Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.1.34 (lipoprotein lipase)
7,025 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Epitope expression was studied in both denatured apolipoprotein B (apo B) on Western blots and in intact low density lipoprotein (LDL) and very low density lipoprotein subfractions VLDL1 (Sf120-400), VLDL2 (Sf60-120), and VLDL3 (Sf20-60) in competitive binding immunoassays with the aid of six monoclonal anti-LDL antibodies. The apo B in all lipoprotein fractions was shown to bind to all antibodies, but significant differences in apo B epitope expression were observed. On the average, the immunoreactivity of VLDL subfractions (expressed as binding affinity and as relative 125I-LDL displacing potency) decreased with increasing flotation rate. Similarly, VLDL1 was less immunoreactive than lipolyzed "remnants" of VLDL1 after treatment with bovine milk lipoprotein lipase. The results indicate that, even when lipoprotein fractions obtained from the same individual and having the same kind of apo B subspecies were compared, significant differences in immunoreactivity occurred due to the modulating effect of other lipoprotein components on apo B epitope expression.
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PMID:Expression of apolipoprotein B epitopes in very low density lipoprotein subfractions. Studies with monoclonal antibodies. 620 98

The effects of experimental nephrosis in rats, produced by puromycin aminonucleoside, include an elevation of plasma levels of all lipoprotein density classes and the appearance of high density lipoprotein (HDL) rich in apoprotein (apo) A-I and deficient in apo A-IV and apo E. The hyperlipoproteinemia is associated with an increase in hepatic synthesis of lipoproteins. The possible role of decreased very low density lipoprotein (VLDL were obtained from nonfasting animals by ultracentrifugation at d 1.006 and included chylomicrons) catabolism and its relationship to the apolipoprotein composition of nephrotic high density lipoproteins (1.063 less than d less than 1.210, or 1.072 less than d less than 1.210 [HDL]) was explored. When 125I-VLDL was injected, the faster plasma clearance of lower molecular weight apolipoprotein B (apo BL) compared with that of higher molecular weight apo BH which is seen in normal rats was not observed in nephrotic rats. Less labeled phospholipid, apo C, and apo E were transferred from VLDL to higher lipoprotein density classes. Heparin-releasable plasma lipoprotein lipase and hepatic lipase activities were decreased by 50% in nephrotic rats compared with pair-fed controls. Perfusion of livers with medium that contained heparin released 50% less lipase activity in nephrotic rats than in controls. When heparin was injected intravenously, significant decreases in plasma levels of triglycerides and significant increases in levels of free fatty acids were observed in both groups of animals. In the nephrotic rats, 86% of the free fatty acids were in the lipoprotein fractions, as compared with 16% in the controls. Heparin treatment did not restore to normal the decreased apo BL clearance in nephrotic rats but it produced an increased amount of apo A-IV and apo E in the plasma HDL. In vitro addition of partially pure lipoprotein lipase to whole serum from nephrotic rats significantly increased the content of apo E in HDL. We conclude that the abnormal apoprotein composition of HDL in experimental nephrosis is the result of altered entry of apolipoproteins from triglyceride-rich lipoproteins, probably because of decreased lipolysis.
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PMID:Catabolism of very low density lipoproteins in experimental nephrosis. 648 Aug 30

