Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0311277 (abdominal obesity)
 2,792 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Results from several recent reports have linked high serum C-reactive protein (CRP) levels to atherosclerotic disease and its complications. The aims of the present study were to investigate the relationship between CRP levels and subclinical atherosclerosis, as measured by ultrasound in the carotid and femoral arteries; and also to examine whether CRP levels are associated with antibodies to oxidized low-density lipoprotein (Ox-LDL). The study group (n = 391) consisted of clinically healthy 58-year-old men recruited from the general population. CRP and antibody titres to Ox-LDL were measured by ELISA. The results showed an association between CRP and ultrasound-assessed subclinical atherosclerosis in the femoral artery (r = 0.14, P = 0.010), and also between CRP and systolic blood pressure, diastolic blood pressure, heart rate, triglycerides, high-density lipoprotein, body mass index, waist-to-hip ratio (WHR), blood glucose, cigarette-years and antibody titres to ox-LDL (r = 0.19, P < 0.001). In this clinically healthy population of 58-year-old men, CRP levels were associated with both intima-media thickness and plaque occurrence in the femoral artery. The association between CRP and femoral atherosclerosis was not independent of smoking, serum LDL cholesterol, or systolic blood pressure. CRP levels were independently related to abdominal obesity measured as WHR, smoking and antibody titres to Ox-LDL.
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PMID:Relationship between C-reactive protein and intima-media thickness in the carotid and femoral arteries and to antibodies against oxidized low-density lipoprotein in healthy men: the Atherosclerosis and Insulin Resistance (AIR) study. 1125 71

Recent data suggest that infections, inflammation and the immune system are involved in the process of atherosclerosis. The aim of the present study was to analyze the association of coronary heart disease (CHD) with three inflammation markers, C-reactive protein (CRP), serum amyloid-A (SAA) and plasma fibrinogen. The cross-sectional study included 1400 men aged 45-74 years, who participated in a cardiovascular risk factor survey in Finland in 1997. Participants with prevalent CHD had markedly higher CRP, SAA and fibrinogen levels than participants without CHD. In logistic regression models, the age, smoking, serum cholesterol and systolic blood pressure adjusted odds ratios (2nd, 3rd and 4th quartile as compared with the 1st quartile) of CHD increased gradually with increasing quartile of CRP (1.90, 2.27, 2.64), SAA (1.68, 1.83, 2.41), and fibrinogen (1.60, 1.95, 2.14). The associations weakened somewhat after further adjustment for indicators of obesity, particularly waist hip-ratio. CRP, SAA and fibrinogen levels were markedly lower among CHD patients using cholesterol-lowering medication as compared to non-users. In conclusion, CRP, SAA and fibrinogen, which are markers of inflammation, were positively and significantly associated with prevalent CHD. Central obesity needs to be considered as a confounding factor in the observed associations. These findings support the hypothesis that cholesterol-lowering drugs have an anti-inflammatory effect.
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PMID:The association of c-reactive protein, serum amyloid a and fibrinogen with prevalent coronary heart disease--baseline findings of the PAIS project. 1139 43

Hypertension, dyslipidemia, impaired glucose tolerance, and obesity remain the major modifiable risk factors for most of the coronary disease afflicting the elderly. The relative risk associated with these established risk factors diminishes with advancing age, but this is offset by a greater absolute and attributable risk. Diabetes is increasing alarmingly in prevalence and operates more powerfully in women, eliminating their coronary disease resistance (relative to men). Interest in this entity now focuses on the insulin resistance syndrome promoted by abdominal obesity that has become so common in the elderly. The isolated systolic hypertension and large pulse pressure that predominate in the elderly is now recognized as a coronary disease hazard. Dyslipidemia, characterized by a high total to high-density lipoprotein cholesterol ratio, is the most predictive lipid profile for coronary disease in the elderly. High triglycerides, accompanied by low high-density lipoprotein cholesterol usually signifies insulin resistance and more atherogenic, small, dense low-density lipoprotein. Left ventricular hypertrophy is an ominous harbinger of coronary disease. Fibrinogen and the leukocyte count are correlated coronary disease risk factors that may indicate unstable lesions. Novel risk factors, such as hemostatic factors, homocysteine, lipoprotein(a), C-reactive protein, and hyperinsulinemia, are worthy of attention, but the efficacy of correcting them in the elderly has not yet been demonstrated. Nor has the efficacy of hormone replacement therapy in women. All the coronary risk factors tend to cluster, and the hazard posed by each is greatly influenced by the burden of coexisting risk factors. High-risk elderly candidates for coronary disease can be efficiently targeted for treatment by global risk assessment, using only the major established risk factors. The distinction between primary and secondary prevention in the elderly is less clear than in the middle-aged because they often have advanced presymptomatic vascular pathology that imposes a coronary event rate comparable to that of the middle-aged who have already sustained a clinical event. Declines in coronary mortality rates in the United States have included the elderly, justifying optimism about the efficacy of preventive measures. Most of the elderly have sufficient remaining life expectancy to warrant vigorous preventive management. Trials of risk factor modification in the elderly indicate that decades of exposure to modifiable risk factors can be countered by measures implemented late in life.
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PMID:Coronary heart disease risk factors in the elderly. 1187 68

