Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0242339 (dyslipidemia)
13,927 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiovascular events in patients with type 2 diabetes mellitus are a major problem in clinical practice, and patients with diabetes have derived less benefit from advances in preventive and interventional cardiology. Tighter goals for metabolic management and attention to nontraditional risk factors may be needed in this patient group. Insulin resistance rather than hyperinsulinemia is thought to underlie cardiovascular disease in patients with diabetes. Insulin resistance is associated with cardiovascular events and a wide range of traditional and nontraditional risk factors for cardiovascular disease (e.g., endothelial dysfunction, dyslipidemia, inflammation, vascular wall abnormalities). Therapy with lifestyle modifications, metformin, or thiazolidinediones (TZDs) corrects many of the abnormalities associated with diabetes in addition to lowering blood glucose and correcting diabetic dyslipidemia. TZDs, acting via the peroxisome proliferator-activated receptor-gamma, affect a number of mediators involved in the development of the cardiovascular complications of diabetes, including lipid profiles, vascular changes, and inflammatory mediators. TZDs decrease plasminogen activator-1 and C-reactive protein levels. They also reduce the extent of thickening of the carotid artery and reduce hyperplasia after coronary stent implantation. Insulin-sensitizing therapy with TZDs is a promising intervention for patients with diabetes at risk for adverse cardiovascular outcomes.
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PMID:Rationale for the use of insulin sensitizers to prevent cardiovascular events in type 2 diabetes mellitus. 1782 42

The metabolic syndrome (MetS) phenotype is typically characterized by visceral obesity, insulin resistance, atherogenic dyslipidemia involving hypertriglyceridemia and subnormal levels of high density lipoprotein-cholesterol (HDL-C), oxidative stress and elevated cardiovascular risk. The potent antioxidative activity of small HDL3 is defective in MetS [Hansel B, et al. J Clin Endocrinol Metab 2004;89:4963-71]. We evaluated the functional capacity of small HDL3 particles from MetS subjects to protect endothelial cells from apoptosis induced by mildly oxidized low-density lipoprotein (oxLDL). MetS subjects presented an insulin-resistant obese phenotype, with hypertriglyceridemia, elevated apolipoprotein B and insulin levels, but subnormal HDL-C concentrations and chronic low grade inflammation (threefold elevation of C-reactive protein). When human microvascular endothelial cells (HMEC-1) were incubated with oxLDL (200 microg apolipoprotein B/ml) in the presence or absence of control HDL subfractions (25 microg protein/ml), small, dense HDL3b and 3c significantly inhibited cellular annexin V binding and intracellular generation of reactive oxygen species. The potent anti-apoptotic activity of small HDL3c particles was reduced (-35%; p<0.05) in MetS subjects (n=16) relative to normolipidemic controls (n=7). The attenuated anti-apoptotic activity of HDL3c correlated with abdominal obesity, atherogenic dyslipidemia and systemic oxidative stress (p<0.05), and was intimately associated with altered physicochemical properties of apolipoprotein A-I (apoA-I)-poor HDL3c, involving core cholesteryl ester depletion and triglyceride enrichment. We conclude that in MetS, apoA-I-poor, small, dense HDL3c exert defective protection of endothelial cells from oxLDL-induced apoptosis, potentially reflecting functional anomalies intimately associated with abnormal neutral lipid core content.
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PMID:Metabolic syndrome features small, apolipoprotein A-I-poor, triglyceride-rich HDL3 particles with defective anti-apoptotic activity. 1786 79

