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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lipids are transported in the blood in four major classes of lipoproteins. The triacylglycerol-rich lipoproteins are chylomicrons and very-low-density lipoproteins (VLDL) which are produced by the small intestine and liver, respectively. These lipoproteins mainly carry fatty acids to adipose tissue and muscle where the triacylglycerol is hydrolysed by lipoprotein lipase. The resulting particles that remain in the blood are chylomicron remnants and low-density lipoprotein (LDL), respectively. The remnant is taken up by the liver via endocytosis which is mediated by a specific receptor for apolipoprotein E (apoE). LDL, which are rich in cholesterol, can also be taken up by the liver or extrahepatic tissues by a receptor-mediated endocytosis that specifically recognises apoB or apoE. 'Nascent' high-density lipoprotein (HDL) particles are secreted by the liver and intestine and then undergo modification to become HDL3 and then HDL2 as they acquire cholesterol ester. They facilitate the reverse transport of cholesterol back to the liver. Little is known of the hormonal regulation of lipoprotein uptake by the liver. Recently, we have shown that insulin and tri-iodothyronine (T3) increase the specific binding of LDL to cultured hepatocytes whereas dexamethasone (a synthetic glucocorticoid) has the opposite effect. The changes in binding produced by insulin and dexamethasone are paralleled by alterations in the rate of degradation of apoB. These findings may in part explain the hypercholesterolaemia and increased risk of premature atherosclerosis that can be associated with poorly controlled diabetes or hypothyroidism.
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PMID:The biochemistry of lipoproteins. 314 85

Using a discriminating gradient separation technique combined with careful analysis of lipid and apolipoprotein (apo) composition, serum lipoproteins of 20 chronically uremic patients have been compared with those of 19 normal controls matched for age and sex. In uremic subjects, serum VLDL concentration was markedly increased. These particles were enriched in protein and cholesterol and relatively poor in triglycerides (TG). They contained more frequently apo B-48, and a decreased proportion of apo E. Expressed in percent, total apo C was normal but the ratio of apo C-III2/apo C-III1 was elevated. Uremic IDL, whose serum concentration was markedly increased, were characterized by an increased proportion of protein. Total uremic LDL whose serum concentration was normal, contained less esterified cholesterol (EC) and more TG than normal LDL, their EC/TG ratio being very low. Moreover, the concentration of the mature subfraction of LDL having a mean density of 1.043 g/ml, was markedly decreased in uremic subjects. Taken together, these anomalies indicate a delayed transformation of VLDL into LDL in chronic renal failure. The decreased concentration of total HDL in uremic subjects was more marked in HDL2 (-46%) than HDL3 (-24%). Both uremic HDL2 and HDL3 were relatively enriched in TG, and uremic HDL3 were poorer in EC than normal HDL3.(ABSTRACT TRUNCATED AT 250 WORDS)
Atherosclerosis 1988 Nov
PMID:Anomalies in composition of uremic lipoproteins isolated by gradient ultracentrifugation: relative enrichment of HDL in apolipoprotein C-III at the expense of apolipoprotein A-I. 314 49

The effects of the artificial triglyceride-phospholipid emulsion (10% intralipid) on HDL subfraction were studied in vivo. After a 14-h fast, subjects received intralipid via a 4-h infusion. Serum lipoproteins were analyzed before and at 4 and 6 h after the start of the infusion. At 4-h the following acute changes by infusion were observed. Triglyceride, phospholipid, free cholesterol, and esterified cholesterol in chylomicrons and VLDL increased. HDL2 as well as triglyceride, phospholipid, free cholesterol and protein within the HDL2 increased, while HDL3 decreased. An increase in HDL3 triglyceride was observed. The masses of apo A-I and A-II in the HDL2 density interval rose while these parameters fell in HDL3. There were decreases of apo C-II and C-III in the HDL subfractions and elevations in chylomicrons and VLDL. The particle size of the HDL subfractions increased. However, most of these acute changes at 4 h tended to disappear by 6 h. These results suggest that there is exchange of lipids and reversible transfer of apo C-II and C-III between HDL subfractions and intralipid, and conversion of HDL3 to HDL2 followed by the reverse conversion of HDL2 to HDL3 as the synthetic emulsion is cleared from the plasma.
Atherosclerosis 1988 Nov
PMID:Changes of HDL subfraction concentration and particle size by intralipid in vivo. 314 50

