Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was designed to analyze the effect of vitamin B-6 supplementation on the lipoprotein profile of chronic hemodialysis patients. Individuals on chronic hemodialysis experience an acceleration of atherosclerosis, which is often accompanied by abnormal lipid metabolism. Although total plasma cholesterol is usually normal, high-density-lipoprotein (HDL) cholesterol is often low. Recently, it has been suggested that the development of atherosclerotic lesions in chronic hemodialysis patients may be the result of a decreased plasma concentration of pyridoxal 5'-phosphate (PLP) and concomitant alterations in plasma amino acid and/or lipoprotein profiles. All subjects in this study were supplemented with 0.97 mmol (200 mg) pyridoxine hydrochloride per day for 28 days; then, concentrations of PLP, total cholesterol, and lipoprotein cholesterol fractions were determined in the plasma. No significant difference was noted in PLP concentration between Group 1 (five post-menopausal women with a history of atherosclerosis who were undergoing maintenance hemodialysis therapy) and Group 2 (six subjects who were non-symptomatic). However, both groups had significant increases in PLP concentrations between the pre- and post-supplementation periods (p less than .01). In contrast, there was a statistically significant difference in total plasma cholesterol and very-low-density- and low-density-lipoprotein (VLDL and LDL) cholesterol concentrations between groups, but no significant changes in total cholesterol or VLDL and LDL cholesterol content were found during vitamin B-6 supplementation. No statistically significant differences in HDL, HDL2, and HDL3 cholesterol concentrations were observed between Group 1 and Group 2 subjects or within either group during vitamin B-6 supplementation.
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PMID:Lack of effect of vitamin B-6 supplementation on the lipoprotein profile of post-menopausal chronic hemodialysis patients. 236 39

One hundred and fifty-four male and 69 female Chinese patients, aged between 40 and 60 years, who had suffered myocardial infarction (MI) were investigated and compared with 216 men and 219 women who had no history or ECG evidence of coronary heart disease. The male MI patients had significantly raised levels of triglycerides (160 mg/dl), cholesterol (194 mg/dl), VLDL-CH (31 mg/dl), apolipoprotein B (122 mg/dl) and apolipoprotein E (4.7 mg/dl) and a lower apolipoprotein A-I level (126 mg/dl) than the control group (triglycerides 131, cholesterol 179, VLDL-CH 26, apo B 102, apo E4.2, and apo A-I 138 mg/dl). The women with MI also had higher values for the atherogenic lipids than the control group (triglycerides 175 vs. 134 mg/dl, cholesterol 218 vs. 186 mg/dl, LDL-CH 128 vs. 104 mg/dl, VLDL-CH 32 vs. 26 mg/dl, apo B 121 vs. 103 mg/dl and apo E 5.4 vs. 4.3 mg/dl), as well as lowered apolipoprotein A-I (128 vs. 144 mg/dl). The Lp(a) levels (men and women considered together) were significantly higher for the MI patients (34.3 mg/dl vs. 26.2 mg/dl). Anti-atherogenic lipoproteins such as HDL-cholesterol, HDL2-CH, HDL3-CH, phospholipids and apolipoprotein A-II, C-II and C-III showed no difference between the groups.
Atherosclerosis 1990 Jun
PMID:Lipids, lipoproteins, apolipoproteins, and other risk factors in Chinese men and women with and without myocardial infarction. 237 89

