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

---

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

The effects of lipolysis of human plasma very low density lipoprotein (VLDL) on the structure and composition of high density lipoproteins (HDL) have been investigated. Lipolysis was performed in a controlled system in vitro containing VLDL (d less than 1.006 g/ml) and HDL3 (d = 1.125-1.210 g/ml) from human plasma and lipoprotein lipase (EC 3.1.1.34) purified from bovine milk. Lipolysis of VLDL caused profound changes in HDL3. Protein, phospholipid, and cholesterol liberated from VLDL during its lipolysis were transferred to the HDL3 particles. As a consequence of this in vitro transfer, the chemical composition and biophysical properties of HDL3 were substantially altered. The newly formed particles exhibited a flotation rate (F01.20) of 6.7 and a hydrated density of 1.110 g/ml. The chemical composition closely resembled that of native HDL2, and their size was slightly larger than that of the precursor HDL3. When HDL3 and postlipolysis HDL2 were subjected to ultracentrifugation under flotation velocity and equilibrium conditions, both proved to be stable particles. These results, when extrapolated to in vivo conditions, suggest an important metabolic relationship between the levels of circulating VLDL and HDL2 in plasma. This relationship now permits a reasonable explanation for numerous in vivo observations in which the levels of VLDL and HDL2 change reciprocally.
...
PMID:Formation of high density lipoprotein2-like particles during lipolysis of very low density lipoproteins in vitro. 21 57

The human plasma high density lipoproteins (HDL) are a heterogeneous ensemble of five proteins associated with both neutral and polar lipids. The sequence of all five proteins are known. ApoA-I and apoA-II are the major protein components; apoC-I, apoC-II and apoC-III are the minor protein components. All these apoproteins spontaneously recombine with phospholipids to give stable lipid-protein complexes and freely exchange between the two major HDL subclasses, HDL2 and HDL3. In addition, ApoC-I, apoC-II, and apoC-III exchange between HDL and very low density lipoproteins. Furthermore, certain HDL apoproteins are activators for plasma enzymes that are important in lipid metabolism. ApoA-I and apoC-I activate lecithin/cholesterol acyltransferase; apoC-II is an activator of lipoprotein lipase. The regions of apoC-I and apoC-II that are involved in the activation of these enzymes have been localized with synthetic peptides. Studies of synthetic and native fragments of apoA-II, apoC-I, apoC-II, and apoC-III as well as model lipid-binding peptides have identified specific regions with structural features common to lipid-binding proteins. These special properties, which include helical potential, sequences with a critical amphipathic length, and high hydrophobicity of the nonpolar side of the amphipathic helix, are the determinants of HDL structure and metabolism.
...
PMID:A review of the unique features of HDL apoproteins. 22 Apr 93

The preheparin and postheparin lipoprotein lipids (cholesterol C and triacylglycerols TAG) were related to the serum insulin and to the postheparin plasma activities of lipoprotein lipase (LPL) and hepatic lipase (HL) in normolipemic human. The positive correlation, although not statistically significant, of insulin level of the LPL activity was found, while no correlation to the HL activity was seen. Under preheparin conditions: 1) both insulin level and LPL activity were negatively related to the VLDL-C/TAG ratio indicating an enrichment of VLDL with TAG, 2) moreover, the LPL activity was positively related to the HDL-C and HDL3-C, 3) the HL activity predominated in relation to the HDL, and particularly to the HDL3, as indicated by negative correlations to the both lipids and to the lipid/apoA-I ratios of HDL and HDL3. This lipid depletion of HDL3 was more expressive due to the TAG, while HDL2 appeared to be relatively enriched with TAG, as suggested by correlations of C/TAG ratios with HL activity. The in vivo acceleration of lipoprotein metabolism by heparin resulted in: 1) the reduction of VLDL-TAG and HDL2-TAG, and in the increase of HDL3-TAG, 2) the appearance of positive relation of HDL2-C to the LPL activity and of opposite relation to the HL activity, 3) the lack of HL correlation to the TAG of HDL and HDL3. Even under these conditions no relation of insulin level to any HDL lipid was revealed. The results suggest that in normal human the HL affects more considerably than LPL the lipid metabolism of HDL subfractions and it does not seem to be under insulin control.
...
PMID:The preheparin and postheparin lipids of high density lipoprotein subfractions: relation to the serum insulin and postheparin plasma lipase activities in normal human. 136 70

