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)

The effect of dietary supplementation of vitamin E on serum cholsterol, triglycerides, lipoproteins and lipoprotein composition was studied in rabbits fed a one per cent cholesterol diet for a period of twelve weeks. Vitamin E supplemented animals were found to maintain significantly lower concentrations of serum cholesterol, triglycerides and very low density lipoproteins (d less than 1.006). The difference in the serum lipid content was mainly in the very low density lipoproteins of d less than 1.006. The possibility of an increased clearance of chylomicron remnants and decreased inhibition of extrahepatic lipoprotein lipase in hypercholesterolemic rabbits as a result of vitamin E supplementation is discussed in the light of the results obtained.
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PMID:Effect of dietary supplementation of vitamin E on serum lipids and lipoproteins in rabbits fed a cholesterolemic diet. 23 11

Albumin carries fatty acids and has also been suggested to act as an antioxidant. In the present work, polyunsaturated fatty acids (linoleic, arachidonic, eicosapentaenoic and docosahexaenoic acids)--but not palmitic and oleic acid--inhibited growth of human hepatoma cells in low albumin concentration (0.5%). Growth inhibition by polyunsaturated fatty acids was prevented by albumin in a dose-related manner in the range 0.7-5.0%. Albumin also protected against growth inhibition following catabolism (by lipoprotein lipase) of very low density lipoproteins. Vitamin E strongly counteracted the inhibitory effect of polyunsaturated fatty acids. Vitamin E and albumin appeared to have additive effects in protecting against growth inhibition by polyunsaturated fatty acids. Indomethacin did not greatly modify the polyunsaturated fatty acids effect. Growth inhibition by polyunsaturated fatty acids, as well as the level of thiobarbituric acid reacting substances (a measure of lipid peroxidation) in growth media, increased with increasing number of fatty acids double bonds. Vitamin E and albumin prevented both thiobarbituric acid reacting substances formation and growth inhibition by polyunsaturated fatty acids. The results suggest that the concentrations of albumin and vitamin E in the incubation medium are essential when studying polyunsaturated fatty acids effects on cell growth.
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PMID:Growth inhibition of human hepatoma cells (HepG2) by polyunsaturated fatty acids. Protection by albumin and vitamin E. 131 55

Vitamin E uptake by Caco-2 cells, a human intestinal cell line, was studied by incubating the cells with alpha-tocopherol/triglyceride emulsions with or without bile activated lipase or lipoprotein lipase. During a 1-h incubation, vitamin E was transferred to Caco-2 cells only in the presence of triglyceride hydrolysis by bile activated lipase and not by lipoprotein lipase. Incubation with either lipase resulted in hydrolysis of approximately 20% of the medium [3H]-triolein to free fatty acids and a 3-5-fold increase in cellular radioactivity. In the absence of lipases but the presence of taurocholate, addition of oleic acid in an amount equal to the molar concentration of triglyceride (5.7 mM) to triglyceride emulsions containing either alpha-tocopherol or cholesteryl ester resulted in an increase in cellular [3H]-triglyceride and alpha-tocopherol or cholesteryl ester. We suggest that the absorption of hydrophobic molecules such as vitamin E may occur in the presence of bile and amphipathic lipids via the uptake of micellar neutral lipids by the intestine.
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PMID:Vitamin E uptake by human intestinal cells during lipolysis in vitro. 229 2

High vitamin E supplementation in the diets of streptozocin-induced diabetic rats eliminates accumulation of lipid peroxides in the plasma and the liver, returns the plasma triglycerides toward normal levels, and increases the activity of lipoprotein lipase. Vitamin E has no effect on the levels of insulin or glucose. These findings suggest that vitamin E increases the total hepatic triglyceride lipase activity by increasing the lipoprotein lipase activity possibly by protecting the membrane-bound lipase against peroxidative damage.
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PMID:Triglyceride-lowering effect of dietary vitamin E in streptozocin-induced diabetic rats. Increased lipoprotein lipase activity in livers of diabetic rats fed high dietary vitamin E. 351 38