Objectives. To examine the associations between smokeless tobacco use, smoking, cardiovascular risk factors, inflammation and ultrasound-assessed measures of atherosclerosis in the carotid and femoral arteries. Subjects. The study was performed in a population-based sample of clinically healthy men (n = 391) all 58 years old. Exclusion criteria were cardiovascular or other clinically overt diseases or continuous medication with cardiovascular drugs. Methods. The habits of smoking and oral moist snuff use were assessed by questionnaires. C-reactive protein (CRP) was assessed by high sensitive enzyme-linked immunosorbent assay (ELISA). Intima-media thickness (IMT) in the carotid bulb, the common carotid artery and the common femoral artery and plaque occurrence were measured by ultrasound. Results. The use of oral moist snuff was associated with serum triglycerides and waist-hip ratio (WHR), but not with CRP or ultrasound-assessed measures of subclinical atherosclerosis. Smoking, on the other hand, was associated with CRP, the components in the metabolic syndrome and IMT as well as plaques in the carotid and femoral arteries. In comparison to never-smokers the current smokers had higher values of WHR, triglycerides, C-reactive protein and IMT in carotid bulb and femoral artery. Ex-smokers were in general more obese and had a femoral IMT that was in-between that of never-smokers and current smokers. Conclusions. Tobacco smoking, but not oral moist snuff use, was associated with carotid and femoral artery IMT, and increased levels of CRP. Current smoking was also associated with abdominal obesity. Ex-smokers though, are generally more obese. Smoking was also associated with hyperinsulinaemia, dyslipidaemia and high blood pressure, i.e. the metabolic syndrome. The inhaled smoke from the combustion of tobacco seems to be an important aetiological factor in the atherosclerotic process.
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PMID:Carotid and femoral atherosclerosis, cardiovascular risk factors and C-reactive protein in relation to smokeless tobacco use or smoking in 58-year-old men. 1190 17

Undernutrition is a frequent complication of evolutive and chronic HIV (human immunodeficiency virus) infection characterized by bodyweight loss and changes in body composition. The Centers for Disease Control and Prevention define AIDS wasting as involuntary loss of more than 10% of body weight, plus more than 30 days of either diarrhea, or weakness and fever. Wasting syndrome has been considered as a case definition of the AIDS disease since 1987. Wasting syndrome is clearly linked to disease progression and death. Despite the progress under the era of highly active antiretroviral therapy (HAART), wasting is still a problem for people with AIDS. A small part of the weight lost is fat. More important is the loss of "lean body mass", which is mostly muscle. Body composition changes during HIV infection are different from those observed in food deprivation. Under the era of HAART, a HIV-associated adipose redistribution syndrome (HARS) was described that associates subcutaneous lipoatrophy and abdominal obesity linked to various metabolic disorders. Several factors contribute to wasting syndrome. Not only low food intake and poor nutrient absorption, but mainly altered metabolism (increased resting energy expenditure) and specific disturbances in protein turnover, which is also increased. Nutritional evaluation of HIV-infected patients should include the measurement of body composition and analysis of nutritional parameters, including albumin, transthyretin and C-reactive protein. Transthyretin seems to be particularly useful to follow the recovery period of malnutrition.
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PMID:Body composition and nutritional parameters in HIV and AIDS patients. 1255 39

