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)

The reality of metabolic syndrome (MS) as a specific entity is debatable. However, the simple measure of waist circumference (>94 cm in men and >80 cm in women) is useful: (1) to check for insulin resistance by measuring serum levels of fasted glucose and insuline, cholesterol, triglycerides; (2) to look for diseases associated with MS such as hypertension, non alcohoolic steatohepatitis, sleep apnea, polycystic ovary disease, hypogonadism and to measure serum levels of ferritine, ALAT, ASAT, urate acid, CRP hs, testosterone and (3) to make obese people aware of their risk of becoming diabetic and to motivate them to change their life style. The utility of exercise and of various diets is discussed as well as the efficiency of drugs acting on different components of MS such as rimonabant, orlistat, metformin, glitazones, telmisartan and testosterone. The importance of political measures to fight the obesity epidemic is underlined.
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PMID:[Metabolic syndrome: jumble syndrome of obesity or specific entity? Which treatment: diet or polypill?]. 1838 74

Lipocalin-2 (also known as neutrophil gelatinase-associated lipocalin [NGAL]) has been described as a promising marker of metabolic syndrome associated with inflammation. The aim of our work was to develop an assay for the determination of lipocalin-2 in human serum and to investigate its levels in healthy volunteers and donors suffering from metabolic syndrome. We also conducted a pilot study on individuals with metabolic syndrome and on healthy probands and measured lipocalin-2 in these individuals. We developed and evaluated the sandwich ELISA method for the quantitative determination of human lipocalin-2 in serum samples. We measured blood pressure, waist circumference, serum cholesterol, triglycerides, HDL cholesterol, LDL cholesterol, insulin, glucose, creatinine, hs-CRP, and adiponectin and calculated the BMI and Quicki insulin sensitivity index. In the study on 153 healthy volunteers, we showed that sex and age are not determinative for lipocalin-2 serum values. Furthermore, we tested 45 individuals with metabolic syndrome; values of lipocalin-2 did not differ (78.8 vs. 80.0 microg/l, p =0.56) from the data of healthy individuals from the first study. Neither group differed with regard to sex or age. Lipocalin-2 correlated with alanine aminotransferase (ALT) (r=-0.3, p<0.01) aspartate aminotransferase (AST) (r=-0.3, p<0.01), cholesterol (r=-0.21, p=0.047), creatinine (r=0.19, p=0.05), and high-sensitivity C-reactive protein (hs-CRP) (r=0.22, p=0.036). No significant correlation was found between serum lipocalin-2 and BMI, waist circumference, blood pressure, triglycerides, HDL, Quicki, or the number of metabolic syndrome components. When study patients with metabolic syndrome were further stratified according to the number of components of metabolic syndrome, serum concentrations of lipocalin-2 did not differ. The results presented demonstrate the analytical competence of the lipocalin-2 assay. However, we assumed that lipocalin-2 is not a routinely usable marker of metabolic syndrome or obesity. The association between serum lipocalin-2 and obesity or metabolic syndrome was not validated in our study.
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PMID:Lipocalin-2: development, analytical characterization, and clinical testing of a new ELISA. 1839 69

Various modifiable risk factors have been associated with inflammation and haemostasis, although the accumulative effects have not yet been examined. We therefore explored additive and independent associations of modifiable risk factors (smoking, alcohol, cholesterol, obesity, hypertension, physical activity) with inflammatory (CRP) and haemostatic (fibrinogen) markers. Data were collected from a sample of 7670 healthy asymptomatic participants (45.9% men, aged 46.2+/-15.6 years). A graded increase in the risk of inflammation (CRP> or =3 mg/L) with increasing numbers of modifiable risk factors was demonstrated (odds ratio for > or =4 risk factors=5.09, 95% CI, 3.96-6.55). Similar associations were found in relation to haemostasis. Central adiposity was the strongest independent predictor of inflammation (OR=3.45, 95% CI, 3.07-3.87) although smoking most strongly predicted haemostasis (OR=2.19, 95% CI, 1.94-2.48). These findings suggest that targeting multiple risk factors is likely to have the greatest benefit for cardiovascular prevention.
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PMID:The accumulative effects of modifiable risk factors on inflammation and haemostasis. 1841 Oct 23

