Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The red cell membrane Li+/Na+exchange is a heteroexchange that operates in either direction across the cell membrane. It binds either Li+ or Na+ on one side of the membrane and it exchanges the transported species for either Li+ or Na+ on the opposite side in a stoichiometric ratio of 1:1. In the population, Li+/Na+exchange is unimodally distributed but skewed to the right. Such distribution results from superimposition of two normal distributions. Many laboratories have shown that red-cell Li+/Na+ exchange is increased in patients with essential hypertension, compared with normotensive controls. Among the various alterations of cell membrane cation transport reported in hypertension, the increase of red-cell Li+/Na+ exchange has been most widely investigated and confirmed. Moreover, increased Li+/Na+ exchange has been found in some clinical conditions related to hypertension, such as overweight and diabetes. Among diabetic patients, Li+/Na+ exchange is particularly high in patients with nephropathy, hypertension, and microalbuminuria, leading to the hypothesis that it can be considered a cellular marker of the risk of developing diabetic nephropathy. Furthermore, it is associated with severe and drug-resistant hypertension, insulin resistance, vascular and cardiac hypertrophy, hyperlipidemia, obesity, family history of hypertension, and of major cardiovascular accidents suggesting that high Li+/Na+ exchange could be a biochemical marker for increased cardiovascular risk. Regardless of its the pathophysiological significance, its measurement could be of clinical use as an intermediate phenotype of increased cardiovascular risk.
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PMID:The Li+/Na+ exchange in hypertension. 1270 53

We examined cellular membrane fatty acid composition and insulin sensitivity in patients with mild essential hypertension and hyperlipidemia, and investigated whether bezafibrate, a lipid-lowering drug, could improve elevated blood pressure and insulin sensitivity in these subjects by ameliorating cellular membrane fatty acid composition. Twenty-seven subjects were recruited. Twelve men with mild essential hypertension [systolic blood pressure (SBP) between 140 mmHg and 160 mmHg] and hypertriglyceridemia (plasma triglyceride concentration over 150 mg/dl) were designated the HL group. Fifteen men with mild essential hypertension and normotriglyceridemia (plasma triglyceride concentration below 150 mg/dl) were designated the NL group. Subjects in the HL group were given bezafibrate 400 mg/dl and those in the NL group were given placebo for 3 months. Bezafibrate significantly reduced SBP (140 +/- 2.6 to 131.8 +/- 2.6 mmHg, mean +/- SEM), diastolic blood pressure (DBP) (87.8 +/- 2.0 to 82.8 +/- 2.6 mmHg), fasting plasma triglyceride concentration (225.5 +/- 23.5 to 102.9 +/- 10.9 mg/dl), fasting plasma insulin concentration (9.6 +/- 0.8 to 7.1 +/- 0.8 microU/ml), and homeostasis model assessment scores (HOMA-R, 2.4 +/- 0.2 to 1.7 +/- 0.2), and significantly improved the insulin sensitivity index (56.0 +/- 3.0 to 70.7 +/- 4.8 mg x l2/mmol x mU x min) in the HL group. Regarding erythrocyte membrane fatty acid composition, bezafibrate reduced the percentages of saturated fatty acids (SFA) and increased the percentage of polyunsaturated fatty acids (PUFA). Plasma triglyceride concentrations were positively correlated with HOMA-R (r = 0.50, p < 0.01) and SFA (r = 0.39, p < 0.05), and negatively correlated with PUFA (r = -0.45, p < 0.05) before administration of placebo or bezafibrate. In conclusion, an improvement of hyperlipidemia by bezafibrate may be attributed to reduction of blood pressure and amelioration of insulin sensitivity. Abnormalities in membrane lipid composition may play an important role in these metabolic disorders.
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PMID:Bezafibrate improves hypertension and insulin sensitivity in humans. 1273 99

Essential hypertension in humans may develop through a combination of genetic and environmental factors. Diet has long been under investigation as a potential effector of blood pressure. A diet high in sucrose or fructose can give rise to hyperlipidemia, insulin resistance and hypertension. Insulin resistance, glucose intolerance and oxidative stress are common features of hypertension. If glucose metabolism through the glycolytic pathway is impaired, as in insulin resistance, there will be a build-up of glyceraldehyde, glyceraldehyde-3-phosphate and dihydroxyacetone phosphate with further metabolism to methylglyoxal, a highly reactive ketoaldehyde. Excess aldehydes can bind sulfhydryl groups of membrane proteins, altering membrane calcium channels, increasing cytosolic free calcium, peripheral vascular resistance and blood pressure. The presence of reactive aldehydes can also lead to oxidative stress. Dietary management through lower sucrose or fructose intake and increased consumption of vitamins improves glucose metabolism, lowers tissue aldehydes, increases anti-oxidant capacity and may also prevent hypertension.
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PMID:Prevention of fructose-induced hypertension by dietary vitamins. 1467 55

