Chitosan Adsorbents Carrying Amino Acids for Selective Removal of Low Density Lipoprotein

2004 ◽  
Vol 32 (2) ◽  
pp. 303-313 ◽  
Author(s):  
Guoqi Fu ◽  
Haofeng Yu ◽  
Zhi Yuan ◽  
Bin Liu ◽  
Bin Shen ◽  
...  
Keyword(s):  
Amino Acids ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Selective Removal ◽  
Low Density

scholarly journals SP414A NOVEL ADSORBENTS FOR SELECTIVE REMOVAL OF LOW DENSITY LIPOPROTEIN

2016 ◽  
Vol 31 (suppl_1) ◽  
pp. i229-i229
Author(s):  
Liu Qiang ◽  
Sun Si ◽  
Yang Tingting ◽  
Han Mei ◽  
Lin Liping ◽  
...  
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Selective Removal ◽  
Low Density

Th-P15:138 Effects of amino acids on the rate of oxidation of low density lipoprotein by iron at PH 4.5

2006 ◽  
Vol 7 (3) ◽  
pp. 523
Author(s):  
L. Satchell ◽  
A. Islam ◽  
M. Hamed ◽  
J. Sharp ◽  
I.S. McCue ◽  
...  
Keyword(s):  
Amino Acids ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density

scholarly journals Acute effects of ethanol on the perfused rat liver. Studies on lipid and carbohydrate metabolism, substrate cycling and perfusate amino acids

1979 ◽  
Vol 184 (1) ◽  
pp. 97-106 ◽  
Author(s):  
David L. Topping ◽  
Dallas G. Clark ◽  
Gerald B. Storer ◽  
Rodney P. Trimble ◽  
Richard J. Illman
Keyword(s):  
Amino Acids ◽  
Carbohydrate Metabolism ◽  
Ketone Bodies ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Fold Increase ◽  
Very Low Density Lipoprotein ◽  
Low Density ◽  
Ethanol Infusion ◽  
Glucose Output

1. Livers from fed rats were perfused in situ with whole rat blood containing glucose labelled uniformly with 14C and specifically with 3H at positions 2, 3 or 6. 2. When ethanol was infused at a concentration of 24μmol/ml of blood the rate of utilization was 2.8μmol/min per g of liver. 3. Ethanol infusion raised perfusate glucose concentrations and caused a 2.5-fold increase in hepatic glucose output. 4. Final blood lactate concentrations were decreased in ethanol-infused livers, but the mean uptake of lactate from erythrocyte glycolysis was unaffected. 5. Production of ketone bodies (3‐hydroxybutyrate+3‐oxobutyrate) and the ratio [3‐hydroxybutyrate]/[3‐oxobutyrate] were raised by ethanol. 6. Formation of 3H2O from specifically 3H-labelled glucoses increased in the order [6-3H]<[3-3H]<[2-3H]. Production of 3H2O from [2-3H]glucose was significantly greater than that from [3-3H]glucose in both control and ethanol-infused livers. Ethanol significantly decreased 3H2O formation from all [3H]glucoses. 7. Liver glycogen content was unaffected by ethanol infusion. 8. Production of very-low-density lipoprotein triacylglycerols was inhibited by ethanol and there was a small increase in liver triacylglycerols. Very-low-density-lipoprotein secretion was negatively correlated with the ratio [3‐hydroxybutyrate]/[3‐oxobutyrate]. Perfusate fatty acid concentrations and molar composition were unaffected by perfusion with ethanol. 9. Ethanol decreased the incorporation of [U-14C]glucose into fatty acids and cholesterol. 10. The concentration of total plasma amino acids was unchanged by ethanol, but the concentrations of alanine and glycine were decreased and ([glutamate]+[glutamine]) was raised. 11. It is proposed that the observed effects of ethanol on carbohydrate metabolism are due to an increased conversion of lactate into glucose, possibly by inhibition of pyruvate dehydrogenase. The increase in gluconeogenesis is accompanied by diminished substrate cycling at glucose–glucose 6-phosphate and at fructose 6-phosphate–fructose 1,6-bisphosphate.

scholarly journals The Trypanosoma cruzi neuraminidase contains sequences similar to bacterial neuraminidases, YWTD repeats of the low density lipoprotein receptor, and type III modules of fibronectin.

