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PubMed1981

Ascites chylomicron: a poor substrate for hepatic triglyceride lipase.

A patient with nephrotic syndrome and morbus Kimura (eosinophilic granuloma) showed chylous ascites. Ascites chylomicrons were analyzed and used to study the substrate specificity of lipoprotein lipase and hepatic triglyceride lipase. Ascites triglyceride and cholesterol concentrations were 191 and 12 mg/dl, respectively. Both apo CII and apo CIII content in ascites were approximately one-third of those of plasma from normal subjects. Ascites chylomicrons were incubated with either lipoprotein lipase or hepatic triglyceride lipase, which were prepared from postheparin plasma using heparin-Sepharose affinity chromatography. Lipoprotein lipase hydrolyzed ascites chylomicrons, while hepatic triglyceride lipase did not. These results suggest different functions of these two lipases in chylomicron catabolism.

Ascites↗
PubMed1992

Serum triglyceride and insulin levels are associated with erythrocyte sodium-lithium counter-transport activity in normoglycaemic individuals.

The relationship between erythrocyte sodium-lithium counter-transport activity, serum insulin, lipids and demographic factors was examined in 93 normoglycaemic predominantly normotensive individuals with mild fasting hypercholesterolaemia (greater than 5.2 mmol/l). The major significant univariate correlates of sodium-lithium counter-transport activity were fasting serum triglycerides, HDL cholesterol, the ratio of fasting glucose: insulin, apo A1, alcohol consumption and apo B. Stepwise multiple regression analysis revealed 24% of the variability in sodium-lithium counter-transport activity could be accounted for by independent contributions of fasting serum triglycerides, alcohol consumption, the fasting glucose/insulin ratio and apo A1 and ANOVA confirmed a significant relationship with fasting insulin measures that was independent of serum triglycerides (P less than 0.05). The relationship between erythrocyte sodium-lithium counter-transport activity and concentrations of serum triglycerides, HDL components, insulin and additionally alcohol consumption, could reflect the influence of those variables on erythrocyte structure and function.

Alcohol Drinking↗
PubMed1977

The effect of treatment with clofibrate on hepatic triglyceride and lipoprotein lipase activities of post heparin plasma in male patients with hyperlipoproteinemia.

Twelve male patients with hyperlipoproteinemia were treated with clofibrate, 1 g twice daily. Serum triglyceride concentration decreased on the average 28 +/- 6%. No significant change of serum cholesterol concentration occurred. Post heparin plasma lipoprotein lipase activity isolated and partially purified by heparin Sepharose affinity chromatography was determined quantitatively. During the clofibrate treatment this enzyme activity increased 48 +/- 9%. The post heparin hepatic triglyceride lipase did not change significantly. The possibility that the serum triglyceride-lowering effect of clofibrate might partly be explained by an increased removal rate of triglyceride rich lipoproteins through increased lipoprotein lipase activity is discussed.

Adult↗
PubMed1978

Incorporation of labelled glucose and glycerol into phospholipids and triglycerides by rat and rabbit aorta.

[1-14C]Glycerol and [U1-14C]glucose were incorporated into aortic phospholipids and triglycerides by isolated rat and rabbit aorta. The major portion of radioactivity was found in the glycerol moiety of triglycerides and phospholipids. Within the range of concentrations studied the rate of incorporation of [1-14C]glycerol was dependent on substrate concentration, whereas the rate of incorporation of [U1-14C]glucose was not. The distribution of radioactivity in the glycerophosphatides was found mainly in phosphatidylserine and phosphatidic acid when [1-14C]glycerol was used as substrate. On the other hand, the major portion of radioactivity was found in phosphatidylcholine when [U1-14C]glucose was the substrate. The incorporation of [1-14C]glycerol and [U1-14C]glucose into aortic triglycerides and phospholipids was markedly increased by aortae obtained from rabbits fed an atherogenic diet as compared to aortae from control animals. Results from double-labeled glycerol containing both [2-3H]glycerol and [1-14C]glycerol indicated that the biosynthesis of triglycerides and phospholipids in the rat aorta did not use phosphatidic acid from the same pool.

Animals↗
PubMed1993

Composition of human low density lipoprotein: effects of postprandial triglyceride-rich lipoproteins, lipoprotein lipase, hepatic lipase and cholesteryl ester transfer protein.