Studies of simultaneous autologous 131I-chylomicron (Sf greater than 400) and 125I-very low density lipoprotein (VLDL) (Sf 20 to 400) apolipoprotein B (apo B) were performed both before (triglyceride level c 1500 mg/dL) and during treatment with stanozolol, a 17 alpha-methyl anabolic androgenic steroid (triglyceride level c 750 mg/dL) in a 74-year-old woman with a past history of recurrent chylomicronemic pancreatitis. Both before and during stanozolol treatment chylomicron apo B disappeared rapidly and directly, little appearing in VLDL and virtually none in intermediate (IDL) or low density lipoproteins (LDL). Multicompartmental analysis indicated that the great majority of chylomicron apo B was removed via an extremely rapid compartment (estimated fractional catabolic rate [FCR], 5.0/h), accounting for 66% before and 88% during stanozolol treatment. The remaining 131I-apo B decayed biphasically, with total Sf greater than 400 residence times of 8.6 hours before and 3.7 hours during stanozolol treatment. Hence, despite a moderately depressed adipose tissue lipoprotein lipase activity, the subject's hypertriglyceridemia did not appear to proceed solely from retarded chylomicron removal, nor was the dramatic decrease in triglyceride in response to stanozolol a function only of the acceleration of such removal. VLDL apo B kinetics were analyzed by a multicompartmental model featuring a rapid, stepwise delipidation chain which proceeds either rapidly to IDL and LDL or to a slowly turning over compartment within VLDL. While VLDL. apo B synthesis remained essentially constant, the major effect of stanozolol was a substantial reduction in the fraction of VLDL apo B diverted to this slowly turning over compartment, which decreased from 5.0% before to 1.2% during treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chylomicron and very low-density lipoprotein apolipoprotein B metabolism: mechanism of the response to stanozolol in a patient with severe hypertriglyceridemia. 648 32

Three patients with Menkes' disease, an inherited disorder of copper transport, were studied to determine whether the copper deficiency was associated with a lipoprotein disorder. Hypocuprinemia was documented in all three cases. Two patients had severe copper and ceruloplasmin deficiencies, whereas the third patient had a less severe deficiency. Hypertriglyceridemia was observed in the first patient, and elevations in triglyceride, cholesterol, apolipoprotein B (ApoB), and apolipoprotein C-III (ApoC-III) occurred predominantly in the very low density lipoprotein fraction (VLDL). This patient had normal lipoprotein lipase activity but mild glucose intolerance. The second patient had a borderline high cholesterol level with normal plasma triglycerides and apolipoproteins, whereas the third patient appeared to have normal total cholesterol but slightly higher triglycerides with elevated plasma apolipoprotein E (ApoE). No striking differences were observed in the chemical composition of all lipoprotein subfractions between patients and controls except that the neutral lipid content of VLDL was higher in patients than in controls. The ApoB was initially normal in molecular weight but degraded faster than the controls during storage. The appearance of the major low density lipoprotein (LDL) fraction of the first two patients was opaque white, in contrast to clear yellow in the third patient and in the age- and diet-matched controls. This abnormal appearance of LDL in these patients was associated with low plasma levels of beta-carotene and ceruloplasmin. These findings suggest that decreased serum copper levels may be associated with lipid and lipoprotein abnormalities and may enhance lipid peroxidation of LDL accounting for the color change.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Studies of lipids, lipoproteins, and apolipoproteins in Menkes' disease. 648 10

The lipid patterns of plasma from 6 patients on hemodialysis (HD) and 6 patients on continuous ambulatory peritoneal dialysis (CAPD) were compared and correlated to plasma toxicity as measured by the survival of human macrophages cultured in vitro. The median values for plasma triglycerides (TG), cholesterol, low density lipoprotein (LDL) cholesterol, apolipoprotein B and lipolytic activities (lipoprotein lipase and hepatic lipase) were insignificantly higher in CAPD plasma than in HD plasma. The median high density lipoprotein (HDL) cholesterol/LDL cholesterol ratio was significantly higher in HD plasma than in CAPD plasma. In both groups systemic heparinization was followed by a significant increase in free fatty acids and in plasma toxicity. The difference in plasma toxicity was insignificant. In the whole group of patients (n = 12) toxicity in post-heparin plasma was correlated to pre-heparin very low density lipoprotein (VLDL) TG, but not to LDL TG. Separately post-heparin toxicity in CAPD plasma was correlated to pre-heparin total TG, VLDL TG and post-heparin LDL TG.
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PMID:The effect of systemic heparinization on plasma lipoproteins and toxicity in patients on hemodialysis and continuous ambulatory peritoneal dialysis. 648 84