1991 ◽  
Vol 174 (1) ◽  
pp. 179-191 ◽  
Author(s):  
M E Pereira ◽  
J S Mejia ◽  
E Ortega-Barria ◽  
D Matzilevich ◽  
R P Prioli
Keyword(s):  
Amino Acids ◽  
Trypanosoma Cruzi ◽  
Low Density Lipoprotein ◽  
Ldl Receptor ◽  
Density Lipoprotein ◽  
Full Length ◽  
Host Cells ◽  
Structure Characteristic ◽  
Low Density ◽  
Type Iii

Trypanosoma cruzi expresses a developmentally regulated neuraminidase (TCNA) implicated in parasite invasion of cells. We isolated full-length DNA clones encoding TCNA. Sequence analysis demonstrated an open reading frame coding for a polypeptide of 1,162 amino acids. In the N-terminus there is a cysteine-rich domain containing a stretch of 332 amino acids nearly 30% identical to the Clostridium perfringens neuraminidase, three repeat motifs highly conserved in bacterial and viral neuraminidases, and two segments with similarity to the YWTD repeats found in the low density lipoprotein (LDL) receptor and in other vertebrate and invertebrate proteins. This domain is connected by a structure characteristic of type III modules of fibronectin to a long terminal repeat (LTR) consisting of 44 full length copies of twelve amino acids rich (75%) in serine, threonine, and proline. LTR is unusual in that it contains at least 117 potential phosphorylation sites. At the extreme C-terminus is a hydrophobic segment of 35 amino acids, which could mediate anchorage of TCNA to membranes via a glycosylphosphatidylinositol linkage. This is the first time a protozoan protein has been found to contain a YWTD repeat and a fibronectin type III module. The domain structure of TCNA suggests that the enzyme may have functions additional to its catalytic activity such as in protein-protein interaction, which could play a role in T. cruzi binding to host cells.

scholarly journals Metabolomic consequences of genetic inhibition of PCSK9 compared with statin treatment

2018 ◽  
Author(s):  
Eeva Sliz ◽  
Johannes Kettunen ◽  
Michael V Holmes ◽  
Clare Oliver-Williams ◽  
Charles Boachie ◽  
...  
Keyword(s):  
Amino Acids ◽  
Statin Therapy ◽  
Lipid Composition ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Statin Treatment ◽  
Metabolic Effects ◽  
Lipid Lowering ◽  
Low Density ◽  
Pcsk9 Inhibitors

ABSTRACTBackgroundBoth statins and PCSK9 inhibitors lower blood low-density lipoprotein cholesterol (LDL-C) levels to reduce risk of cardiovascular events. To assess potential differences between metabolic effects of these two lipid-lowering therapies, we performed detailed lipid and metabolite profiling of a large randomized statin trial, and compared the results with the effects of genetic inhibition of PCSK9, acting as a naturally occurring trial.Methods228 circulating metabolic measures were quantified by nuclear magnetic resonance spectroscopy, including lipoprotein subclass concentrations and their lipid composition, fatty acids, and amino acids, for 5,359 individuals (2,659 on treatment) in the PROspective Study of Pravastatin in the Elderly at Risk (PROSPER) trial at 6-months post-randomization. The corresponding metabolic measures were analyzed in eight population cohorts (N=72,185) using PCSK9 rs11591147 as an unconfounded proxy to mimic the therapeutic effects of PCSK9 inhibitors.ResultsScaled to an equivalent lowering of LDL-C, the effects of genetic inhibition of PCSK9 on 228 metabolic markers were generally consistent with those of statin therapy (R2=0.88). Alterations in lipoprotein lipid composition and fatty acid balance were similar. However, discrepancies were observed for very-low-density lipoprotein (VLDL) lipid measures. For instance, genetic inhibition of PCSK9 showed weaker effects on lowering of VLDL-cholesterol compared with statin therapy (54% vs. 77% reduction, relative to the lowering effect on LDL-C; P=2 × 10−7 for heterogeneity). Genetic inhibition of PCSK9 showed no robust effects on amino acids, ketones, and a marker of inflammation (GlycA); in contrast, statin treatment lowered GlycA levels.ConclusionsGenetic inhibition of PCSK9 results in similar metabolic effects as statin therapy across a detailed lipid and metabolite profile. However, for the same lowering of LDL-C, PCSK9 inhibitors are predicted to be less efficacious than statins at lowering VLDL lipids, which could potentially translate into subtle differences in cardiovascular risk reduction.

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