Insulin resistance and compensatory hyperinsulinemia are recognized not only in type 2 diabetes mellitus(DM) but also in essential hypertension(EHT), hyperlipidemia and obesity; these are known as the components of metabolic syndrome and accumulation of these components increase risk of cardiovascular diseases(CVD). When coronary angiographic findings were evaluated in patients with coronary artery disease(CAD), the severity was higher in CAD with DM than that without DM. Even in CAD without DM, the severity of coronary angiographic findings was higher in CAD with insulin resistance than that without insulin resistance. When residents of rural communities in Japan were followed 8 years, the incidence of CVD was 3.5 times higher in subjects with insulin resistance than those without insulin resistance. One of the intracellular signal transduction of insulin receptor; MAP kinase may be concerned atherosclerotic mechanisms of insulin resistance. These findings suggest that insulin resistance is a significant background of atherosclerosis, and insulin resistance is one of the major facilitation factors of genesis and progression of CVD.
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PMID:[Significance of insulin resistance to atherosclerotic complications in essential hypertension]. 1473 36

Obesity, atherosclerosis, insulin resistance and hyperinsulinemia, hyperlipidemia, essential hypertension, type 2 diabetes mellitus, and coronary heart disease (CHD) are the components of metabolic syndrome X and are associated with elevated plasma levels of C-reactive protein, interleukin-6, and tumor necrosis factor-alpha, which are markers of inflammation. This suggests that metabolic syndrome X is a low-grade, systemic, inflammatory condition. Hence, instituting anti-inflammatory measures might be beneficial in preventing or halting the progress of metabolic syndrome X in high-risk populations.
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PMID:Metabolic syndrome X: an inflammatory condition? 1497 97

Obesity is the one of the fundamental problems in societies of the highly developed countries. In the Framingham study almost linear dependence between cardiovascular mortality and overweight was proven. Moreover, obesity often coexists with different illnesses, such as type 2 diabetes, myocardial ischaemia, essential hypertension, dyslipidemia, arteriosclerosis, renal insufficiency, degenerative changes of joints, cholelithiasis, or some neoplasms. Among methods of treatment of obesity the most known and safe is the low calories content diet. In pharmacotherapy of obesity two medications of new generation i.e. sibutramin and orlistat make up basis at present. The present study is concentrated onto Sibutramin, which acts in the central nervous system. Authors introduce mechanisms of action of the medicine, its participation in termogenesis as well as therapeutic effectiveness. Special attention is dedicated for clinical situations in which decrease of body mass is the key element of therapy, that is essential hypertension, diabetes and hyperlipidemia.
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PMID:[Sibutramine in treatment of obesity. Therapeutic premises in patients with essential hypertension, diabetes, hyperlipidemia]. 1523 Jan 49

The deletion of thiazide-sensitive Na-Cl cotransporter ( TSC, SLC12A3) causes Gitelman's syndrome characterized by low blood pressure, while deletions of the WNK1 ( PRKWNK1) and WNK4 ( PRKWNK4) genes cause familial hypertension known as pseudohypoaldosteronism type II. Recent studies have revealed that cell surface expression of TSC is regulated by WNK1 and WNK4. We hypothesized that molecular variations in TSC, WNK1, and WNK4 could lead to an increased morbidity of hypertension. We identified 52, 35, and 21 polymorphisms in Japanese hypertensives by sequencing the entire coding regions of TSC, WNK1 and WNK4, respectively. Twenty-one representative polymorphisms were genotyped in 1,818 Japanese individuals (771 subjects with hypertension and 1,047 controls) randomly sampled in Suita city. The results indicated that the systolic blood pressure in men with the CT+TT genotype in WNK4 C14717T was 3.1 mmHg higher than those with the CC genotype ( p=0.042) after adjustment with confounding factors such as age, BMI, hyperlipidemia, diabetes mellitus, antihypertensive drug use, smoking, and drinking. Multivariate logistic regression analysis (with adjustment for the same parameters) in men revealed that the odds ratio for the presence of hypertension of the CT+TT genotype in C14717T to the CC genotype was 1.62 ( p=0.010, 95% confidence interval, 1.12-2.33). Association of TSC and WNK1 with hypertension was not observed. In conclusion, our study suggests the possible involvement of WNK4 in essential hypertension in a Japanese general population.
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PMID:Identification of 108 SNPs in TSC, WNK1, and WNK4 and their association with hypertension in a Japanese general population. 1530 83