A preponderance of small, dense low density lipoprotein (LDL) particles has been linked to increased risk of myocardial infarction, and a dense and protein-rich LDL has proved to be a characteristic of patients with manifest coronary heart disease (CHD). The present study focused on metabolic determinants of the LDL subfraction distribution with the emphasis placed on alimentary lipaemia. The relations of plasma levels and composition of light (1.019 < d < 1.040 kg/l) and dense (1.040 < d < 1.063 kg/l) LDL subfractions to postprandial triglyceride-rich lipoproteins (TGRL), postheparin plasma lipase activities and the activity of cholesteryl ester transfer protein (CETP) were studied in 32 men with angiographically ascertained premature coronary atherosclerosis (age 48.8 +/- 3.2 years) and in 10 age matched healthy control men. LDL subfractions were separated by equilibrium density gradient ultracentrifugation of fasting plasma drawn before participants were subjected to an oral fat tolerance test of a mixed meal type. The response of TGRL to the oral fat load was determined by measuring plasma triglycerides, and the apolipoprotein (apo) B-48 and apo B-100 content of Sf 60-400 and Sf 20-60 lipoprotein fractions. At a second visit plasma samples were taken for determination of postheparin plasma lipoprotein lipase (LPL) and hepatic lipase (HL) activities and for measurement of CETP activity. Hypertriglyceridaemic patients had a preponderance of dense LDL particles compared with normotriglyceridaemic patients and controls. The magnitude of the response of TGRL to the oral fat load showed a positive association with the dense LDL apo B concentration (r = 0.32-0.52, P < 0.05), whereas the LPL activity correlated positively with the free (r = 0.50, P < 0.001) and esterified cholesterol (r = 0.45, P < 0.01) and apo B (r = 0.42, P < 0.01) content of the light LDL fraction. The HL activity was found to be inversely associated with the plasma level of light LDL triglycerides (r = -0.38, P < 0.05). In contrast, no relations were noted between CETP activity and plasma concentrations of LDL constituents. Multiple stepwise linear regression analysis with the proportion of total LDL apo B contained in the dense LDL subfraction (% dense LDL apo B) used as the dependent variable indicated that the combined effect of LPL activity and postprandial plasma levels of TGRL (areas under the curve for plasma triglycerides or Sf 60-400 apo B-48) accounted for around 50% of the variability in the distribution of LDL particles between light and dense subfractions.(ABSTRACT TRUNCATED AT 400 WORDS)

Carrier Proteins↗
PubMed1996

Abnormal postprandial apolipoprotein B-48 and triglyceride responses in normolipidemic women with greater than 70% stenotic coronary artery disease: a case-control study.

Because remnants of triglyceride-rich lipoproteins (TRLP) are potentially atherogenic, the postprandial lipoprotein metabolism was studied in 12 normocholesterolemic, normotriglyceridemic women, aged 60 +/- 2 years, with angiographically proven coronary artery disease (CAD+; cholesterol 5.7 +/- 0.1 (S.E.) mmol/l, triglyceride 1.35 +/- 0.10 mmol/l) and in 12 individually matched controls, aged 59 +/- 2 years, without angiographical abnormalities (CAD-; cholesterol 5.1 +/- 0.2 mmol/l and triglyceride 1.16 +/- 0.13 mmol/l). Following an oral retinyl palmitate-fat load, the CAD+ women showed a significantly higher triglyceride response in the chylomicron, or Sf > 1000, fraction (P < 0.05 vs. controls). Total plasma apolipoprotein (apo) B and retinyl palmitate concentrations were similar in both groups. Fasting apo B-48 levels in the d < 1.006 g/ml fraction were significantly higher in CAD+ cases (0.25 +/- 0.03 integrated optical density (iod) units) than CAD- controls (0.15 +/- 0.03; P < 0.05). Furthermore, after the fat load, a greater absolute and incremental apo B-48 response in the intermediate density lipoprotein (IDL) fraction (d = 1.006-1.019 g/ml) was observed in CAD+ cases (incremental area under the curve (Delta-AUC)8: 0.40 +/- 0.12 h.iod) than CAD- controls (0.01 +/- 0.06 h.iod; P = 0.01). Post-heparin hepatic lipase (HL) activities were higher in the CAD+ group: 422 +/- 22 mU/l vs 288 +/- 20 mU/ml in the CAD- group (P < 0.001) while lipoprotein lipase (LPL) activities were identical. The results provide evidence that the metabolism of intestinal TRLP is significantly different in normolipidemic women with angiographically proven CAD compared with individually matched controls without coronary disease. Fasting apo B-48 levels in d< 1.006 g/ml fractions represent a potentially useful marker in women at risk for CAD.

Analysis of Variance↗
PubMed1982

Spouse concordance of plasma cholesterol and triglyceride.

