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)

Twelve different apolipoproteins have been described in human serum. Apo A-I and apo A-II are essential for the structure of the HDL particles and for the function of LCAT activity. Apo B is the main protein in LDL but does also occur in the triglyceride-rich particles. Apo B represents the binding protein for the LDL-receptor pathway. The C-apolipoproteins are located on the surface of VLDL. They are transferred to HDL throughout the catabolism of VLDL and affect lipoprotein lipase activity. This enzyme is also affected by the E-apolipoproteins which occur in the triglyceride-rich particles as well as in HDL. Apo E is the binding site for another specific cell receptor. The concentration and metabolism of apolipoproteins is affected by diet, drugs, hormones, body weight, alcohol, cigarettes, physical exercises, liver and renal diseases. There is a close relation between apolipoproteins and atherosclerosis.
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PMID:[The apolipoproteins in man ]. 675 Feb 20

Fish eye disease (FED) is characterized by severe corneal opacities, causing impaired vision, and dyslipoproteinaemia: hypertriglyceridaemia, raised levels of very low density lipoproteins (VLDL), triglyceride enrichment of low density lipoproteins (LDL) and reduction of high density lipoproteins (HDL). The disease is described in two unrelated families. In both there was a high proportion of low HDL in relatives without eye disease. VLDL, LDL and HDL had normal electrophoretic mobilities. The concentrations of VLDL cholesterol and triglycerides were increased fivefold. LDL cholesterol levels were normal but LDL triglycerides markedly increased. HDL cholesterol was reduced by 90% as were the levels of HDL apolipoproteins. The major part of HDL cholesterol was in the HDL3 fraction. FED HDL were smaller than normal with molecular weights of 115,000 daltons. Lecithin: cholesterol acyltransferase activity and amount of cholesterol esters in serum were normal. Postheparin lipoprotein and hepatic lipases showed normal or subnormal values. Clinically FED differs from other familial conditions with deficiency of HDL such as Tangier disease, LCAT-deficiency and Milano-AI-apoprotein disease. In spite of the extremely low HDL cholesterol FED is not characterized by premature atherosclerosis. Mechanisms for the dyslipoproteinaemia are discussed.
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PMID:Fish eye disease: a new familial condition with massive corneal opacities and dyslipoproteinaemia. 680 51

The effect of bezafibrate on plasma lipids, lipoproteins, apolipoproteins AI, AII and B, and LCAT activity was investigated in 16 hyperlipidemic, non-insulin-dependent diabetes, who were treated for 8 weeks with either placebo or bezafibrate in a double-blind cross-over design. Bezafibrate induced a significant decrease in plasma triglycerides (P less than 0.01), cholesterol (P less than 0.05), VLDL triglycerides (P less than 0.05) and VLDL cholesterol (P less than 0.01), and a significant increase in HDL cholesterol (P less than 0.01), whereas LDL cholesterol remained unchanged. The apolipoprotein AI/apolipoprotein B ratio increased significantly (P less than 0.05), although individual changes in these apolipoproteins were not significant. Apolipoprotein AII increased significantly (P less than 0.05), although individual changes in these apolipoproteins were not significant. Apolipoprotein AII increased significantly (P less than 0.0001) and the apolipoprotein AI/apolipoprotein AII ratio decreased (P less than 0.0001), indicating an increase in the HDL3 rather than the HDL2 fraction. No significant change in LCAT activity was observed.
Atherosclerosis 1982 Jun
PMID:Effect of bezafibrate on plasma lipids, lipoproteins, apolipoproteins AI, AII and B and LCAT activity in hyperlipidemic, non-insulin-dependent diabetics. 681 Sep 4

The classification and metabolism of lipoproteins and their relation to the risk of coronary heart disease are briefly discussed. Cross-sectional studies indicate that people who practice endurance training tend to have higher levels of HDL, but lower plasma concentrations of VLDL, LDL and triglycerides than physically inactive persons of the same age and sex. A similar picture has emerged from longitudinal studies. The effects of physical training on the level of total cholesterol is less certain (but probably also less important since the essential part of plasma cholesterol is present in lipoproteins--LDL and HDL--which are considered to have antagonistic functions in the development of atherosclerosis). Forced training of rats resulted in a lowering of total concentrations of cholesterol (although there are some negative reports) and triglycerides, increased activity of lipoprotein lipase in the muscle, increased activity of the plasma enzyme LCAT (lecithin: cholesterol acyltransferase) and increased excretion of bile acids in the faeces. In human subjects who practice endurance training a similar increase in activity of the above enzymes has been demonstrated and this may be the basis for the effect of training on lipoprotein concentrations in plasma. It is concluded that physical activity of endurance type appears to have a favourable effect on the pattern of lipoproteins in the plasma (rise in HDL, fall in VLDL and LDL), and that consequently such training may have significance for the prevention of coronary heart disease.
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PMID:Physical activity and plasma lipids. 698 9