To explore the interactions of triacylglycerol and phospholipid hydrolysis in lipoprotein conversions and remodeling, we compared the activities of lipoprotein and hepatic lipases on human VLDL, IDL, LDL, and HDL2. Triacylglycerol and phospholipid hydrolysis by each enzyme were measured concomitantly in each lipoprotein class by measuring hydrolysis of [14C]triolein and [3H]dipalmitoylphosphatidylcholine incorporated into each lipoprotein by lipid transfer processes. Hepatic lipase was 2-3 times more efficient than lipoprotein lipase at hydrolyzing phospholipid both in absolute terms and in relation to triacylglycerol hydrolysis in all lipoproteins. The relationship between phospholipid hydrolysis and triacylglycerol hydrolysis was generally linear until half of particle triacylglycerol was hydrolyzed. For either enzyme acting on a single lipoprotein fraction, the degree of phosphohydrolysis closely correlated with triacylglycerol hydrolysis and was largely independent of the kinetics of hydrolysis, suggesting that triacylglycerol removed from a lipoprotein core is an important determinant of phospholipid removal via hydrolysis by the lipase. Phospholipid hydrolysis relative to triacylglycerol hydrolysis was most efficient in VLDL followed in descending order by IDL, HDL, and LDL. Even with hepatic lipase, phospholipid hydrolysis could not deplete VLDL and IDL of sufficient phospholipid molecules to account for the loss of surface phospholipid that accompanies triacylglycerol hydrolysis and decreasing core volume as LDL is formed (or for conversion of HDL2 to HDL3). Thus, shedding of whole phospholipid molecules, presumably in liposomal-like particles, must be a major mechanism for losing excess surface lipid as large lipoprotein particles are converted to smaller particles. Also, this shedding phenomenon, like phospholipid hydrolysis, is closely related to the hydrolysis of lipoprotein triacylglycerol.
...
PMID:Triacylglycerol and phospholipid hydrolysis in human plasma lipoproteins: role of lipoprotein and hepatic lipase. 139 Jun 40

Correction of cardiovascular risk factors is of particular significance in a high-risk population, such as that of diabetic patients. This paper reports the effects of one-month administration of 400 mg/day Bezafibrate (BZF), followed by a two-month wash-out and one-month administration of 500 mg/day Acipimox (APX) or vice versa in a random order in 16 Type 2 diabetic patients with diet-resistant hyperlipidaemia and in good metabolic control (HbA1c less than 8%), on plasma fibrinogen and on their lipid pattern. Metabolic control displayed a nonsignificant improvement (HbA1c) during both treatments (stable body weight). Both BZF and APX produced a 14% decrease in total CHOL (p less than 0.01), whereas BZF was more effective in reducing triglycerides (tg) (-37% vs -15%). The marked BZF-induced Tg reduction was associated with a proportional decrease in Apo B, while an increase in total HDL-, HDL2 and HDL3-CHOL, together with a significant increase in Apo AI, was observed. APX treatment resulted in a HDL2-CHOL increase only (+29%). Both drugs reduced VLDL-CHOL (BZF -37%; APX -15%) and VLDL-Tg (-56% and -34%). In BZF treated patients Apo CIII fell indicating a possible reduction of specific inhibition of lipoprotein lipase activity, while APX affected both Apo CII (+23%) and Apo CIII (-26%) and led to a 62% Apo CII/CIII ratio increase. BZF alone led to a significant 25% decrease in plasma fibrinogen (from 415 +/- 14.3 to 312.1 +/- 18.1 SEM mg/dl, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Comparison of the effects of bezafibrate and acipimox on the lipid pattern and plasma fibrinogen in hyperlipidaemic type 2 (non-insulin-dependent) diabetic patients. 139 77

