Dihomo-γ-Linolenic Acid in Patients with Atherosclerosis: Effects on Platelet Aggregation, Plasma Lipids and Low-Density Lipoprotein-Induced Inhibition of Prostacyclin Generation

1985 ◽  
Vol 54 (04) ◽  
pp. 901-901
Author(s):  
D P Mikhailidis ◽  
M A Barradas ◽  
P Dandona
Keyword(s):  
Platelet Aggregation ◽  
Linolenic Acid ◽  
Plasma Lipids ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density

Dihomo-γ-Linolenic Acid in Patients with Atherosclerosis: Effects on Platelet Aggregation, Plasma Lipids and Low-Density Lipoprotein-Induced Inhibition of Prostacyclin Generation

1984 ◽  
Vol 51 (02) ◽  
pp. 186-188 ◽  
Author(s):  
A Szczeklik ◽  
R J Gryglewski ◽  
K Sladek ◽  
E Kostka-Trąbka ◽  
A Żmuda
Keyword(s):  
Linolenic Acid ◽  
Plasma Lipids ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Thromboxane A2 ◽  
Low Density ◽  
Red Cell ◽  
Double Blind ◽  
Daily Dose ◽  
Antithrombotic Effects

SummaryDihomo-γ-linolenic acid (DHLA), a precursor of monoenoic anti-aggregatory prostaglandins (PGE1, PGD2), was administered for 4 weeks in a daily dose of 1.0 g into 33 patients with atherosclerosis on a basis of a double-blind trial. Comparison of treatment and placebo groups revealed elevation of DHLA in red cell lipids in DHLA-treated subjects. No differences, however, between the two groups could be observed in platelet aggregability, thromboxane A2 generation by platelets, serum cholesterol, PGE1 and PGE2 levels, and in inhibitory activity of low-density lipoproteins against prostacyclin synthetizing system in arteries. The dietary supplementation used did not lead to distinct antithrombotic effects.

scholarly journals Omega-3 fatty acid supplementation in primary nephrotic syndrome: effects on plasma lipids and coagulopathy.

1992 ◽  
Vol 3 (6) ◽  
pp. 1321-1329
Author(s):  
A V Hall ◽  
A Parbtani ◽  
W F Clark ◽  
E Spanner ◽  
M W Huff ◽  
...  
Keyword(s):  
Nephrotic Syndrome ◽  
Platelet Aggregation ◽  
Fish Oil ◽  
Bleeding Time ◽  
Plasma Lipids ◽  
Low Density Lipoprotein ◽  
Urine Volume ◽  
Density Lipoprotein ◽  
Low Density ◽  
Before And After

The effect of fish oil dietary supplementation on the dyslipidemia and coagulopathy of seven patients with nephrotic syndrome and hypoalbuminemia due to primary kidney disease was studied. Plasma lipids, platelet aggregation studies, simplate bleeding time, and fibrinogen levels were determined before and after 6 wk of treatment with fish oil (15 g/day of MaxEPA; 2.7 g of eicosapentenoic acid (EPA) and 1.8 g of docosahexenoic acid. Urea kinetics were determined from urine-urea concentration, urinary proteina, and urine volume. A 3-day dietary intake record was obtained from each patient before and after 6 wk of fish oil supplementation. There was no significant dietary change in protein, fat, or carbohydrate intake over the time period of the study. At study end, total triglycerides decreased from 2.98 +/- 1.31 to 2.18 +/- 1.14 mmol/L (P = 0.002), and very low-density lipoprotein-triglycerides decreased from 2.35 +/- 1.34 to 1.28 +/- 1.07 mmol/L (P = 0.01). Low-density lipoprotein (LDL) cholesterol increased from 5.18 +/- 1.74 to 7.35 +/- 2.83 mmol/L (P = 0.005). No significant changes occurred in bleeding time, platelet count, hematocrit, red blood cell flexibility, or whole blood viscosity. Platelet aggregation responses to collagen and arachidonic acid were consistently reduced after treatment, but there was no change in platelet response to ADP. The platelet membrane phospolipids showed a significantly increased incorporation of EPA after the fish oil diet (P = 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)

Platelet Aggregation and Plasma Lipoproteins in Alcoholics During Alcohol Withdrawal

