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)

In view of the high incidence of hyperlipidemia and the low sialic acid content in the membranes of diabetics, we analyzed the percentage composition of apolipoprotein CII, known as an activator of lipoprotein lipase, and a subspecies of apolipoprotein CIII, an inhibitor of lipoprotein lipase, in triglyceride-rich lipoproteins. CIII can be sub-divided into three groups, CIII0, CIII1 and CIII2, according to sialic acid content by isoelectric focusing gel. In 82 diabetics, serum lipids and lipids in various lipoprotein fractions differed according to treatment, (diet, oral hypoglycemic drug or insulin). CIIIo/CII showed a positive correlation to plasma triglyceride and cholesterol. In the group receiving oral medication (N = 20), CIIIo/CII vs HDL-cholesterol showed a positive correlation, whereas CIII2/CII vs plasma triglyceride showed an inverse correlation. In the insulin group (N = 25), the percentage of CIIIo in VLDL apo C subspecies was inversely correlated with plasma cholesterol. In 38 diabetics whose HbA1 was also examined, CIIIo/CII increased with elevation of HbA1. CIIIo/CII in diabetics with HbA1 higher than 10% was significantly high compared with the index in other diabetics. The percentage of CIII1 in VLDL apo C subspecies was correlated to HbA1 level positively in the diet group but inversely in the insulin group. These results suggest that lipoprotein metabolism in diabetics may vary according to treatment and the sialylation of apolipoprotein may play an important role in determining the severity of this disease.
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PMID:Lipoprotein metabolism in diabetics treated with diet, oral hypoglycemic drug and insulin. 639 41

beta 2-Glycoprotein I (beta 2GI) has recently been identified as a component of circulating plasma lipoproteins. The metabolic role of this apolipoprotein is not known with certainty; it has been reported that beta 2GI has a high affinity for triglyceride-rich particles, causing their selective precipitation by detergents, and activates lipoprotein lipase in the in vitro hydrolysis of artificial lipid emulsions. In the present report, we have evaluated the secondary, tertiary, and quaternary structure of lipid-free beta 2GI. The weight average molecular weight of beta 2GI, as determined by sedimentation equilibrium measurements, was 43,000 in the presence and absence of denaturing agents. Thus, in contrast to other apolipoproteins, apolipoprotein H (apo-H) does not self-associate in aqueous solution. The circular dichroic spectra of apo-H is unusual in that there are no strong negative bands in the far-ultraviolet region of the spectrum; there is a weak positive maximum at 235 nm and a relatively weak negative maximum at 205 nm. Treatment with guanidinium chloride results in a loss of the positive band with only minor changes in the intensity of the band at 205 nm. Apolipoproteins A-I, A-II, C-I, and E, in contrast, have a secondary structure that contains a high percentage of residues in an alpha-helical configuration and undergo major changes in structure at low concentrations of guanidinium chloride. Highly flexible proteins, such as apolipoproteins A-I, A-II, and C-I, absorb rapidly and reversibly to air-water interfaces, whereas more rigid proteins, such as the classical globular proteins, interact with the interface more slowly and irreversibly. This difference is due to the loosely folded tertiary structure of apolipoproteins and the ease with which they can change structure to accommodate a given environment. The surface activity of beta 2GI at neutral pH resembles that of typical globular proteins. Treatment with acid or base, although causing only minor changes in the circular dichroic spectra, resulted in major increases in the rate of absorption to an air-water interface; under these conditions the rates of absorption were similar to that found for apolipoprotein A-I. These results are consistent with a more flexible structure for beta 2GI in acid or base that resembles other loosely folded apolipoproteins. beta 2GI associates with plasma lipoproteins and satisfies all of the criteria to be classified as an apolipoprotein. The secondary, tertiary, and quaternary structure of beta 2GI is, however, quite different from that of other well characterized apolipoproteins. This difference in structure would be expected to affect protein-lipid interactions; the relationship between apo-H and other apolipoproteins may be similar to that proposed for integral versus peripheral membrane proteins.
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PMID:beta 2-Glycoprotein I. Molecular properties of an unusual apolipoprotein, apolipoprotein H. 640 35

The effects of estrogen administration (ethinyl estradiol; 0.1 mg, orally, daily) on plasma lipoprotein metabolism were investigated in five normolipidemic premenopausal females. Estrogen administration resulted in significant (P less than 0.05) mean increases in plasma cholesterol, triglyceride, very low density lipoprotein (VLDL)-cholesterol, and high density lipoprotein (HDL)-cholesterol of 18.8%, 87.0%, 123.1%, and 38.3%, respectively. Analytical ultracentrifugation demonstrated that HDL increases occurred mainly in the HDL2b subfraction (150.0% increase). Lipoprotein compositional analysis showed that estrogen administration caused significant increases in all VLDL and HDL constituents (protein, cholesterol, phospholipid, and triglyceride) as well as VLDL apolipoprotein (apo) B (118.9% increase) and HDL apoA-I (27.4% increase). No significant changes in LDL constituents were noted. Measurement of lipoprotein lipase and hepatic lipase enzymic activity in post-heparin plasma revealed no major change in lipoprotein lipase activity, but showed a significant decrease (43.8%) in hepatic lipase activity during estrogen administration. Radioiodinated VLDL and HDL kinetic data indicated increased VLDL apoB (86.1% rise) and HDL apoA-I (24.9% rise) synthesis during estrogen administration. These data are consistent with the concept that estrogen administration at the dose level studied in premenopausal females causes significant elevations in VLDL and HDL constituents, associated with enhanced production of VLDL apoB and HDL apoA-I.
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PMID:The effects of estrogen administration on plasma lipoprotein metabolism in premenopausal females. 640 8