The beta-very low density lipoproteins (beta-VLDL) that accumulate in type III hyperlipoproteinemic subjects can be divided into two fractions (fraction I and fraction II), which differ in size, lipid composition, and the type of apolipoprotein B (apo-B) present in the particles. The apo-B48-containing particles (fraction I) are of intestinal origin, while apo-B100-containing particles (fraction II) are derived from the liver. Both fractions contain a defective form of apo-E referred to as apo-E2. Intravenous infusion of heparin into two subjects with type III hyperlipoproteinemia resulted in the complete removal of fraction II particles from density less than 1.006 g/ml, while fraction I particles remained at this density. In vitro studies confirmed that fraction I particles did not change density when subjected to hydrolysis with lipoprotein lipase, while fraction II particles shifted to the intermediate density lipoprotein range (approximately equal to 1.02 g/ml). When the beta-VLDL were hydrolyzed by lipoprotein lipase in the presence of density greater than 1.21 g/ml lipoprotein-deficient plasma, the addition of normal apo-E (apo-E3), but not apo-E2, resulted in a shift of fraction II particles to the low density lipoprotein (LDL) range (approximately equal to 1.05 g/ml). Fraction I particles did not undergo a shift to this higher density, supporting previous observations that apo-B48-containing particles are not converted to LDL. The demonstration that apo-B100-containing particles in type III hyperlipoproteinemic subjects could be converted to particles with the density of LDL suggests that apo-E plays a role in the normal conversion of VLDL to LDL. The mutant form of apo-E (apo-E2) found in the beta-VLDL from type III hyperlipoproteinemic subjects appears to impede this conversion, whereas the addition of normal apo-E (apo-E3) allows the processing to occur.
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PMID:Role of apolipoprotein E in the lipolytic conversion of beta-very low density lipoproteins to low density lipoproteins in type III hyperlipoproteinemia. 659 Dec 4

Plasma lipids, lipoproteins, tissue lipoprotein lipase (LPL) and hepatic lipase (H-TGL) were studied in 7 patients with familial hyperchylomicronemia from four different families. Their first-degree relative were also studied. The patients were heterogeneous for the genetic defect; LPL activity was absent in five patients (LPL deficiency) but normal in two. However, these two did not have apo C-II, the physiological activator of LPL (C-II deficiency). There were no significant differences in the clinical picture between patients with LPL deficiency and C-II deficiency. In both mutants, marked hypertriglyceridemia was due to an accumulation of lipoproteins of density less than 1.006 g/ml. The LDL fraction was very reduced and abnormal in composition, presenting a CH/TG ratio of 0.5. The plasma apolipoprotein B (apo B) level was low (67 +/- 5.5 mg/dl) and was transported mainly in the VLDL fraction (26 +/- 3.2 mg/dl) rather than in the LDL fraction (15 +/- 1.4 mg/dl). Very low levels of cholesterol and apolipoprotein A-I in HDL subfractions HDL2 and HDL3 were also recorded. Only 3 out of the 24 first-degree relatives of patients with LPL deficiency showed even a small increase in plasma triglycerides, but 15 had low or low to normal LPL values. H-TGL levels were normal in all subjects. The 4 first-degree relatives of C-II deficiency patients showed normal levels of plasma lipids. LPL and H-TGL, and 2 children of 1 patient showed normal distribution of apo C peptides in their VLDL. A block in chylomicron catabolism, due to the absence of LPL or apo C-II, may lead to a massive accumulation of lipoproteins with a density less than 1.006 g/ml, and a drastic reduction in the LDL and HDL fractions. Low LPL values in the first-degree relatives of LPL deficiency patients might represent a biochemical marker for healthy carriers of LPL deficiency.
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PMID:Familial lipoprotein lipase and apolipoprotein C-II deficiency. Lipoprotein and apoprotein analysis, adipose tissue and hepatic lipoprotein lipase levels in seven patients and their first degree relatives. 665 13