One of the leading problems encountered in patients undergoing peritoneal dialysis is infectious complications including peritonitis. We aimed to investigate the etiology, clinical presentation and therapy of peritonitis attacks in patients undergoing peritoneal dialysis (PD) in two ultimate hospitals in Eskisehir (located at middle Anatolia region of Turkey) over seven years. We determined 179 peritonitis attacks in 74 (62.2%) of 119 patients undergoing PD. The average annual peritonitis incidence in PD patients was found as 0.4. Of 42 patients with multiple peritonitis attacks, seven (16.7%) had relapsing and eight (19%) had recurrent peritonitis. Four (2.2%) of the 179 peritonitis attacks were evaluated as nosocomial peritonitis. The most common findings were abdominal pain (80.4%), cloudy peritoneal fluid (70.9%), increased erythrocyte sedimentation rates (69.3%) and elevated CRP levels (57.5%). Co-morbidities, initial serum albumin reduction, obesity or overweight status and duration of PD catheterization were found as risk factors related to the development of peritonitis in PD patients. The most common causative microorganisms were coagulase-negative staphylococci (21.8%), Staphylococcus aureus (8.9%), Enterococcus spp. (5.6%) and Escherichia coli (3.3%). Eighty two (45.8%) of 179 peritonitis attacks were culture-negative. The antimicrobial agents which have been used for the therapy of peritonitis attacts were cefazolin+ceftazidim (27.9%), cefazolin+amikacin (24%), ceftazidim+vancomycin (9.5%), vancomycin+amikacin (7.3%), vancomycin+amikacin+cefazolin (5.6%), vancomycin alone (5%) and the others (20.7%). Ten (5.6%) patients were placed under hemodialysis due to peritonitis, and seven of 179 attacks in 74 patients who developed peritonitis were fatal (fatality rate: 3.9%). It could be concluded that the patients to undergo PD should be given education about the process, as well the microbiological evaluation of these patients should be looked over. Since gram-positive bacteria were commonly responsible for peritonitis following PD, empirical treatment with vancomycin would lead to more successful results.
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PMID:[Peritonitis related to peritoneal dialysis: evaluation of 179 attacks]. 1869 24

Elevated postprandial lipemia is emerging as a risk factor for obesity-related chronic diseases, such as type 2 diabetes and cardiovascular disease, and is associated with alterations in several metabolic biomarkers of disease. Our goal was to examine the effects of specific polyunsaturated/saturated fatty acid (P/S) ratios on postprandial triacylglycerol (TAG) concentrations and metabolic biomarkers in men with different fasting TAG concentrations through a series of oral fat tolerance tests (OFTT) consisting solely of emulsified lipid. Otherwise healthy men with high (>1.69 mmol/L) fasting TAG (HTAG, n=8) and low fasting TAG (LTAG, n=8) underwent three OFTTs with specific P/S ratios of 0.2, 1.0 and 2.0, respectively, and a total lipid load of 1 g/kg subject body mass. All subjects received each treatment separated by at least 1 week. Postprandial plasma TAG fatty acid composition reflected fatty acids present in the OFTT. All other metabolic responses were independent of the P/S ratio ingested. An accelerated increase in postprandial TAGs was observed in HTAG compared to LTAG. Interleukin (IL)-6 and soluble intercellular adhesion molecule (sICAM)-1 were significantly elevated in HTAG at baseline (P<.05). IL-6 increased significantly following each OFTT (P<.05) in both groups. Postprandial glucose and CRP were significantly exaggerated (P<.05) in HTAG. Overall, HTAG subjects had an accelerated postprandial TAG response and increased concentrations of several inflammatory markers following an OFTT, in the absence of an insulin response. However, P/S ratio had no influence on postprandial lipid and inflammatory parameters.
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PMID:Fasting triacylglycerol status, but not polyunsaturated/saturated fatty acid ratio, influences the postprandial response to a series of oral fat tolerance tests. 1882 81

