are present in skeletal muscle cells, and muscle cells can secrete, in addition to TNFalpha, other cytokines such as IL-1beta or IL-6. Furthermore, the plasma concentration of TNFalpha is elevated in insulin-resistant states associated with obesity and type 2 diabetes. Here we show that TNFalpha increased the amount of glucose transporter (GLUT)-4 at the plasma membrane and also glucose uptake in the L6 muscle cell line stably expressing GLUT4 tagged with the c-myc epitope. Regardless of the state of differentiation of the L6 cells, TNFalpha did not affect the rate of proliferation or of apoptosis. The stimulatory effects of TNFalpha on cell surface GLUT4 and glucose uptake were blocked by nuclear factor-kappaB and p38MAPK pathway specific inhibitors (Bay 11-7082 and SB220025), and these two pathways were stimulated by TNFalpha. Furthermore, although TNFalpha increased IL-6 mRNA and protein expression, IL-6 did not mediate the effects of TNFalpha on cell surface GLUT4 levels, which also did not require de novo protein synthesis. The results indicate that TNFalpha can stimulate glucose uptake in L6 muscle cells by inducing GLUT4 translocation to the plasma membrane, possibly through activation of the nuclear factor-kappaB and p38MAPK signaling pathways and independently of the production of IL-6.
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PMID:The proinflammatory cytokine tumor necrosis factor-alpha increases the amount of glucose transporter-4 at the surface of muscle cells independently of changes in interleukin-6. 1816 26

Inflammatory responses represent a hallmark of numerous pathologies including sepsis, bacterial infection, insulin resistance, and malign obesity. Here we describe an unexpected coactivator function for the nuclear receptor interacting protein 140 (RIP140) for nuclear factor kappaB (NFkappaB), a master transcriptional regulator of inflammation in multiple tissues. Previous work has shown that RIP140 suppresses the expression of metabolic gene networks, but we have found that genetic as well as acute deficiency of RIP140 leads to the inhibition of the proinflammatory program in macrophages. The ability of RIP140 to function as a coactivator for cytokine gene promoter activity relies on direct protein-protein interactions with the NFkappaB subunit RelA and histone acetylase cAMP-responsive element binding protein (CREB)-binding protein (CBP). RIP140-dependent control of proinflammatory gene expression via RelA/CBP may, therefore, represent a molecular rational for the cellular integration of metabolic and inflammatory pathways.
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PMID:Coactivator function of RIP140 for NFkappaB/RelA-dependent cytokine gene expression. 1846

Although eustachian tube dysfunction and bacterial infection have been shown to cause otitis media with effusion (OME), other etiologies are possible. One of the most common medical conditions in children is obesity, which can have effects throughout the body. Little is known, however, about the relationship between obesity and OME. Obesity may result in altered cytokine expression, gastroesophageal reflux disease, or fat accumulation, all of which may contribute to OME. Conversely, OME may induce taste changes through middle ear cavity inflammation, thus contributing to obesity. A similar pattern of taste change has been shown in patients with gustatory nerve anesthesia. Further research on the relationship between obesity and OME may help to determine the exact etiology of OME and contribute to our knowledge about the causes of obesity.
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PMID:Relationship between pediatric obesity and otitis media with effusion. 1981 20

Influenza is a seasonal viral infection associated with significant morbidity and mortality. In 2009, a novel H1N1 influenza A virus emerged and has been classified as a pandemic. In contrast to seasonal influenza, severe disease from pandemic H1N1 seems concentrated in older children and young adults, with almost no cases reported in patients older than 60 yrs. Although patients with underlying cardiopulmonary disease remain at risk, most complications have occurred among previously healthy individuals, with obesity and respiratory disease as the strongest risk factors. Pulmonary complications are common. Primary influenza pneumonia occurs most commonly in adults and may progress rapidly to acute lung injury requiring mechanical ventilation. Secondary bacterial infection is more common in children. Staphylococcus aureus, including methicillin-resistant strains, is an important cause of secondary bacterial pneumonia with a high mortality rate. Treatment of pneumonia should include empirical coverage for this pathogen. Neuromuscular and cardiac complications are unusual but may occur.
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PMID:Complications of seasonal and pandemic influenza. 1993 13

Obesity is an important background of metabolic syndrome progression. Our previous study demonstrated that chemokine CCL2 expression was suppressed in liver of obese mice that were highly susceptible to Listeria monocytogenes infection. We investigated the role of adiponectin in CCL2 expression in obese mice after L. monocytogenes infection. When leptin-deficient obese ob/ob mice were infected intraperitoneally with L. monocytogenes, the elimination of bacteria from spleen, liver, mesenteric lymph nodes and adipose tissue was inhibited in ob/ob mice compared with their heterozygote littermates, ob/? mice. CCL2 expression in the adipose tissue of ob/? mice was enhanced by L. monocytogenes infection, different from ob/ob mice. Similarly, adiponectin expression was not observed in the adipose tissue of ob/ob mice. When mouse adipocyte 3T3-F442A-derived adipocytes were infected with L. monocytogenes, CCL2 expression was transiently up-regulated, following up-regulation of adiponectin expression. Up-regulation of CCL2 in adipocytes by L. monocytogenes infection was suppressed by knocked-down of adiponectin expression and supplementation of recombinant adiponectin partially recovered CCL2 expression. These results suggest that adiponectin is required for appropriate expression of CCL2 that is important for macrophage recruitment in response to bacterial infection.
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PMID:Adiponectin is required for enhancement of CCL2 expression in adipose tissue during Listeria monocytogenes infection. 2004 52


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