The fate and mechanism of removal of apolipoproteins and lipids of human very-low-density lipoproteins were determined in the perfused rat heart. Approx. 50% of the VLDL triacylglycerol was hydrolyzed during a 2 h perfusion. Phospholipid phosphorus, apolipoproteins C-II, C-III and E were quantitatively recovered in the medium. However, there was a loss of unesterified (17 +/- 6%) and esterified (19 +/- 8%) cholesterol from the perfusion medium. Apolipoprotein B was retained by the heart, as determined by the loss of immunoassayable apolipoprotein B (30 +/- 5%) or the uptake of 125I-labelled apolipoprotein of VLDL (9 +/- 2%) from the perfusion medium. The discrepancy in the two methods for estimating apolipoprotein removal was shown to be due to the modification of apolipoprotein B-containing lipoproteins, which was such that they were no longer precipitated with antibodies to apolipoprotein B. The labelled apolipoprotein B, retained by the heart, could be partially released by perfusion of the heart with buffer containing heparin (14 +/- 2%) or trypsin (50 +/- 2%). Labelled apolipoprotein uptake by the heart was reduced by 90% when lipoprotein lipase was first released by heparin or when VLDL was treated with 1,2-cyclohexanedione to modify arginine residues of apolipoproteins. Very little extensive degradation of the apoprotein to low molecular weight material occurred during the 2 h perfusion, since 95% of the tissue label was precipitated by trichloroacetic acid. It is concluded that there is retention of apolipoprotein B, cholesteryl ester and cholesterol by the perfused heart during catabolism of VLDL. The data are consistent with the concept that the retention of apolipoprotein B requires membrane-bound lipoprotein lipase or an interaction with the cell surfaces that is modified by heparin. The overall process also involves arginine residues of apolipoproteins. At least 50% of the labelled apolipoprotein retained in the tissue is associated with lipoprotein lipase and other cell surface sites, while the remainder may be taken up by the cells.
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PMID:Retention of apolipoprotein B and cholesterol by perfused heart during lipolysis of very-low-density lipoprotein. 670 14

The immunoquantification of total apolipoprotein B in human serum has been evaluated by rate and equilibrium nephelometry. The presence of triglyceride-rich lipoproteins spoiled all immunochemical assays and yielded too-high values for apolipoprotein B. The use of detergents improved the results substantially, but results were inaccurate at high triglyceride concentrations. Of many detergents investigated, only Thesit, Kryo Ebo, and Apovax were useful, decreasing the light-scatter signals almost linearly with increasing detergent concentrations. The regression lines, however, were not parallel among the different apo B-containing lipoproteins. Incubating sera or apo B-containing lipoproteins with bovine milk lipoprotein lipase or bacterial triacylglycerol lipase, at concentrations of 100 kU/L, hydrolyzed all of the triglycerides and most of the phosphatidylcholine within 18 h at 37 degrees C Lipase-pretreatment of samples gave optimal correlation between apo B values as determined by nephelometry with those obtained gravimetrically. We also assessed the influence of sample storage, freezing, and thawing on the nephelometric apo B assays.
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PMID:Immunoquantification of total apolipoprotein B in serum by nephelometry: influence of lipase treatment and detergents. 685 Oct 92

Physical, chemical and physiological approaches were used to examine the properties of two very low density lipoproteins, VLDL-I (slow-beta), and VLDL-II (pre-beta), which were isolated by agarose column chromatography from the serum of rhesus monkeys fed either Purina Chow or one of four hyperlipidemic diets containing 0.5-20% cholesterol suspended in either coconut oil, peanut oil, mixed coconut oil and butter fat or lard. In the coconut oil-fed hyperlipidemic animals, the majority of the apolar lipids of VLDL-I was represented by cholesteryl esters. The small percentage of triacylglycerol (15%) had a fatty acid composition which resembled that of the fatty acid in each of the diets. In turn, VLDL-II had a triacylglycerol-rich core and differed from VLDL-I in apolipoprotein distribution (VLDL-I: low molecular weight apolipoprotein B, 36%; apolipoprotein E, 64%; and VLDL-II: high molecular weight apolipoprotein B, 38%; apolipoprotein E, 3%; and apolipoprotein C, 65%). Both VLDLs were hydrolyzed in vitro by milk lipoprotein lipase by first-order kinetics although VLDL-I exhibited a slightly slower reaction rate. When an oral dose of [3H]retinol was given to one of the animals, both VLDLs became labeled but the specific activity of VLDL-I was six times higher than that of VLDL-II and the other lipoproteins. We conclude that VLDL-I represents a cholesteryl ester-rich lipoprotein probably of intestinal origin, whereas VLDL-II may be a particle of hepatic derivation modified by its interaction with the other plasma lipoproteins.
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PMID:Properties and metabolic fate of two very low density lipoprotein subfractions from rhesus monkey serum. 706 52


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