Atherogenic dyslipidemia, manifest by low HDL-cholesterol and high TG levels, is an important component of ATP-III defined metabolic syndrome. Here, we dissected the phenotypic and genetic architecture of these traits by assessing their relationships with other metabolically relevant measures, including plasma adipo-cytokines, highly sensitive C-reactive protein (hsCRP) and LDL particle size, in a large family data set (n=2800) and in an independent set of dyslipidemic cases (n=716) and normolipidemic controls (n=1073). We explored the relationships among these phenotypes using variable clustering and then estimated their genetic heritabilities and cross-trait correlations. In families, four clusters explained 61% of the total variance, with one adiposity-related cluster (including hsCRP), one BP-related cluster, and two lipid-related clusters (HDL-C, TG, adiponectin and LDL particle size; apoB and non-HDL-C). A similar structure was observed in dyslipidemic cases and normolipidemic controls. The genetic correlations in the families largely paralleled the phenotype clustering results, suggesting that common genes having pleiotropic effects contributed to the correlations observed. In summary, our analyses support a model of metabolic syndrome with two major components, body fat and lipids, each with two subcomponents, and quantifies their degree of overlap with each other and with metabolic-syndrome related measures (adipokines, LDL particle size and hsCRP).
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PMID:Genetic and phenotypic architecture of metabolic syndrome-associated components in dyslipidemic and normolipidemic subjects: the GEMS Study. 1788 29

Women who deliver preterm are at increased risk for cardiovascular disease, but mechanisms are not understood. The authors considered that inflammation in women with spontaneous preterm birth (sPTB) might be related to their metabolic profile, such as lipids, and tested this in a nested case-control study from the Pregnancy Exposures and Preeclampsia Prevention Study (1997-2001). Cases were women with sPTB at 34-<37 weeks (n = 76) or < 34 weeks (n = 33). Controls were randomly selected women with term births (n = 228). Early pregnancy inflammation (C-reactive protein: > or = 8 microg/ml) and dyslipidemia (cholesterol: > 230 mg/dl or triglycerides: > 140 mg/dl) were evaluated in serum collected at < 21 weeks. Late pregnancy elevated C-reactive protein (> or = 12 microg/ml) was measured in a subset (n = 295). Polycotomous logistic regression was used to estimate the joint effects of C-reactive protein elevations and dyslipidemia on the risk of sPTB subtypes. After adjustment for race, body mass index, periconceptional vitamin use, and gestational age at sampling, early pregnancy inflammation (odds ratio = 2.9, 95% confidence interval (CI): 1.1, 7.2) and dyslipidemia (odds ratio = 2.0, 95% CI: 1.0, 4.2) were independently associated with sPTB at 34-<37 weeks. The presence of both conditions increased risk of sPTB at < 34 weeks 6.4-fold (95% CI: 1.7, 24.1). Half of the women with early pregnancy inflammation had elevated C-reactive protein late in gestation, and each was independently related to the risk of sPTB at < 34 weeks. The results indicate that some metabolic factors together with inflammation may be related to the risk of sPTB.
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PMID:Inflammation and dyslipidemia related to risk of spontaneous preterm birth. 1790 37

Rheumatoid arthritis is a systemic inflammatory autoimmune disease characterized by symmetric, erosive and chronic synovitis, especially of minor joints. It is associated with increased prevalence of cardiovascular disease and with high mortality. This occurs because of an accelerated atherogenic process, explained by traditional cardiovascular risk factors such as smoking, hypercholesterolemia, age, diabetes mellitus and systemic arterial hypertension. High levels of hemosedimentation velocity and C-reactive protein are directly correlated with increased cardiovascular events. Pro-inflammatory cytokines contribute with endothelial dysfunction, insulin resistance, dyslipidemia, prothrombotic effects and oxidative stress that are at the basis of the atherogenic process. Recent information about atherosclerosis in rheumatoid arthritis allows for identification of the risk factors involved in atherosclerosis that can be best controlled. This could result in a reduced manifestation of the process and its cutback, with consequent decrease of mortality and morbidity related to rheumatoid arthritis.
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PMID:[Rheumatoid arthritis and atherosclerosis]. 1795 59