Changes in the rate of the plasma cholesterol ester production mediated by lecithin: cholesterol acyltransferase (LCAT, E.C. 2.3.1.43) were examined in 15 patients suffering from types II and IV HLP who had been treated for 14 weeks with etiroxate. Whereas the plasma cholesterol concentration decreased significantly only in the initial phase of the therapy, the rate of cholesterol esterification increased gradually and attained at the end of the study a value exceeding by 50% the initial level. The final fractional turnover rate nearly equalled that characteristic for the control group of healthy subjects, in spite of the fact that the concentration of plasma cholesterol in the diseased subjects was higher by 50-100%. Triglyceride concentration decreased only transitorily in the course of the therapy with etiroxate. It is concluded that etiroxate is likely to normalize the rate of cholesterol turnover in the endogenous pool.
Atherosclerosis 1982 Apr
PMID:Rate of LCAT-mediated cholesterol esterification and serum lipids during etiroxate therapy in hyperlipoproteinemia. 707 4

We studied two sisters 29 and 31 years old who had skin and tendon xanthomas, corneal clouding, and severe coronary atherosclerosis. Histologic examination showed collections of lipid-laden histiocytes in the skin. The patients' plasma cholesterol concentrations were 177 and 135 mg per deciliter (4.58 and 3.49 mmol per liter). Levels of high-density-lipoprotein cholesterol were 4 and 7 mg per deciliter (0.1 and 0.2 mmol per liter). Only traces of apolipoprotein A-I were detected in whole plasma. The plasma density fraction from 1.06 to 1.21 g per milliliter contained no high-density lipoprotein on high-pressure liquid chromatography, no apolipoprotein A-I on sodium dodecyl sulfate electrophoresis, and only traces of apolipoprotein A-I on radioimmunoassay. Apolipoprotein C-III was also not detectable. The activity of lecithin-cholesterol acyltransferase was 40 per cent of normal. The half-life of infused normal high-density lipoprotein was three days (normal, 5.8 days). The parents and children of these two patients had low levels of high-density-lipoprotein cholesterol and apolipoprotein A-I. These cases support the hypothesis that low concentrations of high-density lipoprotein promote atherosclerosis.
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PMID:Familial deficiency of apolipoproteins A-I and C-III and precocious coronary-artery disease. 707 8

Plasma unesterified cholesterol is converted to cholesteryl ester by the enzyme lecithin-cholesterol acyltransferase (LCAT). Plasma levels of LCAT were measured by a sensitive double antibody radioimmunoassay in a sample from an adult employee population, ages 20-59 years, in the Pacific Northwest. After adjusting for differences in relative body mass, women had significantly higher LCAT levels (5.90 +/- 1.06, n = 154) than men (5.49 +/- 0.89, n = 83). For ages 20-59 years, LCAT levels showed a slight association with age: r = 0.13 for men and 0.29 for women. LCAT was positively correlated with relative body mass, total cholesterol, and LDL cholesterol. Men who smoked cigarettes had significantly lower LCAT mass than men who did not smoke cigarettes. No statistical differences in mean LCAT values were found between drinkers and nondrinkers. The 5th percentile LCAT value was 4.3 micrograms/ml for both men and women not using hormones. The 95th percentile value was 7.3 micrograms/ml for men and 7.8 micrograms/ml for women regardless of hormone use. Subjects phenotypically LCAT-deficient by clinical criteria and by the absence or near absence of LCAT activity had levels of LCAT mass well below the reference values: 0.73 +/- 0.70, range 0.10 micrograms/ml to 2.65 micrograms/ml, n = 20. Parents or children of LCAT-deficient subjects, i.e., obligate heterozygotes for familial LCAT deficiency, had reduced levels: 3.59 +/- 0.69, range 2.59-4.61 micrograms/ml, n = 19.
Atherosclerosis 1982 Jun
PMID:Population-based reference values for lecithin-cholesterol acyltransferase (LCAT). 711 67