The lipoprotein (LP) fractions VLDL, LDL, HDL2 and HDL3 were prepared by ultracentrifugation of plasma from healthy volunteers and from patients with coronary heart disease (CHD). We investigated the capacity of platelets from healthy volunteers and patients with atherosclerosis to generate thromboxane A2 (TXA2) during spontaneous clotting of whole blood under the influence of the lipoprotein fractions. In our experiments the serum concentration of TXB2, reflecting the capacity of platelets to generate TXA2 during clotting, depends on several factors: the type of LP fraction used, the blood used for generation of TXA2, and for the same LP fraction whether it was taken from plasma of healthy volunteers or patients with CHD. VLDL prepared from plasma of healthy volunteers inhibited but VLDL prepared from plasma of patients with CHD enhanced the TXA2 formation of platelets from healthy volunteers (p less than 0.05, resp.). LDL from CHD patients inhibited the TXA2 formation of platelets from atherosclerotic patients (p less than 0.01). The HDL subfractions HDL2 and HDL3 from healthy volunteers inhibited TXA2 formation by platelets from healthy volunteers as well as those from atherosclerotic patients (p less than 0.05; p less than 0.01, respectively). HDL2 from patients with CHD inhibited only the TXA2 formation of platelets from healthy volunteers (p less than 0.01), whereas HDL3 from CHD patients inhibited only the TXA2 formation of platelets from atherosclerotic patients (p less than 0.01).
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PMID:Modulation of TXA2 generation of platelets by human lipoproteins. 239 69

To study the effects of long-term, self-monitored exercise on the serum lipid profile and body composition of middle-aged non-smoking males, a controlled study was conducted in 61 sedentary, middle-class Swiss men. Thirty-nine men were randomly allocated to jog 2 h/wk for 4 months on an individually prescribed, heart rate-controlled basis, whereas 22 men served as controls. Despite varying adherence to the exercise regimen, the following 4-month net changes (effect in exercise group minus effect in control group) in lipids were seen: HDL cholesterol (C) +0.12 mmol/l (95% CI 0.02, 0.22; P = 0.028), LDL-C +0.08 mmol/l (ns), VLDL-C -0.26 mmol/l (-0.45, -0.07; P = 0.009), total triglycerides (TT) -0.21 mmol/l (ns), HDL-C/total C +0.02 (0.001, 0.05; P = 0.047). The net changes in endurance capacity and resting heart rate in favour of exercisers were significant as well, whereas no significant changes in apolipoprotein levels were seen. Exploratory analyses revealed, for example, associations of the increase in total physical activity with an increase in the HDL-C/total C ratio (r = 0.46; P less than 0.001), and of the change in estimated body fat content with an opposed change in the HDL-C/total C ratio (r = -0.40; P less than 0.001), or an inverse relationship of the change in subcutaneous fat with a change in the HDL2-C level (r = -0.39; P less than 0.001). Multivariable regression analysis suggested that much of the effect of jogging on HDL-C was apparently mediated through a decrease in body fat content. A change in the waist/hip ratio was unrelated to lipoprotein changes but was related to the change of TT level (r = 0.22; P less than 0.05). This study confirms that individually prescribed, unsupervised jogging can increase HDL-C levels and improve the serum lipoprotein profile in self-selected nonsmoking males. Although the effect is modest, it may be relevant to preventive cardiology, given the evidence for a reduction in cardiovascular risk even after apparently small decreases in risk factor levels.
Atherosclerosis 1990 Feb
PMID:Effects of long-term, self-monitored exercise on the serum lipoprotein and apolipoprotein profile in middle-aged men. 240 51

We investigated the progression of carotid atherosclerosis in a population-based sample of 100 Eastern Finnish men aged 42, 48, 54 or 60 years. A high-resolution B-mode ultrasonographic examination was repeated after a follow-up of 24 months for each subject. The intimal-medial thickness (IMT) in the common carotid artery increased by -0.06 mm to 0.90 mm (mean 0.12 mm, SD 0.20 mm). Age (standardised partial coefficient, beta = 0.325, P = 0.0003), serum LDL cholesterol concentration (beta = 0.229, P = 0.0011), pack-years of smoking (beta = 0.274, P = 0.0023), blood leukocyte count (beta = 0.201, P = 0.0239), and platelet aggregability (beta = 0.165, P = 0.0646), measured at baseline, were the strongest predictors of atherosclerosis progression. Neither hypertension, current blood pressure level, serum HDL cholesterol nor serum HDL2 cholesterol concentration at the baseline examination had any association with the change of IMT over 2 yrs.
Atherosclerosis 1990 Feb
PMID:Progression of carotid atherosclerosis and its determinants: a population-based ultrasonography study. 240 52