1986 ◽  
Vol 55 (02) ◽  
pp. 173-177 ◽  
Author(s):  
K Desai ◽  
J S Owen ◽  
D T Wilson ◽  
R A Hutton
Keyword(s):  
Platelet Aggregation ◽  
Alcohol Withdrawal ◽  
Ldl Cholesterol ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Hdl Cholesterol ◽  
Plasma Lipoprotein ◽  
Cholesterol Concentration ◽  
Arachidonic Acid Content ◽  
Low Density

SummaryPlatelet aggregation, platelet lipid composition and plasma lipoprotein concentrations were measured each week in a group of seventeen alcoholics, without overt liver disease, for one month, following acute, total alcohol withdrawal. The platelets were initially hypoaggregable but, within 1-2 weeks of cessation of drinking, they became hyperaggregable and then gradually returned towards normal values. Hyperaggregability could not be explained by increases in either the cholesterol or the arachidonic acid content of the platelets. Plasma very-low-density lipoprotein cholesterol levels remained high throughout the study, but the initially raised levels of high-density lipoprotein (HDL) cholesterol fell by 26%. Low-density lipoprotein (LDL) cholesterol concentration rose by 10% after two weeks of withdrawal but then returned to about the starting level. The resulting changes in the plasma LDL-cholesterol: HDL-cholesterol ratio, which had increased by more than 50% after two weeks of abstinence, essentially paralleled the time course of enhanced platelet reactivity in all but four of the alcoholics. These findings suggest that alterations in plasma lipoprotein concentrations during acute alcohol withdrawal may be a contributory factor to the haemostatic disorders present in such patients.

scholarly journals Modulation of hepatic apolipoprotein B, 3-hydroxy-3-methylglutaryl-CoA reductase and low-density lipoprotein receptor mRNA and plasma lipoprotein concentrations by defined dietary fats. Comparison of trimyristin, tripalmitin, tristearin and triolein

1995 ◽  
Vol 311 (1) ◽  
pp. 167-173 ◽  
Author(s):  
A J Bennett ◽  
M A Billett ◽  
A M Salter ◽  
E H Mangiapane ◽  
J S Bruce ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Plasma Lipids ◽  
Low Density Lipoprotein ◽  
Lipoprotein Metabolism ◽  
Density Lipoprotein ◽  
Dietary Fats ◽  
Low Density ◽  
Mrna Levels ◽  
Expression Of Genes ◽  
Coa Reductase

Different dietary fatty acids exert specific effects on plasma lipids but the mechanism by which this occurs is unknown. Hamsters were fed on low-cholesterol diets containing triacylglycerols enriched in specific saturated fatty acids, and effects on plasma lipids and the expression of genes involved in hepatic lipoprotein metabolism were measured. Trimyristin and tripalmitin caused significant rises in low-density lipoprotein (LDL) cholesterol which were accompanied by significant reductions in hepatic LDL receptor mRNA levels. Tripalmitin also increased hepatic expression of the apolipoprotein B gene, implying an increased production of LDL via very-low-density lipoprotein (VLDL) and decreased removal of LDL in animals fed this fat. Hepatic levels of 3-hydroxy-3-methylglutaryl-CoA reductase mRNA did not vary significantly between the groups. Compared with triolein, tristearin had little effect on hepatic gene expression or total plasma cholesterol. However, it caused a marked decrease in VLDL cholesterol and a rise in LDL cholesterol such that overall it appeared to be neutral. Lipid analysis suggested a rapid desaturation of much of the dietary stearate. The differential changes in plasma lipids and hepatic mRNA levels induced by specific dietary fats suggests a role for fatty acids or a metabolite thereof in the regulation of the expression of genes involved in lipoprotein metabolism.

Changes in plasma lipids and low-density lipoprotein peak particle size during and after acute myocardial infarction

2002 ◽  
Vol 89 (4) ◽  
pp. 460-462 ◽  
Author(s):  
Carlo M Barbagallo ◽  
Manfredi Rizzo ◽  
Angelo B Cefalù ◽  
Davide Noto ◽  
Antonio Scimeca ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Particle Size ◽  
Plasma Lipids ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density

scholarly journals An essential role for lysophosphatidylcholine in the inhibition of platelet aggregation by secretory phospholipase A2