In worldwide studies, interleukin-6 (IL-6) is implicated in age-related disturbances. The aim of the present report was to determine the possible association of IL-6 -174 C/G promoter polymorphism with the cytokine profile as well as with the presence of selected cardiovascular risk features. This was a cross-sectional study on Brazilian women aged 60 years or older. A sample of 193 subjects was investigated for impaired glucose regulation, diabetes, hypertension, and dyslipidemia. Genotyping was done by direct sequencing of PCR products. IL-6 and C-reactive protein were quantified by high-sensitivity assays. General linear regression models or the Student t-test were used to compare continuous variables among genotypes, followed by adjustments for confounding variables. The chi-square test was used to compare categorical variables. The genotypes were consistent with Hardy-Weinberg equilibrium proportions. In a recessive model, mean waist-to-hip ratio, serum glycated hemoglobin and serum glucose were markedly lower in C homozygotes (P = 0.001, 0.028, and 0.047, respectively). In a dominant hypothesis, G homozygotes displayed a trend towards higher levels of circulating IL-6 (P = 0.092). Non-parametric analysis revealed that impaired fasting glucose and hypertension were findings approximately 2-fold more frequent among G homozygous subjects (P = 0.042 and 0.043, respectively). Taken together, our results show that the IL-6 -174 G-allele is implicated in a greater cardiovascular risk. To our knowledge, this is the first investigation of IL-6 promoter variants and age-related disturbances in the Brazilian elderly population.
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PMID:Association between the -174 G/C promoter polymorphism of the interleukin-6 gene and cardiovascular disease risk factors in Brazilian older women. 1799 65

Gestational diabetes (GDM) has increased risk of diabetes (DM2), a coronary artery disease (CAD) equivalent. The aim of this study was to determine the prevalence of impaired glucose metabolism (IGM) in GDM and its association with risk factors for CAD. A cohort of 109 women with GDM underwent a glucose tolerance test which classified them into three groups: diabetic (DM2) (fasting glucose (G) >or=126mg/dl or plasma glucose 2h (2-h G) >or=200mg/dl); impaired glucose tolerance (IGT) (G 100-125mg/dl and/or 2-h G 140-199mg/dl); and normal (N) (G<100mg/dl and/or 2-h<140mg/dl). They were compared for pre-gestational (PBMI) and current (CBMI) body mass index, systolic (SBP) and diastolic blood pressure (DBP), G, lipids, fibrinogen and C-reactive protein (hsCRP). Thirty two months after delivery, 17.4% presented DM2, 39.4% IGT and 43.1% were N. PBMI, CBMI, SBP and DBP were significantly higher in the DM2 than N. G was higher in DM2 and IGT. HDL-cholesterol (HDL-C) was higher in the N (p=0.02) and the triglycerides (TG) were higher in DM2 (p=0.02). The groups showed significantly different levels of hsCRP (p=0.002). We conclude that the high prevalence of IGM, overweight/obesity, dyslipidemia and altered inflammatory markers, make GDM a high-risk situation for CAD.
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PMID:Prevalence of the impaired glucose metabolism and its association with risk factors for coronary artery disease in women with gestational diabetes. 1804 23

The aim of the study was to investigate the role of serum C-reactive protein (CRP) level as a risk factor in predicting metabolic syndrome (MS), hypertension, atherogenic dyslipidemia, type 2 diabetes mellitus, and coronary heart disease. We prospectively evaluated 1270 men and 1320 women, aged 30 to 89 years, who had serum CRP determinations and a mean 4.3 years' follow-up. The CRP values were log-transformed for calculations. Metabolic syndrome was defined by the Adult Treatment Panel III criteria modified for male abdominal obesity. Prediction of outcome was performed by excluding from analysis the particular outcome variable existing at baseline examination. Smoking men had higher age-adjusted estimated CRP concentrations (P < .001), whereas smoking women had lower CRP (P = .027) than never smokers. Risk of developing an elevated (> or =2 mg/L) CRP was predicted significantly by baseline CRP in both sexes and by apolipoprotein (apo B), current smoking, and family income in men, when adjusted for 5 further variables. Baseline CRP levels predicted atherogenic dyslipidemia when adjusted for age, baseline dyslipidemia values, and apo B tertiles and predicted incident hypertension independent of age, waist circumference, and smoking status. After adjustment for sex, age, and the 5 MS components, CRP predicted newly developing MS, with a hazard ratio (HR) of 1.16 (95% confidence interval, 1.02-1.32). When adjusted for sex, age, baseline glucose, waist circumference, and apo B tertiles, diabetes was significantly predicted by CRP in women (HR, 1.31) alone. Sex- and age-adjusted CRP level identified also those that progressed to diabetes independent of a fasting glucose >100 mg/dL (HR, 1.39; 95% confidence interval, 1.21-1.59), although not in men. In the prediction of incident coronary heart disease, CRP contributed to 7 established risk factors including waist circumference with a significant 1.18-fold HR. C-reactive protein is both an independent significant predictor and a risk factor of cardiometabolic risk among Turkish adults, additive to MS components, whereby risk is modulated by sex, smoking habit, and apo B.
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PMID:Serum C-reactive protein is an independent risk factor predicting cardiometabolic risk. 1819 Oct 50

