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)

Metabolic syndrome is characterized by a group of risk factors for cardiovascular diseases, such as abdominal obesity, low high-density lipoprotein (HDL) cholesterol, elevated triglycerides, elevated arterial blood pressure, insulin resistance or impaired glucose tolerance. A number of studies focused on the relationship between alcohol consumption and prevalence of metabolic syndrome and its individual components. Ethanol can either aggravate the syndrome or prevent it--this depends primarily on the amounts and types of alcohol beverages consumed. It is commonly believed that moderate alcohol consumption is associated with a decreased incidence of metabolic syndrome and beneficial effects on plasma lipid levels, waist circumference and fasting plasma glucose. Of all the components of metabolic syndrome, the most beneficial effect of ethanol arises from an increase in plasma HDL cholesterol levels. The relationship between alcohol consumption and incidence of metabolic syndrome is more pronounced among red wine drinkers because polyphenoles contained in red wine increase the activity of endothelial nitric oxide synthase (eNOS), which plays a key role in the pathogenesis of metabolic syndrome. Decreased activity of this enzyme contributes to the development of insulin resistance, arterial hypertension and dyslipidemia. Stimulation of eNOS activity, which participates in the transport of HDL molecules, may provide an explanation for the mechanism of the increase in plasma levels of this particular lipid fraction in response to ethanol. Endothelial nitric oxide synthase requires the presence of antioxidants, which prevent both inactivation of nitric oxide in the reaction with peroxide anions and the accumulation of peroxynitrates.
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PMID:[Effect of ethanol on metabolic syndrome]. 1796 96

Endothelial dysfunction plays an essential role in the development and progression of atherosclerotic lesions. Endothelial nitric oxide synthase (eNOS) and endothelin-1 (ET-1) are considered important molecules in the endothelial dysfunction process. The aim of the present study was to evaluate the role of eNOS and ET-1 (EDN1) gene polymorphisms as susceptibility markers for acute coronary syndrome (ACS). Six polymorphisms (rs1799983, rs2070744, rs1800783, rs3087459, rs1800541, and rs5369) of eNOS and EDN1 genes were analyzed by 5' exonuclease TaqMan genotyping assays in a group of 452 patients with ACS and 283 healthy controls. The results showed increased frequencies of the A allele of the END1-914 C>A (rs3087459) polymorphism in ACS patients when compared to controls (OR=1.56, Pc=0.01). Under an additive model, the "AA" genotype was associated with an increased risk of developing ACS, adjusted for gender, hypertension, dyslipidemia, alcohol consumption, smoking, and diabetes (OR=1.56, p=0.045). Linkage disequilibrium analysis showed one EDN1 haplotype (AT) with increased frequency in ACS patients when compared to healthy controls (OR=1.65, Pc=0.0015). The "AT" haplotype was associated with the risk of developing ACS after adjusting for cardiovascular risk factors using multiple logistic analysis. In this case, the adjusted OR was 1.73 for the AT haplotype (Pc=0.0018). In summary, resulting data suggest that the END1-914 C>A gene polymorphism could be involved in the risk of developing ACS in Mexican individuals.
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PMID:The -974C>A (rs3087459) gene polymorphism in the endothelin gene (EDN1) is associated with risk of developing acute coronary syndrome in Mexican patients. 2403 3