We investigated the prevalence of carotid atherosclerosis and its association with serum lipoprotein cholesterol fractions in 412 Eastern Finnish men ages 42, 48, 54, or 60 years who were examined between February and December 1987 in the Kuopio Ischaemic Heart Disease Risk Factor Study. Carotid atherosclerosis was assessed with high-resolution B-mode ultrasonography. Of the participants, 37% had thickening of the intimal or medial layer of the arterial wall, 10% had plaques, 2% had stenosis in the right or left common carotid artery or in the carotid bifurcation, and only 51% were free of any detectable carotid atherosclerosis. The prevalence of atherosclerosis was 14.1%, 32.0%, 67.7%, and 81.9% in the four age groups, respectively. The mean age-adjusted serum low density lipoprotein (LDL) cholesterol concentration was 3.67 mmol/l (142 mg/dl) in men free of carotid atherosclerosis and 4.02 mmol/l (155 mg/dl) in those with at least intimal thickening (p = 0.003 for difference). The mean age-adjusted serum cholesterol concentration in the high density lipoprotein (HDL) fraction was 1.34 mmol/l (52 mg/dl) in the atherosclerosis-free and 1.27 mmol/l (49 mg/dl) in the atherosclerotic men (p = 0.029 for difference). There was a similar difference in both the serum HDL2 and the HDL3 cholesterol levels. Serum LDL and HDL (inverse) cholesterol were significant determinants of severity of carotid atherosclerosis in a multivariate regression model adjusting for age, obesity, plasma fibrinogen, cigarette-years, and duration of hypertension. Our data reveal the high prevalence of atherosclerosis in middle-aged Eastern Finnish men and provide further evidence of the roles of LDL and HDL cholesterol in atherosclerosis.
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PMID:Prevalence of carotid atherosclerosis and serum cholesterol levels in eastern Finland. 319 22

Dietary plant proteins may lower plasma cholesterol and LDL concentrations in hypercholesterolemic patients when substituted for animal proteins, particularly in diets with low cholesterol and saturated fat content. Plant protein diets appear, however, to be without effect on plasma lipoprotein levels in normal subjects. In the present study, we have examined whether the origin of the dietary protein, i.e. plant (soy) or animal (casein), affects the plasma lipoproteins in normolipidemic subjects when these proteins are presented as components of diets low in cholesterol and saturated fat. The study followed a crossover design. Five men and 5 women consumed liquid formula diets containing 20% of calories as casein or soy protein, 28% as fat (mainly monounsaturated), and 52% as carbohydrate; the intake of cholesterol was less than 100 mg per day. The two dietary periods, each of 1 month duration, were separated by an interim period of 1 month on self-chosen food. Following an initial 30% reduction of cholesterol and LDL plasma levels on both diets, the concentrations of each of the major lipoprotein classes (VLDL, IDL, LDL, HDL2 and HDL3) were similar during the two experimental dietary periods. Body weights were essentially constant. Dietary soy protein and casein could not be distinguished in their effects on the plasma concentrations and chemical composition of the major lipoprotein classes in normolipidemic subjects.
Atherosclerosis 1988 Jul
PMID:Effects of soy protein and casein in low cholesterol diets on plasma lipoproteins in normolipidemic subjects. 321 60