Most actions of glucocorticoids (GCs) are mediated by the glucocorticoid receptor (GR). The interindividual response to GCs varies considerably, as demonstrated by a variable suppressive response to 0.25-mg dexamethasone (DEX). Several polymorphisms in the gene coding for the GR have been described. It is unclear to what extent the observed response variability is due to GR polymorphisms or to other factors. However, at least three polymorphisms seem to be associated with altered GC sensitivity and changes in body composition and metabolic parameters. The N363S polymorphism has been associated with increased sensitivity to GCs, increased insulin response to DEX, a tendency towards lower bone mineral density, and increased body mass index (BMI). However, other reports found no associations with BMI. Another polymorphism, previously described as a BclI restriction fragment length polymorphism, recently was identified as a C --> G nucleotide change. The G allele also was associated with increased sensitivity to GCs. In middle-aged subjects, the G allele of this BclI polymorphism was associated with increased abdominal obesity, while at older age, a lower BMI was found, accompanied by a tendency towards lower lean body mass. A third polymorphism consists of two linked, single-nucleotide mutations in codons 22 and 23, of which the second mutation results in an amino acid change from arginine (R) to lysine (K). In contrast to the other polymorphisms, this ER22/23EK polymorphism was associated with a relative resistance to GCs. In line with this, ER22/23EK carriers had lower total cholesterol and low-density lipoprotein cholesterol levels as well as lower fasting insulin concentrations and a better insulin sensitivity. C-reactive protein levels were lower in ER22/23EK carriers, as was found in a different population of elderly males. In accordance with this healthy metabolic profile, we found in this population a significantly better survival in ER22/23EK carriers after a 4-year follow-up. GCs also affect the brain. Although a certain level of cortisol is essential for proper brain functioning, excessive GC levels have been shown to negatively affect brain morphology and functions. At older age, we found that the risk of dementia and white matter lesions was lower in ER22/23EK carriers. GCs are also important in the regulation of body fat distribution. At young age, we observed sex-specific differences in body composition. Male ER22/23EK carriers were taller, had more muscle mass, and were stronger than noncarriers. In young females, ER22/23EK carriers had tendencies towards smaller waist and hip circumferences and lower body weight. Another polymorphism (TthIIII) was not associated with altered GC sensitivity. In conclusion, these polymorphisms in the GR gene may contribute considerably to the observed variability in GC sensitivity. As a result, they are associated with several differences in body composition and metabolic factors.
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PMID:Polymorphisms in the glucocorticoid receptor gene and their associations with metabolic parameters and body composition. 1474 9

Increasing efforts are being made to address, in public health policy (PHP), both the persistence of nutritional deprivation in economically disadvantaged communities, and the increase in so-called "chronic disease" (abdominal obesity, diabetes, cardiovascular disease, certain cancers, osteoporosis, arthritides, and inflammatory disease) in communities at all stages of economic development. The problems in the "chronic disease" descriptor are that its origins may be as early as conception, rather than during the postnatal lifespan, or even in previous generations; it may appear abruptly or slowly; and it may be amenable to environmental and behavioural intervention well into its course and in older age groups. It is also not necessarily "non-communicable", a qualifier often used for "chronic disease" (chronic non-communicable disease or CNCD) and often has inflammatory features, for example the inflammatory marker C-reactive protein is a predictor of macrovascular disease and ischaemic events can, in part, be prevented in the affected by influenzal vaccination. The nexus between immunodeficiency, inflammatory processes and nutritional status which is characteristic of "infective" and food-borne illness, is also more and more evident in "chronic disease". It may be more helpful to consider "chronic disease" as "eco-disease" with its environmental and behavioural contributors, and to regard that which is clearly nutritionally dependent as "eco-nutritional disease".
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PMID:Nutrition and prevention of chronic diseases: a unifying eco-nutritional strategy. 1505 57