Blood ◽  
1995 ◽  
Vol 86 (11) ◽  
pp. 4166-4174 ◽  
Author(s):  
Y Yuan ◽  
SP Jackson ◽  
HH Newnham ◽  
CA Mitchell ◽  
HH Salem
Keyword(s):  
Platelet Aggregation ◽  
Phospholipase A2 ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Plasma Lipoproteins ◽  
Ionophore A23187 ◽  
Low Density ◽  
Secretory Phospholipase A2 ◽  
Secretory Phospholipase ◽  
Inhibition Of Platelet Aggregation

The release of secretory phospholipase A2 (sPLA2) into the mammalian circulation may contribute to the development of hemorrhagic and inflammatory diseases. sPLA2 has previously been shown to alter the behavior of platelets, leukocytes, and endothelial cells, although the molecular basis for these cellular effects has not been established. Our studies indicate that the inhibition of platelet aggregation by snake, bee venom, and pancreatic sPLA2 is dependent on a plasma cofactor. This cofactor resides within the lipoprotein fraction of plasma, with 54%, 31%, and 11% of the activity present in the high- density lipoprotein (HDL), low-density lipoprotein (LDL), and very low density lipoprotein (VLDL) fractions, respectively. Delipidation of HDL and LDL was associated with the complete loss of platelet-inhibitory activity. Incubation of purified sPLA2 with the HDL fraction of plasma resulted in the time-dependent generation of lysophosphatidylcholine (lysoPC). The formation of lysoPC correlated with the inhibition of platelet aggregation. Purified lysoPC (10 to 100 micrograms/mL) inhibited platelet aggregation and dense granule release induced by thrombin (0.05 U/mL), collagen (1 micrograms/mL), ionophore A23187 (2 mumol/L), ADP (12.5 mumol/L), and adrenaline (3.2 mumol/L). The inhibition of platelet aggregation by lysoPC was dose-dependent and correlated with decreased fibrinogen binding to glycoprotein IIb-IIIa. Our studies indicate that the enzymatic generation of lysoPC from plasma lipoproteins is essential for the sPLA2-mediated inhibition of platelet activation in the presence of albumin. These results raise the possibility that the toxic effects of circulating sPLA2 may be due in part to the generation of the bioactive lysophospholipid, lysoPC.

Effect of aging and obesity on the expression of dyslipidaemia in children from families with familial combined hyperlipidaemia

2006 ◽  
Vol 112 (2) ◽  
pp. 131-139 ◽  
Author(s):  
Ewoud ter Avest ◽  
Allan D. Sniderman ◽  
Sebastian J. H. Bredie ◽  
Albert Wiegman ◽  
Anton F. H. Stalenhoef ◽  
...  
Keyword(s):  
Plasma Lipids ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Indirect Evidence ◽  
Low Density ◽  
Tissue Mass ◽  
Adipose Tissue Mass ◽  
And Gender ◽  
Genetically Determined

The aim of the present study was to delineate the mechanism(s) responsible for the increased secretion of VLDL (very-low-density lipoprotein) particles in patients with FCH (familial combined hyperlipidaemia). In 194 young adults (<25 years of age) recruited from families with FCH, we investigated how plasma lipids, (apo)lipoproteins and BMI (body mass index) varied with age. Furthermore, we performed a 5-year follow-up study of clinical and biochemical characteristics of a subset of this population (n=85) stratified by apoB (apolipoprotein B) levels (below or above the 75th percentile adjusted for age and gender). Plasma apoB concentration (r=0.45, P<0.0001), triacylglycerol (triglyceride) concentration (r=0.45, P<0.0001), LDL (low-density lipoprotein) subfraction profile (r=−0.46, P<0.0001) and BMI (r=0.51, P<0.0001) were significantly associated with age. Plasma apoB concentration in the hyperapoB group was already elevated at a young age, whereas other characteristics of FCH, as observed in adults, including triacylglycerol levels >1.5 mmol/l and/or small-dense LDL, were observed only sporadically. After the 5-year follow-up, BMI increased in both groups, and this increase was associated with changes in apoB (r=0.27, P<0.05), triacylglycerol (r=0.30, P<0.01), VLDL cholesterol (r=0.22, P<0.05), VLDL triacylglycerol (r=0.25, P<0.05) and high-density lipoprotein cholesterol (r=−0.27, P<0.05). In conclusion, we have found indirect evidence of a primary, presumably genetically determined, increase in plasma apoB concentration occurring early in life of offspring from families with FCH. However, aging-related post-maturation increases in adipose tissue mass also appear to contribute to an aggravation and/or modulation of this genetically determined apoB overproduction.

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