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Query: UMLS:C0948265 (metabolic syndrome)
 24,271 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The insulin resistance syndrome, otherwise known as the metabolic syndrome, describes a cluster of cardiovascular and metabolic abnormalities, which are strongly associated with overweight and obesity. The importance of the syndrome is due to its increased rates of cardiovascular morbidity and mortality. Insulin resistance is also characterized by elevated free fatty acid (FFA) levels. In otherwise healthy human subjects, elevation of FFA impairs endothelial function. This appears to be largely the result of blunting of nitric oxide-dependent tone, most likely at the level of the endothelial isoform of nitric oxide synthase (eNOS). Some of the potential mediatory mechanisms include oxidative stress, proinflammatory cytokines, C-reactive protein, or endogenous inhibitors of eNOS. Regardless of the mechanism(s) that mediates the effects of increased FFA on the vasculature, impaired vascular function is likely to account, at least in part, for the increase in cardiovascular mortality in subjects with the insulin resistance syndrome.
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PMID:FFAs: do they play a role in vascular disease in the insulin resistance syndrome? 1566 14

Advances in adipose tissue biology over the past 10 years have led to an improved understanding of the mechanisms linking obesity with the metabolic syndrome and other complications. Obesity is characterized by a chronic, systemic low-grade state of inflammation. Biomarkers of inflammation, such as the leukocyte count, tumor necrosis factor-alpha (TNF-alpha), interleukin 6 (IL-6), and C-reactive protein, are increased in obesity, associated with insulin resistance, and predict the development of type 2 diabetes and cardiovascular disease. It is now clear that the adipocyte is an active participant in the generation of the inflammatory state in obesity. Adipocytes secrete a variety of cytokines, including IL-6 and TNF-alpha, that promote inflammation. Moreover, recent studies suggest that obesity is associated with an increase in adipose tissue macrophages, which also participate in the inflammatory process through the elaboration of cytokines. An improved understanding of the role of adipose tissue in the activation of inflammatory pathways may suggest novel treatment and prevention strategies aimed at reducing obesity-associated morbidities and mortality.
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PMID:The evolving role of inflammation in obesity and the metabolic syndrome. 1566 21

Relatively limited contemporary information is available about the magnitude of, and factors associated with, the metabolic syndrome in adult men and women. The purpose of our observational study was to describe the prevalence and predictors of the metabolic syndrome in a sample of employed adults attending a worksite cardiovascular screening program. The study sample consisted of 871 men and women between the ages of 21 and 77 years from 6 locations of the parent company. These individuals attended an employer-sponsored cardiovascular screening and wellness program during 2003. A standardized questionnaire was administered to all study participants and a number of different coronary risk factors were measured. Approximately 27% of the study sample was classified as having the metabolic syndrome. Men, persons with a history of hypertension, heart disease, or stroke, sedentary individuals, and those with an increased heart rate and higher levels of C-reactive protein were associated with presence of the metabolic syndrome. A relatively similar risk factor profile was noted in persons without a self-reported history of prior cardiovascular disease. The results of our cross-sectional observational study suggest that the prevalence of the metabolic syndrome is considerable. A number of demographic, comorbid, and other factors are associated with this syndrome. Increased attention to the metabolic syndrome, and modification of predisposing factors, remains of considerable public health and clinical importance.
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PMID:Metabolic syndrome in a screened worksite sample: prevalence and predictors. 1566 35

Female sexual dysfunction (FSD) is a significant public health problem. We assessed the prevalence of FSD in premenopausal women with the metabolic syndrome as compared to the general female population. Compared with the control group (N = 80), women with the metabolic syndrome (N = 120) had reduced mean full Female Sexual Function Index (FSFI) score (23.2+/-5.4 vs 30.1+/-4.7, P < 0.001), reduced satisfaction rate (3.5+/-1.1 vs 4.7+/-1.2, P < 0.01), and higher circulating levels of C-reactive protein (CRP: 2.2 (0.6/4.9) vs 0.8 (0.2/2.9) mg/l, median (interquartile range), P = 0.01). There was an inverse relation between CRP levels and FSFI score (r = -0.32, P=0.02). Investigation of female sexuality is suggested for patients with the metabolic syndrome.
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PMID:The metabolic syndrome: a cause of sexual dysfunction in women. 1614 28