The lipid and lipoprotein profile was examined in male patients with acute myocardial infarction (AMI) at the time of infarction (group A) and in male patients who had survived AMI 2-3 years before the study (group B), and compared to that of healthy controls. The myocardial infarction (MI) patients exhibited similar total cholesterol and LDL-cholesterol levels as the controls. However, the LDL mass concentration was higher in patients than in controls (P less than 0.01 for group A, P less than 0.001 for group B). In composition, patients' LDL in both groups was rich in protein and triglycerides but poor in cholesterol. The compositional changes in patient LDL were evident at all levels of LDL-cholesterol. The mean total HDL and HDL2 mass concentrations were lower in patients than in controls (P less than 0.001 for both groups), but there was no difference in HDL3 levels. Upon admission to hospital the patients with AMI at the time of examination (group A) had higher serum total triglyceride concentration than controls, but on the fasting morning samples serum triglyceride and VLDL lipid levels did not differ between patients and controls. Patients who had survived AMI 2-3 years prior to study (group B) exhibited higher serum total triglyceride and VLDL levels than the control subjects. On stepwise discriminant analysis, HDL2 protein concentration was the single best variable for distinguishing between patients and controls. The most powerful discriminatory parameter was the HDL/LDL protein ratio or the HDL2/LDL protein ratio.
Atherosclerosis 1988 Nov
PMID:Serum lipoproteins in patients with myocardial infarction. 321 82

Two separate studies were carried out with acipimox, a new antilipolytic agent with long-lasting activity. First, in a randomized, double-blind, cross-over study a dose of 750 mg/day of acipimox versus placebo was employed for 60 days in 11 patients with type IV hyperlipoproteinemia. Mean plasma triglyceride levels were reduced after acipimox compared to placebo (434 +/- 60 vs 777 +/- 224 mg/dl, P less than 0.01). Serum total cholesterol fell also significantly after acipimox compared to placebo. No significant alteration was observed in the HDL2/HDL3 ratio or in the concentration or composition of the HDL subfractions. Six patients with severe hypertriglyceridemia (2 type IV and 4 type V) and low lipoprotein lipase (LPL) activity took part in a second, open study, lasting for 9 months. Acipimox was given at a dose of 750 mg/day for the first 6 months and 1200 mg/day for the last period. The response of serum total and VLDL triglycerides was inconsistent. HDL cholesterol was significantly raised (+33.3%) after 9 months of treatment due to changes of HDL2 and HDL3 cholesterol, phospholipid and protein concentrations. LPL activity was markedly reduced in adipose tissue at 9 months. No significant changes occurred in postheparin plasma LPL activity. In contrast, hepatic lipase activity showed a reduction of about 25% from 6 months of treatment onwards.
Atherosclerosis 1988 Feb
PMID:Effects of acipimox on serum lipids, lipoproteins and lipolytic enzymes in hypertriglyceridemia. 327 68

This study compared the effects of continuous subcutaneous insulin infusion (CSII) and conventional insulin therapy (CIT) on serum lipid and lipoprotein levels in type I diabetic patients during 1 year cross-over study (6 months on CSII and 6 months on CIT). The study group consisted of 28 normolipidemic and nonobese diabetic patients (14 males and 14 females) aged 31 +/- 2 yr. The glycemic control was moderate (HbA1 10.2 +/- 0.3%) before starting the study. During the first 6 months, the HbA1 level fell significantly in the CSII group (from 10.4 +/- 0.5% to 9.8 +/- 0.4%, P less than 0.05), but remained unchanged in patients on CIT. During the second 6 months after cross-over no significant alterations in HbA1 levels were observed in either group. HDL-cholesterol (HDL-chol) rose by 38% during the first 6 months in the patients using CSII (P less than 0.001) and by 18% in the CIT group (P less than 0.005). The rise in HDL-chol was accounted for by an increase in both HDL2-chol and HDL3-chol subfractions. Following the shift from CIT to CSII, HDL2-chol rose further (P less than 0.05), whereas HDL3-chol remained unchanged. When CSII was changed to CIT, the HDL3-chol level decreased (P less than 0.02), but HDL2-chol remained constant. There was no correlation between HDL-cholesterol and HbA1 levels or between the changes in either variable. HDL2-chol was 35% higher in females when compared to males at entry, and it rose in both sexes during CSII. HDL3-chol elevated during CSII only in females. CSII or CIT treatments did not cause significant changes in cholesterol or triglyceride levels of VLDL or LDL lipids during the study. Thus, even a mild improvement in glycemic control during CSII is associated with a rise in HDL-chol, particularly the HDL2 subfraction.
Atherosclerosis 1987 Apr
PMID:High density lipoprotein subfractions during continuous insulin infusion therapy. 330 Jun 67