An abnormal level of serum lipids may be one of the major risk factors for the development of atherosclerosis in patients with chronic renal failure (CRF). In the present study, the effect of polyunsaturated fatty acid-rich and low carbohydrate diet on serum lipids and HDL-cholesterol was studied in 6 nonnephrotic and nondialyzed patients with CRF on an isocaloric basis. Serum triglycerides decreased significantly from 2.08 +/- 0.93 mmol/l (183 +/- 82 mg/dl) to 1.49 +/- 0.83 mmol/l (131 +/- 73 mg/dl) by consumption of polyunsaturated diet (p less than 0.01). The 'HDL-cholesterol ratio' increased significantly and LCAT decreased on a polyunsaturated diet. In conclusion, the consumption of a polyunsaturated fatty acid-rich diet tends to normalise increased serum triglycerides and lowered 'HDL-cholesterol ratio' in patients with CRF and may be effective for prevention of atherosclerotic vascular sequellae.
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PMID:Effects of a polyunsaturated fatty acid-rich diet on serum lipids in patients with chronic renal failure. 712 70

In order to compare the mass-activity distribution of lecithin-cholesterol acyltransferase (LCAT) among plasma lipoproteins separated by various ultracentrifugal or chromatographic procedures, we have quantified the enzyme by an electroimmunoassay technique using a specific antibody raised in the rabbit. This antibody, when added to whole serum, inhibited all of the enzyme activity present in it. The percent mass distribution of the enzyme among the lipoproteins isolated by rate-zonal ultracentrifugation (d 1.00-1.36 g/ml, SW 40 rotor, 37 000 rpm, 16 h) was as follows: very low density lipoproteins (VLDL), 0; low density lipoproteins (LDL), 6.2; HDL2, 6.5; HDL3, 12 and d greater than 1.21 g/ml fraction, 75. Measurement of LCAT activity of each lipoprotein fraction against mixed single bilayer lecithin-cholesterol vesicles (molar ratio, 4:1) containing apo A-I, indicated that VLDL, LDL and HDL2 were inactive or minimally active under the experimental conditions used, whereas HDL3 and the d greater than 1.21 g/ml fraction contained 17.5 and 79.9% of the total enzyme activity. Prolonged ultracentrifugation of the LCAT-containing lipoproteins resulted in the recovery of activity in the lipoprotein-free infranatant. In studies with lipoproteins linked to Sepharose 4B, LCAT was found to bind LDL, HDL2, and HDL3. It is concluded that LCAT is present in all the major lipoproteins except for VLDL. The activity appears to be dependent, at least in part, on the type of lipoproteins to which the enzyme is associated with.
Atherosclerosis 1982 Oct
PMID:In vitro mass: activity distribution of lecithin--cholesterol acyltransferase among human plasma lipoproteins. 715 89

Because lecithin-cholesterol acyltransferase (LCAT) has been shown to carry out acylation of lysolecithin as well as hydrolysis of lecithin in addition to an esterification of cholesterol, the cofactor requirements of the three reactions catalyzed by the enzyme were studied. The purified enzyme required apolipoprotein A-I (apo A-I) for both the phospholipase A2 activity (release of free fatty acids from lecithin) and cholesterol esterification, whereas, low density lipoprotein (LDL) was required for the acylation of lysolecithin. Apo A-I and lecithin liposomes could not substitute for LDL for the activation of lysolecithin acyltransferase activity. Removal of apo A-I from the LDL preparation by affinity chromatography did not affect the activation of lysolecithin acylation, indicating that the contaminating apo A-I is not responsible for the activation. LDL facilitates cholesterol esterification in presence of labelled lecithin liposomes by providing the unesterified cholesterol. Removal of contaminating apo A-I, however, abolishes this LCAT activity which could be restored by addition of pure apo A-I. Lysolecithin inhibits both phospholipase A2 and LCAT activities, but LDL appeared to attenuate the effects of lysolecithin, in addition to stimulating the acylation of lysolecithin. These results show that apo A-I is not obligatory for all the reactions carried out by the enzyme, and that LDL plays an important role in the regulation of the hydrolysis and acylation reaction carried out by the enzyme.
Atherosclerosis 1982 Nov
PMID:Studies on the cofactor requirement for the acylation and hydrolysis reactions catalyzed by purified lecithin-cholesterol acyltransferase. Effect of low density lipoproteins and apolipoprotein A-i. 715 94


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