The purpose of this study was to determine whether benign hereditary leukopenia-neutropenia in Yemenites may be reflective of an absent or a lesser degree of chronic low grade inflammation that has been documented to exist in most apparently healthy subjects. The white blood cell count (WBCC), fibrinogen as well as high sensitivity C-reactive protein (hs-CRP) concentrations were determined in a group of apparently healthy individuals during their routine health screening program. These inflammatory biomarkers in a group of 82 Yemenite Jews were compared to those measured in a group of 1817 individuals whose parents immigrated to Israel from Central and East Europe, from countries surrounding the Mediterranean Sea as well as the Middle East. The two study groups were matched for possible confounding factors that may have an influence on the intensity of the microinflammatory response including age, gender, body mass index, components of the metabolic syndrome and the Ten Year Calculated Coronary Heart Disease Framingham Risk Score. The expected reduced WBCC was noted in the group of Yemenite Jews (6.99 +/- 1.64 versus 5.88 +/- 2.06 x 10(3)/microL cells, P = 0.001). However, they had significantly enhanced concentrations of hs-CRP, the respective values being 2.1 +/- 2 versus 1.4 +/- 2.4 mg/L in men (P = 0.002) and 2.5 +/- 2.2 versus 1.4 +/- 2.9 in women (P < 0.0005). An increased concentration of fibrinogen was found in the Yemenite Jews, although the difference was not statistically significant in men. Thus, the leukopenia-neutropenia in Yemenite Jews is probably not an expression of an absent or lesser degree of chronic low grade inflammation. These findings shed more light on the potential mechanisms that are responsible for the low WBCC in this particular ethnic group.
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PMID:Benign hereditary leukopenia-neutropenia does not result from lack of low grade inflammation. A new look in the era of microinflammation. 1572 95

Women with Turner syndrome (TS) have increased risks of atherosclerosis, diabetes mellitus, and obesity. We hypothesized that women with TS have adverse metabolic or inflammatory markers for cardiovascular disease compared with normal women and estrogen-deficient controls. This was a cross-sectional study conducted at University College London Hospitals, UK. One hundred seventeen estrogen-treated women with TS and normal fasting blood glucose were compared with 30 age-matched normal controls and 31 estrogen-treated women with 46,XX premature ovarian failure (POF). The main outcome measures were markers of the metabolic syndrome, including the adipokines IL-6 and leptin, and C-reactive protein (CRP). TS women were more obese than controls (waist circumference, 79.9 +/- 12.4, 73.5 +/- 6.9, and 74.7 +/- 8.6 cm in TS, normal subjects, and POF controls, respectively; P = 0.005; body mass index, 26.8 +/- 5.8, 23.7 +/- 3.2, and 22.9 +/- 3.4 kg/m2; P < 0.001). This obesity was associated with increased CRP (2.9 +/- 1.5, 0.8 +/- 1.0, and 1.2 +/- 0.9 mg/liter; P < 0.001) and IL-6 concentrations (1.5 +/- 0.7, 1.0 +/- 1.5, and 1.2 +/- 0.5 pg/ml; P = 0.014), but lower fasting serum insulin (4.7 +/- 2.3, 6.3 +/- 3.0, and 6.9 +/- 2.9 mIU/ml; P = 0.004), glucose (83 +/- 11, 90 +/- 7, and 90 +/- 7 mg/dl; P < 0.001), and leptin (10.2 +/- 6.3, 14.4 +/- 7.6, and 14.8 +/- 8.1 ng/ml; P = 0.048). Triglyceride concentrations were similar in TS and POF women and were greater than in normal controls (97 +/- 53, 97 +/- 53, and 71 +/- 27 mg/dl; P = 0.024). We conclude that women with TS have various physical and biochemical features suggestive of the metabolic/insulin resistance syndrome, but there is a discrepancy among CRP, IL-6, and leptin, with leptin and fasting insulin concentrations being lower than expected for the degree of obesity. Obesity and estrogen therapy do not fully explain these findings. Women with TS may have specific metabolic defects contributing to cardiovascular risk.
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PMID:Adipokine dysregulation in turner syndrome: comparison of circulating interleukin-6 and leptin concentrations with measures of adiposity and C-reactive protein. 1572 8

Atherosclerotic cardiovascular disease (CVD), a leading cause of morbidity and mortality in the general population, is also an increasing cause for concern for HIV-infected patients. A number of risk factors for CVD are also associated with HIV disease and HIV therapy, particularly insulin resistance, metabolic dyslipidemia, and inflammation. For example, atherogenic dyslipidemia, a side effect of HIV therapy, is an established risk for CVD in the non-HIV-infected population. As our understanding of atherosclerotic disease evolves, new markers of CVD risk have been identified, including metabolic syndrome definitions and C-reactive protein, a marker of inflammation. Use of these markers, in association with established risk factor guidelines, may serve as important tools in helping HIV physicians implement drug regimens that allow optimum management of metabolic complications associated with HIV and HAART, and thereby reduce CVD risk. The objective of this article is to review the mechanisms of atherosclerotic CVD and to discuss risk factors and markers that can be applied in the evaluation and treatment of CVD in the HIV-positive population.
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PMID:Atherosclerotic cardiovascular disease risk in the HAART-treated HIV-1 population. 1576 7