The inflammatory marker C-reactive protein (CRP) is a highly promising cardiovascular risk factor. The data associating high sensitivity CRP (hsCRP) to atherosclerotic vascular disease, especially coronary artery disease, are strong, consistent and have been tested across many populations. Multivariate analysis shows that hsCRP has an independent predictive value to the prediction of coronary artery disease along with the conventional cardiovascular risk factors such as sex, age, cigarette smoking, blood pressure, diabetes, elevated total cholesterol (or low density lipoprotein cholesterol) and high density lipoprotein cholesterol. Retrospective analysis of published clinical trials show that individuals with elevated hsCRP benefit from the use of acetylsalicylic acid and/or the statin class of medication. Before implementing a public health policy that includes the measurement and clinical decision-making algorithm using hsCRP, several conditions must be met. Among them, a better understanding of the biology of CRP, an indepth scrutiny at the link between hsCRP levels, the metabolic syndrome, and abdominal obesity and finally, clinical trials, currently underway that will test the hypothesis that patients with elevated levels of hsCRP but a normal low density lipoprotein-cholesterol benefit from a pharmacological intervention for cardiovascular prevention in a primary prevention setting.
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PMID:Preventive cardiology: move over low density lipoprotein cholesterol, hello C-reactive protein? 1530 11

High-sensitivity C-reactive protein (hs-CRP) levels are closely associated with adiposity and predict coronary heart disease and type 2 diabetes mellitus. However, relationships of CRP to adiponectin and other markers of insulin resistance have been inadequately researched in children. We measured fasting serum levels of adiponectin, insulin, hs-CRP, and lipoproteins, and recorded the anthropometric profile and percentage of body fat (%BF; bioimpedance method) in 62 (36 normal weight, 26 overweight) healthy, urban, postpubertal Asian Indian males (aged 14 to 18 years). Serum levels of adiponectin were lower (P = not significant [NS]), whereas those of fasting insulin (P = .01) and hs-CRP (P = .02) were higher in overweight subjects. Adiponectin levels inversely correlated with body mass index (BMI; r = -0.26, P < .05), %BF (r = -0.24, P < .05), fasting insulin (r = -0.32, P < .05) and insulin resistance measured by the homeostasis model of assessment (HOMA-IR; r = -0.31, P < .05), but not with hs-CRP levels. Fasting insulin and hs-CRP levels correlated significantly with BMI, %BF, waist circumference (WC), waist-to-hip circumference ratio (W-HR), and triceps and subscapular skinfold thickness. The correlation of adiponectin with insulin sensitivity was independent of abdominal obesity, but became nonsignificant after controlling for BMI and %BF. Further, BMI was an independent predictor of adiponectin levels and the ratio of adiponectin and %BF was an independent predictor of fasting insulin levels. Although adiponectin levels did not correlate with hs-CRP levels, we observed dichotomous relationships of adiponectin and hs-CRP levels with generalized and abdominal obesity, respectively. We conclude that generalized obesity affects the adiponectin-insulin relationship in postpubertal Asian Indian males; however, the relationship of adiponectin with hs-CRP needs further evaluation.
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PMID:Adiponectin, insulin resistance, and C-reactive protein in postpubertal Asian Indian adolescents. 1537 91

Development of hypertension has been linked to chronic low-grade inflammation. However, it is not known whether this connection is mediated by features of the metabolic syndrome or smoking, or their changes, which themselves have been linked to inflammation. We studied the predictive value of highly sensitive C-reactive protein (hs-CRP), smoking, and abdominal obesity to the development of hypertension in an 11-year follow-up of a population-based study cohort comprising 379 middle-aged normotensive men. During the follow-up, 124 men (33%) developed hypertension. Men with hs-CRP > or =3.0 mg/L were 2.8x (95% confidence interval, 1.2 to 6.6) more likely to develop hypertension than with hs-CRP <1.0 mg/L even after adjustment for features of the metabolic syndrome, lifestyle factors, and their changes. Cigarette smoking was also associated with development of hypertension independently of inflammation and other confounders. Waist girth increased more in men who quit smoking than in other men. An increase in waist girth during follow-up strongly predicted incident hypertension. The decrease in smoking was not associated with a lower risk of hypertension in age-adjusted analyses. Hypertension is preceded by low-grade chronic inflammation in middle-aged white men independently of smoking or features of the metabolic syndrome. Furthermore, smoking may be a risk factor for hypertension. Although stopping smoking is beneficial with respect to health outcomes, the subsequent increase in weight and waist girth associated with smoking cessation may offset the decrease in the risk of hypertension that one may otherwise expect.
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PMID:Inflammation, abdominal obesity, and smoking as predictors of hypertension. 1549 31


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