Type 2 diabetes mellitus is associated with elevated plasma triglyceride levels, low high-density lipoprotein cholesterol, and a high incidence of cardiovascular disease. Hydroxymethylglutaryl-coenzyme A reductase inhibitors and fibrates are frequently used in the treatment of diabetic dyslipidemia, but their specific impact on the inflammation processes involved in atherosclerosis remains to be fully characterized. The objective of this 2-group parallel study was to investigate the differential effects of a 6-week treatment with either atorvastatin 20 mg/d alone (n = 19) or micronized fenofibrate 200 mg/d alone (n = 19) on inflammation, cell adhesion, and oxidation markers in type 2 diabetes mellitus subjects with marked hypertriglyceridemia. In addition to the expected changes in lipid levels, atorvastatin decreased plasma levels of C-reactive protein (-26.9%, P = .004), soluble intercellular adhesion molecule 1 (-5.4%, P = .03), soluble vascular cell adhesion molecule 1 (-4.4%, P = .008), sE-selectin (-5.7%, P = .02), matrix metalloproteinase 9 (-39.6%, P = .04), secretory phospholipase A(2) (sPLA(2)) (-14.8%, P = .04), and oxidized low-density lipoprotein (-38.4%, P < .0001). On the other hand, fenofibrate had no significant effect on C-reactive protein levels and was associated with reduced plasma levels of sE-selectin only (-6.0%, P = .04) and increased plasma levels of sPLA(2) (+22.5%, P = .004). These results suggest that atorvastatin was potent to reduce inflammation, oxidation, and monocyte adhesion in type 2 diabetes mellitus subjects with marked hypertriglyceridemia, whereas fenofibrate decreased sE-selectin levels only and was associated with an elevation of sPLA(2) levels.
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PMID:Differential effect of atorvastatin and fenofibrate on plasma oxidized low-density lipoprotein, inflammation markers, and cell adhesion molecules in patients with type 2 diabetes mellitus. 1824 11

Recent data indicate a rise in obesity both in children and adolescents in developing countries. The overall prevalence of overweight/obesity in urban children in New Delhi has shown an increase from 16% in 2002 to about 24% in 2006-2007. Our recent data show that the prevalence among adolescent children was 29% in private schools and 11.3% in government funded schools. While India already has highest number of patients with type 2 diabetes mellitus (T2DM) globally, rapid rise of obesity in children is the prime reason for increasing insulin resistance, the metabolic syndrome, dyslipidemia, polycystic ovarian syndrome and raised levels of C-reactive protein. Excess body fat, thick truncal subcutaneous fat, and abdominal adiposity are important predisposing factors for development of insulin resistance in Asian Indian children. As compared to other ethnic groups, children with ancestral origin in South Asia manifest adiposity, insulin resistance and metabolic perturbations earlier in life and these derangements are of higher magnitude than white Caucasian children. Since the metabolic syndrome and obesity track into adulthood, these clinical entities need to be recognized early for effective prevention of T2DM and coronary heart disease. Therapeutic lifestyle changes, maintenance of high levels of physical activity and normal weight are most important prevention strategies. Both high-risk surveillance and cost-effective population intervention programs are urgently needed. In this context, we have launched one of the largest program ("MARG", The Path) to curb childhood obesity in India.
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PMID:Childhood obesity in Asian Indians: a burgeoning cause of insulin resistance, diabetes and sub-clinical inflammation. 1829 30


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