Vitamin E is the term used for eight naturally occurring fat-soluble nutrients. Alpha-tocopherol predominates in many species and has the highest biological activity. Vitamin E is absorbed via the lymphatic pathway and transported in association with CM. Vitamin E is carried in plasma by lipoproteins. It is secreted by the liver in nascent VLDL with a preferential incorporation of alpha-tocopherol. Most of the plasma vitamin E is in LDL and in HDL. Vitamin E is exchanged readily between lipoproteins: tocopherol in HDL readily transfers to apolipoprotein B-containing lipoproteins (VLDL, LDL), with little return of tocopherol from the apolipoprotein B-containing lipoproteins to HDL. The mechanisms of tissue uptake of vitamin E from the lipoproteins is poorly understood. This uptake may occur during catabolism of triacylglycerol-rich lipoproteins by the activity of lipoprotein lipase, via the LDL receptor or by nonreceptor-mediated uptake. Vitamin E may act to prevent the initiation/progression of spontaneous atherosclerosis. This concept is based on in-vitro data: vitamin E influences the responses of cells (vascular endothelial cells, leukocytes, vascular smooth muscle cells) and the modification of lipoproteins (especially LDL) which, at least in principle, could contribute to the initiation/progression of spontaneous atherosclerosis. In vivo studies are clearly required to establish the extent and mode of vitamin E's antiatherosclerotic impact and, hence, its therapeutic potential.
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PMID:[Vitamin E: metabolism and role in atherosclerosis]. 784 Apr 27

We have found that in rats the peroxide content of chylomicrons (CM) is determined by the lipid peroxide concentration in the diet, indicating that dietary lipid peroxides are incorporated into the lymph CM. Moreover, these incorporated lipid peroxides influence the normal CM metabolism. When radiolabeled CM were injected into rats, there was no difference in the initial plasma removal between CM prepared from oil with low peroxide content (control CM) and CM prepared from oil with high peroxide content (oxidized CM). However, the tissue distribution of the labels indicated that the hepatic uptake of CM decreased with increasing lipid peroxide content of CM. At 10 min after injection of CM, liver uptake of cholesterol label was 48.39 +/- 3.08% for control CM and 31.41 +/- 10.73% for oxidized CM. Vitamin E enrichment of control CM increased their hepatic uptake to 61.07 +/- 0.83%. Additionally, binding of oxidized CM to the heart endothelium increased from 2.55 to 3.60% compared with binding of control CM. When the hydrolysis of control and oxidized CM by endothelial lipoprotein lipase (LPL) was tested in a heart perfusion system, we found that after 30 min, 56.51 +/- 5.81% of control and 76.82 +/- 1.75% of oxidized CM were not hydrolyzed and remained in the perfusate. Thus our results indicate that the altered metabolism of oxidized CM may be related to a reduced hydrolysis rate by endothelial LPL.
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PMID:Effect of dietary lipid peroxides on metabolism of serum chylomicrons in rats. 846 Jul 7

A method for vitamin E (alpha-tocopherol) measurement in rat adipose tissue and mammary gland has been developed and validated. Tissues were homogenized in ethanol-water (1:1) and extracted with n-hexane. Vitamin K1 was used as internal standard. Separation was performed by HPLC with methanol-water (96.5:3.5) as eluent in a Nucleosil C18 column (15 x 0.46 cm) at 40 degrees C. Detection was by fluorescence with excitation at 295 nm and emission at 350 nm for vitamin E and at 330 and 440 nm for vitamin K1. Standards and tissue extracts were checked for linearity giving correlation coefficients over 0.99 in a range of concentrations from 0.56 to 4.51 nmol/g in adipose tissue and from 2.18 to 17.4 nmol/g in mammary gland tissue. Intra-assay precision (R.S.D.) varied between 3 and 4%, whereas inter-assay precision was between 8 and 9%. Recoveries ranged between 95 +/- 3% and 98 +/- 11% for the two tissues, respectively. Vitamin E was measured in rats that had previously received one oral dose of this vitamin. Whereas vitamin E content in adipose tissue did not differ between late-pregnant and virgin rats, it was significantly higher in mammary gland of pregnant rats, and this difference could be related to the enhanced lipoprotein lipase activity in this group.
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PMID:Simplified method for vitamin E determination in rat adipose tissue and mammary glands by high-performance liquid chromatography. 981 22

Natural vitamin E includes four tocopherols and four tocotrienols. RRR-alpha-tocopherol is the most abundant form in nature and has the highest biological activity. Although vitamin E is the main lipid-soluble antioxidant in the body, not all its properties can be assigned to this action. As antioxidant, vitamin E acts in cell membranes where prevents the propagation of free radical reactions, although it has been also shown to have pro-oxidant activity. Non-radical oxidation products are formed by the reaction between alpha-tocopheryl radical and other free radicals, which are conjugated to glucuronic acid and excreted through the bile or urine. Vitamin E is transported in plasma lipoproteins. After its intestinal absorption vitamin E is packaged into chylomicrons, which along the lymphatic pathway are secreted into the systemic circulation. By the action of lipoprotein lipase (LPL), part of the tocopherols transported in chylomicrons are taken up by extrahepatic tissues, and the remnant chylomicrons transport the remaining tocopherols to the liver. Here, by the action of the "alpha-tocopherol transfer protein", a major proportion of alpha-tocopherol is incorporated into nascent very low density lipoproteins (VLDL), whereas the excess of alpha-tocopherol plus the other forms of vitamin E are excreted in bile. Once secreted into the circulation, VLDL are converted into IDL and LDL by the action of LPL, and the excess of surface components, including alpha-tocopherol, are transferred to HDL. Besides the LPL action, the delivery of alpha-tocopherol to tissues takes place by the uptake of lipoproteins by different tissues throughout their corresponding receptors. Although we have already a substantial information on the action, effects and metabolism of vitamin E, there are still several questions open. The most intriguing is its interaction with other antioxidants that may explain how foods containing small amounts of vitamin E provide greater benefits than larger doses of vitamin E alone.
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PMID:Vitamin E: action, metabolism and perspectives. 1151 85