Spouse concordance for plasma cholesterol and triglyceride was studied in 1971 spouse pairs including 545 spouse pairs married 40 or more years. Both lipids showed modest but statistically significant age corrected Kendall Tau-B correlations; 0.046 (P = 0.005) for cholesterol and 0.070 (P = 0.0001) for triglycerides. Concordance was not explained by season of sampling or by selective mortality. Relative weight was positively correlated in spouse pairs and appeared to explain much of the observed correlations in cholesterol and triglycerides. Spouse pairs also showed positive correlations for cigarette smoking and egg and milk consumption, though these behavioral variables explained little of the concordance for cholesterol and triglycerides. Lipid concordance was highest in marriages of the shortest (1-9 yr) and longest (40 + yr) durations, as was relative weight concordance, suggesting an interaction between duration of marriage and environmental and/or selective factors affecting plasma lipids.

Animals↗
PubMed1995

Oral administration of homocysteine leads to increased plasma triglycerides and homocysteic acid-additional mechanisms in homocysteine induced endothelial damage?

Increased plasma homocyst(e)ine is strongly correlated with occlusive arterial diseases. A series of different hypotheses have been reported including involvement of free oxygen radicals and therefore oxidative stress. We determined plasma homocyst(e)ine and homocysteic acid levels after oral low dose homocysteine thiolactone administration to rats for a period of six weeks. Plasma levels of homocyst(e)ine and triglycerides were significantly elevated in the group fed homocysteine thiolactone. GC/MS determination of ketone body formation showed that the underlying mechanism for the increase of triglycerides seems to be inhibition of fatty acid oxidation. Homocysteic acid was detected in the experimental group exclusively. The present study showing a homocyst(e)ine correlated increase of plasma triglycerides by the inhibition of fatty acid oxidation may well propose an additional role of triglycerides for vascular pathology. The presence of homocysteic acid in the experimental group only would support the free oxygen radical hypothesis for the development of vascular changes but homocysteic acid as a potent neurotransmitter could play an independent role in the pathogenesis.

Administration, Oral↗
PubMed1977

Effect of clofibrate on postheparin plasma triglyceride lipase activities in patients with hypertriglyceridemia.

The lipoprotein lipase (LPL) and hepatic triglyceride lipase (HL) activities of postheparin plasma were determined by a specific immunochemical method in 17 patients with primary hyperlipoproteinemia before and during treatment with clofibrate. The drug caused a significant reduction of serum cholesterol (11%) and triglyceride (45%) levels. Postheparin plasma LPL activity rose in all subjects, the average change being 46% (p less than 0.001). The increase of LPL was positively correlated to the pretreatment LPL activity. There was no correlation between the serum triglyceride concentration and postheparin LPL activity either before or during clofibrate administration. On the other hand, in the clofibrate responders there was a weak correlation between the relative changes of triglyceride concentration and LPL activity (r = 0.43, p less than 0.05). During clofibrate treatment the LPL activity of the hypertriglyceridemic patients was significantly higher than the corresponding value of untreated healthy normoglyceridemic subjects of similar age. The postheparin plasma HL activity was not influenced by clofibrate.

Adult↗
PubMed1979

Serum cholesterol and triglycerides in children with growth hormone deficiency.

To test the hypothesis that hyperlipidemia is characteristic of growth hormone deficiency in childhood, we have measured serum cholesterol and triglyceride concentrations in 24 euthyroid children with growth hormone deficiency. Although modest elevations of cholesterol and/or triglyceride above the 95th percentile for age, race, and sex were present in 46% of the children studied, the mean (+/- 1 SD) cholesterol of 173 +/- 36 mg/dl and the mean triglyceride of 80 +/- 42 mg/dl were not significantly different from published normal mean values. Administration of human growth hormone for 4 mo to 15 of these subjects did not alter these mean cholesterol and triglyceride values, but did result in a marked improvement in the growth rate. Some individuals (n = 6) with a subnormal growth response to therapy and/or a low serum thyroxine and high serum cholesterol were treated for an additional 4 mo with growth hormone and thyroid hormone together. There was a statistically significant decrement in serum cholesterol in this group. We conclude that modest hyperlipidemia does exist in some children with growth hormone deficiency. Subclinical hypothyroidism may play a role in the hypercholesterolemia of some children, as may growth hormone deficiency itself. Any association of growth hormone and lipid metabolism remains to be clarified.

Adolescent↗
PubMed1982

Studies on the possible function of beta 2-glycoprotein-I: influence in the triglyceride metabolism in the rat.