We have evaluated a simple dextran sulphate precipitation method for measuring high density lipoprotein cholesterol (HDL) subfractions and have used this method to measure plasma HDL2 and HDL3 in a group of 28 patients with primary gout. These patients were found to have significantly lower levels of plasma HDL and HDL2 than a group of healthy controls, matched for age and sex and of similar body mass index (BMI); no significant difference in mean levels of the HDL3 subfraction was found however. We have confirmed the high prevalence of hypertriglyceridaemia in subjects with gout compared to controls and the mean serum triglyceride levels were significantly higher (P less than 0.01) in the gout group than in controls. We have also shown that subjects with high serum triglyceride levels tend to have low plasma HDL2 concentrations, a finding which is consistent with an inverse relationship between these two parameters. These lipid abnormalities may partly explain the high prevalence of premature atherosclerosis in patients with primary gout.
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PMID:The measurement of high density lipoprotein subfractions in patients with primary gout using a simple precipitation method. 241 36

Plasma levels of dehydroepiandrosterone sulfate (DHEA-S), testosterone, dihydrotestosterone (DHT) androstenedione, sex hormone-binding globulin (SHBG), lipoproteins, apolipoproteins and high density lipoprotein (HDL) subfraction were measured in 32 men aged 26-40 years after myocardial infarction (MI) suffered at least 3-4 months prior to the study, who were normocholesterolemic and had angiographically demonstrated coronary occlusion. The control group consisted of 76 healthy men aged 25-40 years. Blood samples were obtained in the morning from fasting subjects. A significant decrease in plasma DHEA-S and DHT levels were found in MI patients. Also, a significant decrease in HDL-cholesterol, HDL2-cholesterol (HDL2-C) and apolipoprotein A-I, an increase in apolipoprotein B and LDL-cholesterol (LDL-C) levels were observed in those patients as compared with healthy men. However, there were no differences in testosterone, androstenedione and SHBG concentrations between the groups. Significant correlations between testosterone and HDL2-C (r = 0.46, P less than 0.01), as well as between DHEA-S and HDL3-C (r = 0.39, P less than 0.05) levels in MI patients were observed. These results suggest that decreased levels of plasma DHEA-S and DHT may promote the development of coronary atherosclerosis in men.
Atherosclerosis 1989 Oct
PMID:Decreased plasma dehydroepiandrosterone sulfate and dihydrotestosterone concentrations in young men after myocardial infarction. 253 16

Human erythrocytes were incubated for 5 h at 37 degrees C with lipoproteins (LP), preliminary oxidized to different extent, as assessed by thiobarbituric acid (TBA) test. Cholesterol content in the cells was increased by 12-14% after incubation with low-density lipoproteins (LDL) along with augmentation of order parameter and rotational correlation time of spin-labeled stearic acids incorporated into membranes. If erythrocytes were incubated with oxidized LDL, containing 2.5-4 times more TBA-reactive material than native ones, cellular content of cholesterol was increased by 24-28%. In contrast, high-density lipoproteins (HDL2 and HDL3) removed cholesterol from cell membranes, when incubated with erythrocytes. This was followed by increased fluidity of membrane lipid phase as detected by the spin probe method. Oxidation of HDL2 and HDL3 decreased their ability to accept cholesterol from cell membranes. No detectable accumulation of TBA-reactive material was observed in the samples during the incubation. The antioxidant, butylated hydroxytoluene (BHT), in the concentration of 10(-5) M did not influence the cholesterol transfer between LP and erythrocytes. Hence, the effects of lipid peroxidation (LPO) on the cholesterol transfer seem to result from LP alterations by oxidation rather than from free radical reactions occurring during the incubation. By increasing cholesterol-donating ability of LDL and inhibition of cholesterol-accepting capacity of HDL lipid peroxidation in LP may activate cholesterol accumulation in blood vessel cells and thus contribute to atherosclerosis.
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PMID:Free radical lipid oxidation affects cholesterol transfer between lipoproteins and erythrocytes. 255 Mar 31