In the rare familial disorder fish-eye disease, hypertriglyceridaemia is associated with elevated levels of very-low-density lipoprotein (VLDL) and enrichment of low-density lipoprotein (LDL) with triglyceride. The kinetic basis of the dyslipoproteinaemia was investigated by studying the metabolism of the apolipoprotein-B moeity of VLDL, intermediate-density lipoprotein (IDL) and LDL in a 68-year-old woman with this condition. The major kinetic abnormality was a pronounced reduction in the rate of fractional conversion of VLDL-B to IDL-B and of IDL-B to LDL-B, suggesting that the dyslipoproteinaemia represents accumulation in plasma of partly degraded products of VLDL metabolism. This kinetic disorder has features in common with type-III hyperlipoproteinaemia. In studies in vitro no defect in the enzyme, activator or substrate components of the lipoprotein lipase or hepatic lipase systems was observed.
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PMID:Studies of lipoprotein metabolism in a patient with fish-eye disease. 643 21

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

In order to study the effects of chronic alcoholism, 3 groups of patients were investigated and compared to 10 healthy controls. Group I consisted of 9 heavy drinkers, who exhibited type V hyperlipidemia (HLP) under alcohol intake. Group II consisted of 7 patients, who previously had type V HLP under the influence of alcohol. At the time of the investigation, however, they had ceased alcohol drinking for at least 6 months and were normolipidemic. Group III consisted of 7 heavy drinkers without hyperlipidemia. Compared to controls, group I had significantly decreased plasma concentrations of high density lipoproteins2 (HDL2) and HDL3 (both P less than 0.01); activities of post-heparin lipoprotein lipase (LPL) and hepatic lipase (HTGL) as well were excessively decreased (both P less than 0.01). In group III LPL was also decreased (P less than 0.01), but HTGL was distinctly (P less than 0.01) higher than in controls. No such differences could be demonstrated for the patients of group II. Acute alcohol withdrawal from a patient suffering from alcoholism with HLP led to a sharp increase of LPL with a simultaneous decrease of VLDL within 2 days and a more delayed increase of LDL, HDL2 and HTGL, all reaching normal values within 12 days after cessation of alcohol drinking. With respect to the apolipoprotein (apo) composition of HDL2, patients of group I and group III exhibited a significantly lower percentual content of apo C-I at the expense of a significantly higher content of apo A-II as compared to controls and patients of group II. In group I and II, the percentual content of apo D in HDL2 was significantly higher than in controls and in group III. It is concluded that severe alcohol intake strongly impairs LPL in patients with HLP. The pronounced increase of HTGL in some patients (group III) may protect these individuals from HLP. The increased content of apo D in HDL2 may be a possible primary trait for alcohol-inducible HLP.
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PMID:Post-heparin lipolytic activities and alterations of the chemical composition of high density lipoproteins in alcohol-induced type V hyperlipidemia. 649 35

The effects of aging on serum lipids, lipoproteins and apolipoprotein C subclasses in very low density lipoprotein (VLDL) were investigated in healthy male subjects aged from the 1st to the 9th decade. The serum cholesterol, phospholipid and triglyceride concentrations, the serum beta-lipoprotein concentration determined immunologically, and the beta-lipoprotein percentage determined by electrophoresis showed the lowest levels in the 2nd decade, increased gradually with age, attained the highest level in the 6th to 7th decade and slightly declined in the 9th decade. The VLDL-low density lipoprotein (LDL) cholesterol level changed almost in parallel with the serum total cholesterol level, but the HDL cholesterol level and the apolipoprotein A concentration remained almost constant showing no age-related change. The free cholesterol percentages in every lipoprotein fraction and the apolipoprotein content in LDL were higher in the subjects in the 6th and 7th decade than those in the 2nd to 3rd decade. The apo C II/C III ratio in VLDL increased with age. These data suggest that the ability to active lipoprotein lipase may not be impaired but the lecithin:cholesterol acyltransferase (LCAT) activity declines with age.
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PMID:Changes with aging in serum lipoproteins and apolipoprotein C subclasses. 657 6