Natural vitamin E includes four tocopherols and four tocotrienols. RRR-alpha-tocopherol is the most abundant form in nature and has the highest biological activity. Although vitamin E is the main lipid-soluble antioxidant in the body, not all its properties can be assigned to this action. As antioxidant, vitamin E acts in cell membranes where prevents the propagation of free radical reactions, although it has been also shown to have pro-oxidant activity. Non-radical oxidation products are formed by the reaction between alpha-tocopheryl radical and other free radicals, which are conjugated to glucuronic acid and excreted through the bile or urine. Vitamin E is transported in plasma lipoproteins. After its intestinal absorption vitamin E is packaged into chylomicrons, which along the lymphatic pathway are secreted into the systemic circulation. By the action of lipoprotein lipase (LPL), part of the tocopherols transported in chylomicrons are taken up by extrahepatic tissues, and the remnant chylomicrons transport the remaining tocopherols to the liver. Here, by the action of the "alpha-tocopherol transfer protein", a major proportion of alpha-tocopherol is incorporated into nascent very low density lipoproteins (VLDL), whereas the excess of alpha-tocopherol plus the other forms of vitamin E are excreted in bile. Once secreted into the circulation, VLDL are converted into IDL and LDL by the action of LPL, and the excess of surface components, including alpha-tocopherol, are transferred to HDL. Besides the LPL action, the delivery of alpha-tocopherol to tissues takes place by the uptake of lipoproteins by different tissues throughout their corresponding receptors. Although we have already a substantial information on the action, effects and metabolism of vitamin E, there are still several questions open. The most intriguing is its interaction with other antioxidants that may explain how foods containing small amounts of vitamin E provide greater benefits than larger doses of vitamin E alone.
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PMID:Vitamin E: action, metabolism and perspectives. 1157 97

The aim of this experiment was to clarify the contribution of the alpha-tocopherol transfer activity of lipoprotein lipase (LPL) to vitamin E transport to tissues in vivo. We studied the effect of Triton WR1339, which prevents the catabolism of triacylglycerol-rich lipoproteins by LPL on vitamin E distribution in rats. Vitamin E-deficient rats fed a vitamin E-free diet for 4 wk were injected with Triton WR1339 and administered by oral gavage an emulsion containing 10 mg of alpha-tocopherol, 10 mg of gamma-tocopherol, or 29.5 mg of a tocotrienol mixture with 200 mg of sodium taurocholate, 200 mg of triolein, and 50 mg of albumin. alpha-Tocopherol was detected in the serum and other tissues of the vitamin E-deficient rats, but gamma-tocopherol, alpha- and gamma-tocotrienol were not detected. Triton WR1339 injection elevated (P<0.05) the serum alpha-tocopherol concentration and inhibited (P<0.05) the elevation of alpha-tocopherol concentration in the liver, adrenal gland, and spleen due to the oral administration of alpha-tocopherol. Neither alpha-tocopherol administration nor Triton WR1339 injection affected (P>or=0.05) the alpha-tocopherol concentration in the perirenal adipose tissue, epididymal fat, and soleus muscle despite a high expression of LPL in the adipose tissue and muscle. These data show that alpha-tocopherol transfer activity of LPL in adipose tissue and muscle is not important for alpha-tocopherol transport to the tissue after alpha-tocopherol intake or that the amount transferred is small relative to the tissue concentration. Furthermore, Triton WR1339 injection tended to elevate the serum gamma-tocopherol (P=0.071) and alpha-tocotrienol (P=0.053) concentrations and lowered them (P<0.05) in the liver and adrenal gland of rats administered gamma-tocopherol or alpha-tocotrienol. These data suggest that lipolysis of triacylglycerol-rich chylomicron by LPL is necessary for postprandial vitamin E transport to the liver and subsequent transport to the other tissues.
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PMID:Triton WR1339, an inhibitor of lipoprotein lipase, decreases vitamin E concentration in some tissues of rats by inhibiting its transport to liver. 1723 9


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