Serum glycated albumin (GA) is the clinical markers reflecting recent plasma glucose levels. We have previously clarified that serum GA levels are low for obesity and chronic inflammation is involved in the obesity-associated decrease in GA levels through acceleration of albumin catabolism. The present study investigated whether smoking, which is a representative factor that increases CRP, affects serum GA levels. One hundred and three male subjects with normal glucose tolerance (70 nonsmokers, 33 smokers) were enrolled in this study. Smokers and nonsmokers displayed no significant differences in fasting plasma glucose (FPG), oral glucose tolerance test 2-h glucose and HbA(1C). CRP levels were significantly higher in smokers than in nonsmokers (P < 0.05). Serum GA levels were significantly lower in smokers than in nonsmokers (P < 0.05). Stepwise multivariate regression analysis identified FPG and age as positively associated, and BMI and smoking as negatively associated with serum GA levels. In conclusion, serum GA levels were significantly lower in smokers than in nonsmokers. Smoking was identified as a significant negative explanatory variable for serum GA levels. These findings suggest that the inflammation-induced acceleration of albumin metabolism may be involved in the mechanism by which smoking is associated with serum GA levels.
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PMID:Serum glycated albumin levels are influenced by smoking status, independent of plasma glucose levels. 1883 52

Insulin resistance and obesity are intimately related to a chronic low grade systemic inflammation. Interleukin-6 (IL-6) may influence the pathogenesis of obesity-related diseases. The aim of this study is to investigate the effect of body's fat mass on the relationships between -174G/C IL-6 promoter gene polymorphism, IL-6 circulating level and insulin resistance. A population of 150 Caucasian women was studied, subdivided according to their body composition in non-obese (NW), Normal Weight Obese (NWO) and preobese-obese (OB). The NWO subjects were found in an intermediate position between the NW and OB subjects in terms of body weight, fat mass percentage (FM%), abdominal FAT%, hs-CRP and plasma triglyceride level. Fasting plasma IL-6 concentration was positively correlated with the homeostasis model assessment for insulin resistance (HOMA-IR) in all subjects analyzed (P=0.0014). In NWO and OB women a significantly increased IL-6 mean value was observed compared with NW subjects. In G/G population, the IL-6 plasma level of NWO and OB was significantly higher with respect to NW. No significant differences of IL-6 concentrations were observed in the three groups carrying G/C genotype. NWO and OB women homozygous for the allele C have significantly lower value of IL-6 with respect to NW subjects. IL-6 concentration was positively correlated with FM% in G/G (R(2)=0.397, P<0.001) and was negatively correlated in C/C (R(2)=0.459, P=0.002). No significant correlation was observed in G/C genotype (R(2)=0.041, P=0.173). In conclusion our study confirms that, at least in Italian Caucasian females, the FM% is a major determinant of an increase in IL-6 production and insulin resistance. -174 G/C IL-6 promoter polymorphism represents a marker which could help to identify, time in advance, "vulnerable" individuals at risk of age and obesity related diseases.
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PMID:Body composition and -174G/C interleukin-6 promoter gene polymorphism: association with progression of insulin resistance in normal weight obese syndrome. 1899 89

Platelet hyporesponsiveness to the anti-aggregatory effects of nitric oxide (NO) occurs commonly in association with myocardial ischemia and coronary risk factors, often co-exists with endothelial dysfunction and represents an independent marker of long-term cardiovascular risk. We sought to determine whether polycystic ovary syndrome (PCOS), which has been postulated as a cardiovascular risk factor in women, is independently associated with this phenomenon. Twenty-four young women with PCOS (mean age 32.1+/-1.3) were evaluated in lean (n=12) and obese (n=12) subgroups, and compared with age-matched lean normals (n=12). Platelet aggregation and its inhibition by the nitric oxide donor sodium nitroprusside (SNP) were assessed and compared with vascular endothelial function. Plasma concentrations of malondialdehyde (MDA), N(G),N(G)-dimethyl-L-arginine (ADMA) and hs-CRP were measured as markers of oxidative stress, endothelial dysfunction and inflammation, respectively. Circulating endothelial progenitor cell (EPC) counts were also documented. In both PCOS subgroups, which demonstrated hyperaggregability to ADP, responses to SNP inhibition of aggregation (the principal end-point of the study) were significantly impaired (P<0.01 for both), as were their endothelium-dependent vascular responses to salbutamol (P<0.05 for both). However, vasomotor responses to nitroglycerin and circulating EPC counts did not vary between groups. PCOS subjects also had significantly elevated ADMA, MDA and hs-CRP levels relative to normals (all P<0.05). Impairment of SNP response remained unaltered after mean 30+/-2.4 months follow-up in PCOS subjects. We conclude that in PCOS subjects, independent of obesity and associated insulin resistance, profound and reproducible impairment of platelet responsiveness to NO is an additional component of cardiovascular homeostatic disturbance.
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PMID:Polycystic ovary syndrome is associated with severe platelet and endothelial dysfunction in both obese and lean subjects. 1902 16