Seven rats were infused with 14C-labeled Intralipid at a constant rate of 0.38 ml per hour over a time period of 4 hours. Four rats served as controls and received an infusion of 0.15 M NaCl or of serum albumin two hours after the start of the experiment. In these animals the plasma triglyceride concentration rose linearly from 30 to 240 min and paralleled the total blood radioactivity. The triglyceride concentrations at the end of the experiments were about 25 times as high as at the beginning. Three rats receiving 2 hr after the start an additional infusion of beta 2-glycoprotein-I at a rate of 10 mg per hr showed a markedly enhanced triglyceride removal from the plasma, reaching a steady state which lasted for more than 30 min. It is concluded that beta 2-glycoprotein-I affects the triglyceride clearance under these experimental conditions.

Animals↗
PubMed1984

Lipid and lipoprotein triglyceride and cholesterol interrelationships: effects of sex, hormone use, and hyperlipidemia.

The interrelationships of lipid and lipoprotein cholesterol and triglyceride concentrations in normolipidemic and hyperlipidemic employees of the Pacific Northwest Bell Telephone Company were examined bivariately using correlation analysis and multivariately by factor analysis. Application of the latter resulted in the identification of three distinct lipoprotein lipid clusters, which succinctly describes their metabolic relationships. Among normolipidemic subjects, the interrelationships were found to be similar in male and female subjects, but hormone use by women considerably altered interrelationships that involved high-density lipoprotein cholesterol (HDL-C) and triglyceride. Among hyperlipidemic subjects, we found that elevation in cholesterol level alone rarely altered relationships, but elevation in triglyceride level either alone or in conjunction with an elevation in cholesterol concentration was associated with substantial changes in relationships involving the low-density lipoprotein (LDL) fraction. In many instances, positive relationships between LDL cholesterol (LDL-C) and other lipoprotein lipids became inverse in the presence of triglyceride elevation. We conclude that hormone use by women and hypertriglyceridemia with or without an elevation in cholesterol level clearly alter lipoprotein relationships, whereas pure hypercholesterolemia does not. These alterations provide a basis for investigating pathophysiologic mechanisms in hypertriglyceridemia.

Adult↗
PubMed1990

Effect of triiodothyronine on triglyceride synthesis in human fibroblasts in different types of hypertriglyceridemia.

Fibroblasts from 12 normotriglyceridemic subjects and 30 hypertriglyceridemic patients and family members were used to investigate triglyceride synthesis and the influence of triiodothyronine on it. The monolayers were incubated for 72 hours with and without the thyroid hormone, followed by incorporation studies of radiolabeled acetic acid or palmitic acid into the cellular triglyceride fraction. Triiodothyronine had no influence on triglyceride synthesis of normal cell lines and of cells derived from patients with secondary hypertriglyceridemia, whereas fibroblasts from endogenous type IV patients showed higher rates of triglyceride synthesis under identical conditions. Values for type IV were in the range of 134% to 466% of the hormone-free control incubations. In cultures derived from patients with familial combined hyperlipidemia, no stimulation by triiodothyronine was observed: values were in the range of 64% to 144% of the hormone-free controls. Three out of four lines with type V gave "normal" values and are supposed to represent secondary hypertriglyceridemia, whereas one line may express endogenous type IV. The evidence obtained in vitro with cultured cells indicates different metabolic defects in endogenous type IV and familial combined hyperlipidemia; it also shows the biochemically heterogenous nature of the disease "hypertriglyceridemia."

Acetates↗
PubMed1991

Tumor necrosis factor-alpha, interleukin-1, and interferon alpha stimulate triglyceride synthesis in HepG2 cells.

Tumor necrosis factor-alpha (TNF-alpha), interleukin-1 (IL-1), and interferon alpha (IFN-alpha) stimulate hepatic lipogenesis in vivo. We now show that TNF-alpha, IL-1, and IFN-alpha stimulate lipogenesis as measured by the incorporation of 3H-glycerol into triglyceride in cultured HepG2 cells. Incubation of HepG2 cells for approximately 24 hours with TNF or IL-1 was required to see stimulation of lipogenesis, with this effect increasing over the next four days. TNF stimulated lipogenesis by 2.4-fold after 72 hours of incubation, while a 3.5-fold stimulation was seen with IL-1. The half maximal concentration for TNF stimulation of hepatic lipogenesis was 4 ng/mL, while that for IL-1 was 0.3 ng/mL. Cells treated with TNF or IL-1 also showed increased secretion of labeled triglyceride into the media. IFN-alpha stimulated the incorporation of 3H-glycerol into triglyceride by 39% after 72 hour's incubation. In contrast, IFN-gamma had no effect on lipogenesis in HepG2 cells. These data suggest that cytokines can directly stimulate the synthesis of triglycerides in cultured Hep G2 liver cells in vitro.