Atherosclerosis is the major cause of death in the world. Fasting and postprandial hyperlipidaemia are important risk factors for coronary heart disease (CHD). Recent developments have undoubtedly indicated that inflammation is pathophysiologically closely linked to atherogenesis and its clinical consequences. Inflammatory markers such as C-reactive protein (CRP), leucocyte count and complement component 3 (C3) have been linked to CHD and to hyperlipidaemia and several other CHD risk factors. Increases in these markers may result from activation of endothelial cells (CRP, leucocytes, C3), disturbances in adipose tissue fatty acid metabolism (CRP, C3), or from direct effects of CHD risk factors (leucocytes). It has been shown that lipoproteins, triglycerides, fatty acids and glucose can activate endothelial cells, most probably as a result of the production of reactive oxygen species. Similar mechanisms may also lead to leucocyte activation. Increases in triglycerides, fatty acids and glucose are common disturbances in the metabolic syndrome and are most prominent in the postprandial phase. People are in a postprandial state most of the day, and this phase is proatherogenic. Inhibition of the activation of leucocytes, endothelial cells, or both, is an interesting target for intervention, as activation is obligatory for adherence of leucocytes to the endothelium, thereby initiating atherogenesis. Potential interventions include the use of unsaturated long-chain fatty acids, polyphenols, antioxidants, angiotensin converting enzyme inhibitors and high-dose aspirin, which have direct anti-inflammatory and antiatherogenic effects. Furthermore, peroxisome proliferator activating receptor gamma (PPARgamma) agonists and statins have similar properties, which are in part independent of their lipid-lowering effects.
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PMID:Lipaemia, inflammation and atherosclerosis: novel opportunities in the understanding and treatment of atherosclerosis. 1576 89

Regular exercise offers protection against all-cause mortality, primarily by protection against cardiovascular disease and Type 2 diabetes mellitus. The latter disorders have been associated with chronic low-grade systemic inflammation reflected by a two- to threefold elevated level of several cytokines. Adipose tissue contributes to the production of TNF-alpha, which is reflected by elevated levels of soluble TNF-alpha receptors, IL-6, IL-1 receptor antagonist, and C-reactive protein. We suggest that TNF-alpha rather than IL-6 is the driver behind insulin resistance and dyslipidemia and that IL-6 is a marker of the metabolic syndrome, rather than a cause. During exercise, IL-6 is produced by muscle fibers via a TNF-independent pathway. IL-6 stimulates the appearance in the circulation of other anti-inflammatory cytokines such as IL-1ra and IL-10 and inhibits the production of the proinflammatory cytokine TNF-alpha. In addition, IL-6 enhances lipid turnover, stimulating lipolysis as well as fat oxidation. We suggest that regular exercise induces suppression of TNF-alpha and thereby offers protection against TNF-alpha-induced insulin resistance. Recently, IL-6 was introduced as the first myokine, defined as a cytokine that is produced and released by contracting skeletal muscle fibers, exerting its effects in other organs of the body. Here we suggest that myokines may be involved in mediating the health-beneficial effects of exercise and that these in particular are involved in the protection against chronic diseases associated with low-grade inflammation such as diabetes and cardiovascular diseases.
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PMID:The anti-inflammatory effect of exercise. 1577 55

As a growing number of patients with low low-density lipoprotein cholesterol levels are diagnosed with atherosclerosis, research has shifted toward markers of inflammation in an attempt to improve global cardiovascular risk prediction. These markers include cytokines, cell adhesion molecules, and acute phase reactants like high sensitivity C-reactive protein, an innate immune response protein. When measured with new high-sensitivity assays, levels of high sensitivity C-reactive protein have proven to predict future cardiovascular risk at all levels of low-density lipoprotein cholesterol, at all levels of the Framingham Risk Score, and at all levels of the metabolic syndrome. Among apparently healthy men and women, levels of high sensitivity C-reactive protein of <1, 1-3, and >3 mg/L distinguish between those at low, moderate, and high risk for future cardiovascular disease, respectively. In clinical practice, high sensitivity C-reactive protein should be used along with lipid evaluation as part of global risk assessment. Improved knowledge of cardiovascular risk should lead to improved compliance with both lifestyle and pharmacologic interventions designed to prevent future cardiovascular events.
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PMID:High sensitivity C-reactive protein in clinical practice. 1578 90


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