Digestion of the human apolipoprotein (apo) A-II gene with the endonuclease MspI produces fragments of 3.0 or 3.7 kb, reflecting the presence or absence of a polymorphic site within an Alu sequence 3' to the gene. Patients with hypertriglyceridemia have been shown to have an increased prevalence of the 3.0 kb allele. To explore this observation further, plasma lipoprotein lipids were studied in a random sample of fasted middle-aged Caucasian men, of which 59 were 3.0 kb homozygotes, 24 were heterozygotes, and 2 were 3.7 kb homozygotes. After adjusting for the effects of age, height, weight, alcohol intake and cigarette consumption by covariance analysis, no statistically significant associations were present between genotype and the concentrations of triglyceride in whole plasma or the d less than 1.019 g/ml fraction of plasma (i.e., VLDL + IDL). Nor were the cholesterol concentrations in VLDL + IDL, low density lipoprotein (LDL, d = 1.019-1.063 g/ml), high density lipoprotein (HDL), HDL2 or HDL3 related to genotype. In an independent comparison of eight 3.0 kb homozygotes and eight 3.7 kb homozygotes (all Caucasians) drawn from a different community, genotype was unrelated to the triglyceride or cholesterol concentrations in VLDL (d less than 1.006 g/ml), IDL + LDL (d = 1.006-1.063 g/ml) or HDL, after adjustment for the effects of covariates. These results suggest that the MspI polymorphism of the apo A-II gene is not associated with genetic variation that significantly affects triglyceride transport in the majority of men.(ABSTRACT TRUNCATED AT 250 WORDS)
Atherosclerosis 1989 May
PMID:Plasma lipoprotein lipids in relation to the MspI polymorphism of the apolipoprotein AII gene in Caucasian men. Lack of association with plasma triglyceride concentration. 256 9

The structure of lipoproteins is described, followed by a description of the structure and function of low density lipoproteins (LDL) which carry cholesterol to cells, and high density lipoproteins (HDL) which remove cholesterol. The process of atherosclerosis is then indicated. When LDL accumulates in plasma, it is deposited in macrophages which metabolize all the components of LDL except the cholesterol ester which becomes a foam cell. HDL converts foam cells back to macrophages. The presence of HDL and HDL2 allows foam cells to secrete cytoplasmic cholesterol and an apoprotein E which coats HDL2 and allows the recognition and removal of cholesterol in blood and by receptors in he liver. Atherosclerosis can be predicted from the effect of the HDL and LDL on foam cell formation, i.e., more foam cells means more HDL, particularly HDL2, and the less likely atherosclerosis will develop. The link between oral contraceptives (OCs) and atherosclerosis is that with estrogen LDL cholesterol levels decrease, while there are increases with progestins; HDL and HDL2 increase with estrogen and decrease with progestins. HDL3 is unaffected by estrogen. The effects of progestins are dependent on a number of other factors. Longterm clinical trials of OCs and their effects on lipoproteins are identified from Johns Hopkins and George Washington University studies. The longterm trail results are given. Total cholesterol rose regardless of the 3 different progestins. Compounds containing dl-norgestrel in higher doses raised LDL levels more than ethynodiol diacetate or norethindrone. In low doses, levels of LDL also rose but ethynodiol diacetate rose least in 6 months. Apoprotein B also rose in a similar fashion. Norgestrel lowers HDL considerably and HDL2 in higher or lower doses; there were more differences in ethynodiol diacetate or norethindrone. All 3 preparations raised HDL3 similarly. Norgestrel decreases apoprotein levels in high doses and apoprotein is unaffected at low doses; low apoprotein is linked to coronary artery disease. Increases occurred with ethynodiol diacetate and norethindrone. New triphasic compounds are under investigation, and show low HDL at 6 but not 12 months, but consistently raise LDL. Lipoprotein phospholipids research findings are also revealed as well as other related research. Adverse effects may be seen for many years after OC use, so low doses are recommended.
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PMID:Effects of oral contraceptives on circulating lipids and lipoproteins: maximizing benefit, minimizing risk. 257 64


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