Lipolysis of human very low density lipoproteins (VLDL) by lipoprotein lipase (LPL) was inhibited in the presence of high density lipoproteins (HDL), anti-apolipoprotein (apo) CII, and by increasing the VLDL free cholesterol content but not with anti-apo CIII or lipoprotein-free plasma. The experiments lend direct evidence that the composition of VLDL and their milieu are important determinants of lipolysis by LPL. Apo CIII may not be critical in LPL mediated VLDL catabolism.
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PMID:Effect of human high density lipoproteins, anti-apolipoproteins CII and CIII, and hydrolysis of very low density lipoprotein (VLDL) cholesterol ester on VLDL catabolism in vitro. 658 72

Apolipoprotein (apo) C-II is a cofactor for lipoprotein lipase, the enzyme that catalyzes the hydrolysis of triglycerides on plasma triglyceride-rich lipoproteins. The complete coding sequence of apoC-II mRNA has been determined from an apoC-II clone isolated from a human liver cDNA library. A 17-base-long synthetic oligonucleotide based on amino acid residues 5-10 of apoC-II was utilized as a hybridization probe to select recombinant plasmids containing the apoC-II sequence. Two thousand four hundred clones were screened and one apoC-II cDNA clone containing 500 bases was identified. DNA sequence analysis of this clone revealed a 101 amino acid C-II apolipoprotein containing a 22 amino acid signal peptide attached to the amino terminus of the 79 amino acid residue plasma apoC-II. The amino acid sequence of apoC-II determined by nucleic acid analysis is in agreement with the recently determined sequence of plasma apoC-II isolated from normal subjects. The determination of the complete cDNA sequence of apoC-II and the availability of a cDNA probe of apoC-II will facilitate our analysis of the biosynthesis and processing as well as the genomic organization of apoC-II in normal subjects and patients with dyslipoproteinemias characterized by hypertriglyceridemia.
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PMID:Human apolipoprotein C-II: complete nucleic acid sequence of preapolipoprotein C-II. 659 4

To elucidate the mechanism by which apolipoprotein C-II (apoC-II) enhances the activity of lipoprotein lipase (LpL), discoidal phospholipid complexes were prepared with apoC-III and di[(14)C]palmitoyl phosphatidylcholine (DPPC) and containing various amounts of apoC-II. The rate of DPPC hydrolysis catalyzed by purified bovine milk LpL was determined on the isolated complexes. The rate of hydrolysis was optimal at pH 8.0. Analysis of enzyme kinetic data over a range of phospholipid concentrations revealed that the major effect of apoC-II was to increase the maximal velocity (V(max)) some 50-fold with a limited effect on the Michaelis constant (K(m)). V(max) of the apoC-III complex containing no apoC-II was 9.2 nmol/min per mg LpL vs. 482 nmol/min per mg LpL for the complex containing only apoC-II. The effect of apoC-II on enzyme kinetic parameters for LpL-catalyzed hydrolysis of DPPC complexes was compared to that on the parameters for hydrolysis of DPPC and trioleoylglycerol incorporated into guinea pig very low density lipoproteins (VLDL(p)) which lack the equivalent of human apoC-II. Tri[(3)H]oleoylglycerol-labeled VLDL(p) were obtained by perfusion of guinea pig liver with [(3)H]oleic acid. Di[(14)C]palmitoyl phosphatidylcholine was incorporated into the VLDL(p) by incubation of VLDL(p) with sonicated vesicles of di[(14)C]palmitoyl phosphatidylcholine and purified bovine liver phosphatidylcholine exchange protein. The rates of LpL-catalyzed hydrolysis of trioleoylglycerol and DPPC were determined at pH 7.4 and 8.5 in the presence and absence of apoC-II. In the presence of apoC-II, the V(max) for DPPC hydrolysis in guinea pig VLDL(p) increased at both pH 7.4 and pH 8.5 (2.4- and 3.2-fold, respectively); the value of K(m) did not change at either pH (0.23 mm). On the other hand, the kinetic value of K(m) for triacylglycerol hydrolysis in the presence of apoC-II decreased at both pH 7.4 (3.05 vs. 0.54 mm) and pH 8.5 (2.73 vs. 0.62 mm). These kinetic studies suggest that apoC-II enhances phospholipid hydrolysis by LpL in apoC-III-DPPC discoidal complexes and VLDL(p) mainly by increasing the V(max) of the enzyme for the substrates, whereas the activator protein primarily causes a decrease in the apparent K(m) for triacylglycerol hydrolysis.-Shirai, K., T. J. Fitzharris, M. Shinomiya, H. G. Muntz, J. A. K. Harmony, R. L. Jackson and D. M. Quinn. Lipoprotein lipase-catalyzed hydrolysis of phosphatidylcholine of guinea pig very low density lipoproteins and discoidal complexes of phospholipid and apolipoprotein: effect of apolipoprotein C-II on the catalytic mechanism.
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PMID:Lipoprotein lipase-catalyzed hydrolysis of phosphatidylcholine of guinea pig very low density lipoproteins and discoidal complexes of phospholipid and apolipoprotein: effect of apolipoprotein C-II on the catalytic mechanism. 668 42


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