The Na+/Ca2+ exchanger (NCX) is a membrane protein involved in calcium homeostasis, catalyzing the exchange of one Ca2+ ion for three Na+ ions across the cell membrane. The Na+/Ca2+ exchange has been suggested to play a role in the pathogenesis of hypertension. Therefore, we examined whether genetic variations in NCX1 were associated with hypertension. Among 15 polymorphisms identified in 96 hypertensive subjects by sequencing the entire exon and promoter regions of NCX1, 7 representative polymorphisms with a minor allele frequency of greater than 4% were genotyped in 1,865 individuals, of whom 787 were hypertensive and 1,072 were normotensive. These subjects were residents of Suita City and were randomly selected as a population for the Suita cohort study. Multivariate logistic regression analysis performed after adjusting for age, body mass index, hyperlipidemia, diabetes mellitus, smoking, and drinking revealed that the -23200T>C and -23181T>C polymorphisms in the 5' upstream region of exon 1c were significantly associated with hypertension in men (-23200T>C: CC vs. TC+TT: odds ratio=0.61; 95% confidence intervals: 0.39 to 0.97; p =0.04) and in women (-23181T>C: CC vs. TC+TT: odds ratio=1.45; 95% confidence intervals: 1.04 to 2.02; p =0.03), respectively. Thus, our study suggests that NCX1 is one of the genes related to susceptibility to essential hypertension in the Japanese general population.
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PMID:Association of genetic polymorphisms of sodium-calcium exchanger 1 gene, NCX1, with hypertension in a Japanese general population. 1578 3

Primary hypertension is well known to occur in children, but the characteristics of such children are changing due to the influence of the obesity epidemic. In view of this, we conducted a cross-sectional study of 70 children [age 13.3+/-4 years (mean +/- SD)] with primary hypertension referred to a specialized pediatric hypertension clinic. Secondary hypertension had been excluded after a standardized diagnostic evaluation. Isolated systolic hypertension was present in 62.9% of subjects. Family history of hypertension was present in 86.2%, and 52.9% were obese (BMI > or =95th percentile). BMI was weakly correlated with systolic BP (r =0.28,P =0.10) and was significantly correlated with total cholesterol (r =0.36,P =0.005) and triglycerides (r =0.42,P =0.01). Mean plasma renin activity (PRA) was 3.1+/-2.7 ng/ml/h. PRA was correlated with diastolic but not systolic BP. Patients with high PRA had higher diastolic BP and lower BMI compared to those with low PRA. Left ventricular hypertrophy was present in 24%. Mean 24-h systolic BP load by ambulatory BP monitoring was 52+/-24%; mean 24-h diastolic BP load was 18+/-16%; BP loads were greater in patients with high PRA. These data suggest that primary hypertension in children is characterized by systolic BP elevation, positive family history and obesity. Hyperlipidemia accompanies primary hypertension in obese children, and left ventricular hypertrophy is common. Patients with high PRA have more severe BP elevation. Future studies should focus on further defining the pathophysiology of primary hypertension in children, including the roles of renin and insulin resistance, so that improved methods of prevention and treatment can be developed.
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PMID:Characteristics of children with primary hypertension seen at a referral center. 1586 53

Adrenomedullin (AM) has various physiological actions on the cardiovascular system, including vasodilatation, diuresis, natriuresis, inhibition of aldosterone secretion, and increases of the cardiac output, all of which cause hypotension. Since AM plays a role in the pathophysiology of vascular diseases, genes controlling AM might be involved in the development and etiology of essential hypertension (EH). However, there have been few studies examining the relationship between the AM gene and hypertension. The aims of this study were to genotype some of the genetic markers for the human AM gene in Japanese subjects, and via a haplotype-based case-control study, assess the association between and the AM gene and EH or its risk factors, such as hyperlipidemia, renal damage, and proteinuria. We genotyped 205 EH patients and 210 age-matched normotensive (NT) individuals for two single nucleotide polymorphisms of rs4399321, rs7944706 and a microsatellite polymorphism located approximately 5,400 base pairs downstream of the 3' end of the human AM gene. The overall distribution in each variant and haplotype did not significantly differ between the two groups. However, after dividing the groups into those subjects with and without proteinuria, the haplotype analysis revealed a positive association. In conclusion, a possible mutation linked to the haplotype may indicate a genetic predisposition for proteinuria in EH.
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PMID:Haplotype-based case-control study revealing an association between the adrenomedullin gene and proteinuria in subjects with essential hypertension. 1609 66


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