Lipoprotein lipase enhances binding at 4 degrees C of human plasma lipoproteins (chylomicrons, VLDL, intermediate density lipoprotein, LDL, and HDL3) to cultured fibroblasts and hepG-2 cells and to extracellular matrix. Heparinase treatment of cells and matrix reduces the lipoprotein lipase enhanced binding by 90-95%. Lipoprotein lipase causes only a minimal effect on the binding of lipoproteins to heparan sulfate deficient mutant Chinese hamster ovary cells while it promotes binding to wild type cells that is abolished after heparinase treatment. With 125I-LDL, lipoprotein lipase also enhances uptake and proteolytic degradation at 37 degrees C by normal human skin fibroblasts but has no effect in heparinase-treated normal cells or in LDL receptor-negative fibroblasts. These observations prove that lipoprotein lipase causes, predominantly, binding of lipoproteins to heparan sulfate at cell surfaces and in extracellular matrix rather than to receptors. This interaction brings the lipoproteins into close proximity with cell surfaces and may promote metabolic events that occur at the cell surface, including facilitated transfer to cellular receptors.
...
PMID:Lipoprotein lipase enhances binding of lipoproteins to heparan sulfate on cell surfaces and extracellular matrix. 143 Feb 23

We measured lipoproteins, apolipoproteins, lipoprotein lipase (LPL), hepatic triglyceride lipase (HTGL), lecithin: cholesterol acyltransferase (LCAT) and parameters of calcium metabolism to evaluate the roles of these enzymes and hypertriglyceridemia for impaired high-density lipoprotein (HDL) metabolism in chronic renal failure, and to examine the impact of altered calcium homeostasis on the lipoprotein-regulating enzymes. The subjects were 25 healthy volunteers and 66 uremic patients, 24 treated with hemodialysis (HD) and 42 with continuous ambulatory peritoneal dialysis (CAPD). Lipoprotein analysis revealed: (1) reduction in HDL cholesterol especially in HDL2 subfraction; (2) increase in HDL triglyceride; and (3) decreased ratio of HDL2 cholesterol to HDL3 cholesterol in both HD and CAPD patients. Simple regression analysis showed: (1) a positive correlation between VLDL triglyceride and triglyceride/cholesterol ratio of HDL; (2) positive correlations of LPL level in post-heparin plasma to cholesterol concentrations in HDL2, HDL3 and total HDL, and to apolipoproteins A-I and A-II; and (3) inverse correlations of HTGL to HDL2 cholesterol and to the ratio of HDL2 cholesterol/HDL3 cholesterol. Multiple regression analysis of HDL cholesterol indicated positive association with LPL and inverse correlation with VLDL triglyceride. Four variables including LPL, HTGL, LCAT and VLDL triglyceride explained 51.5% of the variation of HDL cholesterol. HDL2 cholesterol was associated positively with LPL and negatively with VLDL triglyceride in the model. HDL3 cholesterol was associated positively with LPL, HTGL and LCAT and inversely with VLDL triglyceride. Stepwise multiple regression analysis indicated that independent predictors of HTGL were gender, parathyroid hormone levels by a mid-portion assay, ionized calcium and age, and that those of LCAT were ionized calcium and age.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Impaired metabolism of high density lipoprotein in uremic patients. 150 22

A comprehensive assessment of lipoprotein compositional/metabolic response to incremental caloric ethanol (EtOH) doses ranging from low to moderate to high was undertaken using male squirrel monkeys. Control monkeys were maintained on a chemically defined, isocaloric liquid diet, while experimental primates wee fed increasing doses of alcohol (6, 12, 18, 24, 30, and 36% of energy) substituted isocalorically for carbohydrate at 3-month intervals. Liver function tests and plasma triglyceride were normal for all animals. Plasma cholesterol showed a transient increase at the 12% caloric dose that was attributed solely to an increase in high density lipoprotein (HDL). A more pronounced increase in plasma sterol, beginning at 24% and continuing to 36% EtOH, was the result of increments in both HDL and low density lipoprotein (LDL) cholesterol, although the contribution by the latter was substantial primarily at the 36% dose. Plasma apolipoprotein elevations (HDL apolipoprotein A-I, LDL apolipoprotein B) generally accompanied the lipoprotein lipid increases, although the first atherogenic response for LDL became manifest as a significant increase in apolipoprotein B at 18% EtOH calories. Postheparin plasma lipoprotein lipase was not affected by dietary alcohol, whereas hepatic triglyceride lipase activity showed significant increases at higher (24 and 36%) EtOH doses. Plasma lecithin-cholesterol acyltransferase activity was normal at the 6 and 12% EtOH doses, but exhibited a significant reduction beginning at 18% and continuing to 36% EtOH. Alterations in these key lipoprotein regulatory enzymes may represent the underlying metabolic basis for the observed changes in lipoprotein levels and our earlier findings of HDL2/HDL3 subfraction modifications. Results from our study indicate that in squirrel monkeys, moderate (12%) EtOH caloric intake favors an antiatherogenic lipoprotein profile (increases HDL, normal LDL levels, and lecithin-cholesterol acyltransferase activity), whereas higher doses (24-36%) produce both coronary-protective (increases HDL) and atherogenic (increases LDL) responses. Moreover, the 18% EtOH level represents an important transition dose which signals early adverse alterations in lipoprotein composition (increases apolipoprotein B) and metabolism (decreases lecithin-cholesterol acyltransferase).
...
PMID:Alcohol produces dose-dependent antiatherogenic and atherogenic plasma lipoprotein responses. 157 Mar 59