Carcinoma, Hepatocellular↗
PubMed1984

Increased plasma and aortic triglycerides in rabbits after acute administration of 2,3,7,8-tetrachlorodibenzo-p-dioxin.

Administration of a single nonlethal dose (20 micrograms/kg) of 2,3,7,8-tetrachlorodibenzo-p-dioxin to New Zealand male rabbits, both on a standard and on a cholesterol (0.5% in the diet) regimen, resulted in a significant increase of plasma triglyceride levels. Triglycerides were particularly raised in the very low-density lipoprotein fraction; no significant apolipoprotein changes, as assessed by an analytical isoelectrofocusing procedure, could be determined. Concomitant to the increased triglyceridemia, aortic triglycerides were also significantly elevated in 2,3,7,8-tetrachlorodibenzo-p-dioxin-pretreated rabbits, both on the standard and on the cholesterolemic regimen. These findings suggest that 2,3,7,8-tetrachlorodibenzo-p-dioxin, possibly by inhibiting triglyceride breakdown, may induce an atherogenic form of hypertriglyceridemia in a standard experimental model of atherosclerosis.

Animals↗
PubMed1991

Phospholipase C mediated inhibition of factor VII requires triglyceride-rich lipoproteins.

The reduction of plasma factor VII (FVII) activity by phospholipase C (PLC), in vitro, has been proposed as a possible indication of a risk of cardiovascular disease. The ability of PLC to reduce FVII activity was found to require calcium ions and the presence of triglyceride-rich lipoproteins (e.g. chylomicra and very-low density lipoproteins) rather than high or low density lipoproteins. The PLC-mediated reduction of FVII activity was prevented by pre-incubation of PLC with chylomicra, before adding FVII, and this suggests that PLC may act on triglyceride-rich lipoproteins already bound to FVII in order to reduce FVII activity. At optimal PLC concentration, the extent of the reduction in FVII activity was proportional to the concentration of chylomicra. The detergent, Tween, prevented any loss of FVII activity, in both plasma and purified systems, if it was present at the beginning of the incubation with PLC. Addition of Tween, but not EDTA, after inhibition of FVII activity had occurred, caused a partial restoration of FVII activity. It is concluded that PLC reduces FVII activity by modifying triglyceride-rich lipoproteins to a form which binds to FVII, independently of calcium ions, and which inhibits procoagulant activity. The detection of PLC-sensitive procoagulant activity. The detection of PLC-sensitive FVII activity may therefore have no greater significance than the measurement of plasma triglyceride levels in predicting a risk of cardiovascular disease.

Calcium Chloride↗
PubMed1991

Gemfibrozil predictably lowers triglycerides but does not significantly change plasminogen activator inhibitor activity in hypertriglyceridemic patients with a history of thrombosis.

Impaired fibrinolysis due to high plasminogen activator inhibitor levels is present in patients with a variety of thrombotic diseases. Plasminogen activator inhibitor levels correlate with triglyceride levels and are elevated in patients with hypertriglyceridemia. Treatment of asymptomatic hypertriglyceridemic patients with diet or medication results in improvement of fibrinolytic parameters. To determine if similar improvements in fibrinolysis occur during treatment of hypertriglyceridemia in patients with a history of venous thrombosis and impaired fibrinolysis due to high plasminogen activator inhibitor levels, 5 patients were given gemfibrozil. Triglyceride levels and fibrinolytic response to venous occlusion were determined before and after 30 days of treatment. Gemfibrozil therapy resulted in a predictable decrease in triglyceride levels in all patients, a reduction that was statistically significant (p = 0.04). There was no significant change in fibrinolytic variables during gemfibrozil therapy. Independent factors appear to control the plasminogen activator inhibitor and triglyceride levels in patients with a history of venous thrombosis.

Cholesterol↗
PubMed1995

Antithrombotic activity of a symmetrical triglyceride with eicosapentaenoic acid and gamma-linolenic acid in guinea pig mesenteric microvasculature.

The antithrombotic effect of a synthetic symmetrical triglyceride having eicosapentaenoic acid (EPA) at positions 1 and 3, and gamma-linolenic acid (GLA) at position 2 was investigated. Administration of the triglyceride significantly increased thrombus formation time and thrombotic occlusion time induced by light irradiation and a fluorescent dye in guinea pigs after 14 days administration compared to that of soybean oil. The antithrombotic effect of the triglyceride was similar to that of EPA ethyl ester. Administration of the triglyceride increased GLA, dihomo-gamma-linolenic acid (DGLA) and EPA contents in plasma and the liver, and the ratio of DGLA to arachidonic acid. These results might be responsible for this antithrombotic effect.

8,11,14-Eicosatrienoic Acid↗