Recent work shows a high prevalence of low testosterone and inappropriately low LH and FSH concentrations in type 2 diabetes. This syndrome of hypogonadotrophic hypogonadism (HH) is associated with obesity, and other features of the metabolic syndrome (obesity and overweight, hypertension and hyperlipidemia) in patients with type 2 diabetes. However, the duration of diabetes or HbA1c were not related to HH. Furthermore, recent data show that HH is also observed frequently in patients with the metabolic syndrome without diabetes but is not associated with type 1 diabetes. Thus, HH appears be related to the two major conditions associated with insulin resistance: type 2 diabetes and the metabolic syndrome. CRP concentrations have been shown to be elevated in patients with HH and are inversely related to plasma testosterone concentrations. This inverse relationship between plasma free testosterone and CRP concentrations in patients with type 2 diabetes suggests that inflammation may play an important role in the pathogenesis of this syndrome. This is of interest since inflammatory mechanisms may have a cardinal role in the pathogenesis of insulin resistance. It is relevant that in the mouse, deletion of the insulin receptor in neurons leads to HH in addition to a state of systemic insulin resistance. It has also been shown that insulin facilitates the secretion of gonadotrophin releasing hormone (GnRH) from neuronal cell cultures. Thus, HH may be the result of insulin resistance at the level of the GnRH secreting neuron. Low testosterone concentrations in type 2 diabetic men have also been related to a significantly lower hematocrit and thus to an increased frequency of mild anemia. Low testosterone concentrations are also related to an increase in total and regional adiposity, and to lower bone density. This review discusses these issues and attempts to make the syndrome relevant as a clinical entity. Clinical trials are required to determine whether testosterone replacement alleviates symptoms related to sexual dysfunction, and features of the metabolic syndrome, insulin resistance and inflammation.
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PMID:Hypogonadotrophic hypogonadism in type 2 diabetes, obesity and the metabolic syndrome. 1907 78

Fatigue is a serious health concern in the elderly. Sex differences exist in adiposity, systemic inflammation, physical activity/fitness and fatigue; however, the relations among these variables remain inadequately characterized impeding the development of fatigue prevention strategies. Measures of adiposity, C-reactive protein, physical activity, aerobic fitness, fatigue, sleep quality and depression were obtained from 127 community-dwelling older adults. Although similar in age (70 y) and BMI (28.0kg/m(2)) women (n=80) reported 63% greater fatigue than men (p=0.04). Adiposity (r=0.44), CRP (r=0.29), physical activity (r=-0.26) and fitness (r=-0.41) were related to fatigue in women (all p<0.05), but not in men. Depression was also related to fatigue in women (r=0.37), and was the only variable related to fatigue in men (r=0.42). In women, fatigue was independently explained (all p<0.05) by CRP (6.6%), depression (6.3%), physical activity (5.8%), and adiposity (3.9%); however, in men, only depression explained variance in fatigue (12.0%). CRP was 40% higher and adiposity 12% higher in women reporting fatigue compared to those with no fatigue; no such differences existed in men. Obese women perceived a greater degree of fatigue than non-obese women, but this was not the case in men. Women report more fatigue than men which was independently associated with inflammation, depression, physical activity and adiposity, whereas in men the only independent predictor was depression. Strategies to prevent fatigue may differ in older women and men, especially with regard to inflammation, physical activity and adiposity.
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PMID:Sex differences in the relationship between obesity, C-reactive protein, physical activity, depression, sleep quality and fatigue in older adults. 1913 24


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