Numerous studies have shown that a high accumulation of abdominal fat is associated with metabolic complications and with an increased risk of coronary heart disease. The present study examined the effects of changes in body fatness and in the level of abdominal fat on metabolic variables in a sample of 13 obese premenopausal women, aged 38.8 +/- 5.3 (SD) yr. Women exercised for 90 min at approximately 55% of maximal aerobic power (VO2 max) four to five times a week for a period of 14 mo. The training program induced a significant increase in VO2 max and a mean reduction in body fat mass of 4.6 kg (P less than 0.01), with no change in fat-free mass. Measurement of adipose tissue areas by computed tomography indicated a greater loss of abdominal fat compared with midthigh adipose tissue (P less than 0.05). The training program also produced significant reductions in the insulinogenic index measured during an oral glucose tolerance test and in plasma cholesterol (Chol), low-density lipoprotein (LDL)-Chol, and apolipoprotein (apo) B levels (P less than 0.05). Training also significantly increased plasma high-density lipoprotein (HDL)-apo A-I and HDL2-Chol levels and decreased plasma HDL3-Chol concentration (P less than 0.05). Whereas no change in postheparin plasma lipoprotein lipase activity was noted, a significant decrease in postheparin plasma hepatic triglyceride lipase activity was observed after training (P less than 0.005). Metabolic responses were not correlated with changes in VO2 max but were significantly correlated with the reduction in body fat mass and/or with the loss of deep abdominal fat.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Loss of abdominal fat and metabolic response to exercise training in obese women. 187 79

Considering the long-term effects of the commonly used antihypertensive agents, there appear to be no apparent adverse effects with calcium antagonists and angiotensin converting enzyme (ACE) inhibitors. The literature available concerning the effects of thiazide diuretics and beta-blockers is extensive and rather confusing. In the case of thiazide diuretics, a review of the literature indicates that in the short-term (therapy for less than six months) thiazide diuretics induce a rise in total cholesterol, total triglycerides and low density lipoprotein (LDL) cholesterol, with a possible fall in high density lipoprotein (HDL). If this was translated into long-term effects it could be associated with an increased risk of atherosclerotic disease. However, the long-term effects (therapy for more than six months) are unclear. Several large-scale trials of antihypertensive therapy using diuretics have suggested that the use of diuretics may have reduced the rate of decline of cholesterol levels which would otherwise have occurred. The literature on the effects of beta-blockers on blood lipids and lipoproteins is extensive and conflicting. The most consistent finding is a rise in triglycerides and there is some evidence that this may be due to the inhibition of lipoprotein lipase. Some authors have found an associated fall in total HDL cholesterol. However, analysis of the effects on the main HDL subfractions (HDL2 and HDL3) show an increase in HDL2 and a decrease in HDL3, which may counteract the possibly detrimental reduction in total HDL. Since triglyceride levels have only weak relationship to atherosclerotic risk it seems unlikely that beta-blockers significantly increase this risk.
...
PMID:Long-term effects of antihypertensives on blood lipids. 197 62


1 2 3 4 5 6 7 8 9 10 Next >>

---