Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.1.34 (lipoprotein lipase)
 7,025 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The R219K polymorphism in the ATP-binding cassette transporter 1 gene ( ABCA1) has been associated with reduced severity of atherosclerosis, fewer coronary events, decreased triglycerides and a trend to increased HDL in men with coronary heart disease (CHD). This study examined the frequency and the effect on CHD and plasma lipids of the polymorphism in patients of both sexes attending a lipid out-patient clinic. The overall frequency of the K allele was 0.26. It was lower in patients with CHD (0.21) than in those without (0.27) but this was not statistically significant. Amongst patients with elevated Lp(a) the frequency of the K allele was significantly lower in those with CHD (0.16) than in those without (0.29). There were no statistically significant differences in total cholesterol, LDL, HDL, apoB or apoAI between carriers and non-carriers. When patients with probable secondary hypertriglyceridaemia (triglycerides >1000 mg/dl), type 2 diabetes and carriers of lipoprotein lipase polymorphisms associated with hypertriglyceridaemia were excluded, the K allele was significantly associated with reduced triglycerides but only in patients with apoE 3/3 genotype. In conclusion, we provide additional evidence that the R219K polymorphism in the ABCA1 gene either directly or as a result of linkage disequilibrium with additional functional variant(s), has a protective effect against CHD and is associated with lower plasma triglycerides in sub-groups of patients with hyperlipidaemia.
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PMID:The association of the R219K polymorphism in the ATP-binding cassette transporter 1 ( ABCA1) gene with coronary heart disease and hyperlipidaemia. 1270 Aug 93

Patients with nephrotic syndrome (NS) have one of the most pronounced secondary changes in lipoprotein metabolism known, and the magnitude of the changes correlates with the severity of the disease. These changes are of a quantitative as well as a qualitative nature. All apolipoprotein B (apo B)-containing lipoproteins, such as very-low-density lipoproteins (VLDL), intermediate-density lipoproteins (IDL), low-density lipoproteins (LDL), and lipoprotein(a) [Lp(a)], are elevated in nephrotic syndrome. High-density lipoproteins (HDL) are reported to be unchanged or reduced. In addition to these quantitative changes, the lipoprotein composition is markedly changed, with a higher ratio of cholesterol to triglycerides in the apo B-containing lipoproteins and an increase in the proportion of cholesterol, cholesterol ester, and phospholipids compared with proteins. Also apolipoproteins show major changes, with an increase in apolipoprotein A-I, A-IV, B, C, and E. Particularly the changes in apo C-II, which is an activator of the enzyme lipoprotein lipase (LPL), and apo C-III, an inhibitor of LPL, with an increase of the C-III to C-II ratio, might contribute to the impaired lipoprotein catabolism in NS. The mechanisms for these changes in lipoprotein metabolism are discussed in this review as far as they are known. Furthermore, the tremendous elevations of Lp(a) in nephrotic syndrome and its primary and secondary causes are reviewed. Primary causes became recently apparent by a significantly higher frequency of low-molecular-weight apo(a) phenotypes in patients compared with controls. The secondary causes were shown by an increase of Lp(a) in all apo(a) isoform groups. Because Lp(a) is an LDL-like particle that is usually included in the measured or calculated LDL cholesterol fraction, the influence of the extremely high Lp(a) levels in NS on the measurement of LDL cholesterol is discussed.
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PMID:Dyslipidemia and nephrotic syndrome: recent advances. 1582 92

Very low-density lipoprotein (VLDL) receptor is a member of the low-density lipoprotein (LDL) receptor family. It binds triglyceride rich lipoprotein (TGRL) but not LDL, because it recognizes apolipoprotein (apo)E only but not apoB. The VLDL receptor functions as a peripheral lipoprotein receptor in concert with lipoprotein lipase (LPL) in heart, muscle, adipose tissue and macrophages. In contrast to the LDL receptor, VLDL receptor binds apo E2/2 VLDL and apoE3/3 VLDL particles, and its expression is not down-regulated by intracellular lipoproteins. It has been reported that both LDL-cholesterol (LDL-C) and postprandial triglyceride (chyromicron and VLDL remnants) are risk factors for human atherosclerotic cardiovascular disease (ASCVD). True ligands such as lipoprotein particles of the VLDL receptor are chyromicron remnant (CMR) and VLDL remnant (postprandial hyperlipidemia). Although the oxidized LDL (oxLDL)-scavenger receptors pathway is considered to be the main mechanism for macrophage foam cell formation, it seems that the TGRL-LPL-VLDL receptor pathway is also involved. Since Lp(a) is one of the ligands for the VLDL receptor, the Lp(a)-VLDL receptor pathway is another potential alternative. The expression of VLDL receptor protein in mouse macrophages is modest compared to that in rabbit and human macrophages, both in vitro and in vivo. Therefore, we need to elucidate the mechanism of human ASCVD not by using the mouse model and scavenger receptors pathway but instead using the rabbit model and VLDL receptor pathway, respectively.
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PMID:Triglyceride Rich Lipoprotein -LPL-VLDL Receptor and Lp(a)-VLDL Receptor Pathways for Macrophage Foam Cell Formation. 2842 82


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