Lipoprotein abnormalities constitute a major risk for development of cardiovascular disease. These substances, which are comprised of various lipids and proteins (apoproteins), are influenced by specific enzymes which effect their concentrations. It has been demonstrated that elevated total cholesterol and LDL cholesterol are directly associated with the development of coronary artery disease, whereas HDL cholesterol has an inverse relationship with coronary heart disease (CHD). Although more controversial, triglycerides may also be directly associated with coronary atherosclerosis. Favourable changes in lipid levels have been shown to reduce coronary mortality. Exercise may constitute a non-pharmacological approach to lipoprotein therapy. Many exogenous factors also influence lipoprotein concentrations. Changes in diet, body composition, age, as well as medication and alcohol usage may directly alter lipid levels. In addition, they can be artificially affected by the analytical method. The immediate effects of one to several bouts of physical activity appear to influence lipoprotein level. A reduction in triglycerides has been shown after physical exertion, especially among trained individuals and those with hypertriglyceridaemia. These acute changes may reflect the utilisation of both muscle and plasma triglycerides as fuels during exertion. After more prolonged training, changes in lipoproteins may also occur. However, since exercise is accompanied by many co-variables which also favourably alter these levels (e.g. lower percentage of body fat, dietary alterations), it is difficult to determine the direct effect of regular physical activity. Initial studies of exercise training's effects on total cholesterol did not differentiate changes in HDL and LDL cholesterol. Subsequent research has observed these specific cholesterol fractions. Consistent reduction in LDL cholesterol levels have not been convincingly demonstrated. Although HDL cholesterol has been shown to increase in certain studies, the response has been variable in other investigations. These latter responses may have been due to the fact that HDL cholesterol changes may be dependent on levels prior to conditioning. Assessment of HDL cholesterol subfractions (HDL2 and HDL3), which could additionally impact on cardiovascular risk reduction, have shown favourable increases in HDL2, but as yet these HDL moieties have not been adequately investigated. Reductions in triglyceride levels after training among those with elevated values and beneficial apoprotein changes post-training have been reported, although few studies exist.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The effect of exercise on lipid metabolism in men and women. 331 16

To reveal the presence of atherogenic potential in the blood serum obtained from patients with angiographically assessed coronary atherosclerosis we used primary cultures of subendothelial cells isolated by collagenase from unaffected human aortic intima. Earlier, we have demonstrated that such cultures are made up mostly of typical and modified smooth muscle cells. Within 24 hours of cultivation with a 40% sera of patients suffering from coronary atherosclerosis, the total intracellular cholesterol level increased twofold to fivefold. Cultivation with the sera of healthy subjects had no effect on the intracellular cholesterol level. The sera of patients were separated by ultracentrifugation into two fractions: total lipoprotein fraction containing the main classes of lipoproteins and a lipoprotein-deficient fraction. The former, but not the lipoprotein-deficient fraction, was characterized by atherogenicity (i.e., the ability to induce the accumulation of intracellular cholesterol). Lipoproteins of the patients' serum were separated into main classes: low density lipoproteins (LDL), very low density lipoproteins (VLDL), and high density lipoproteins (HDL2 and HDL3). An atherogenic component of the serum capable of stimulating the deposition of intracellular cholesterol was represented by LDL and, in one case, by VLDL, but not by other classes of lipoproteins. LDL and other lipoproteins isolated from the blood serum of healthy subjects failed to raise the cholesterol content in cultured cells; that is, they were nonatherogenic.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Blood serum atherogenicity associated with coronary atherosclerosis. Evidence for nonlipid factor providing atherogenicity of low-density lipoproteins and an approach to its elimination. 334 73


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