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PubMed1986

Is the level of serum triglyceride a significant predictor of coronary death in "normocholesterolemic" subjects? The Paris Prospective Study.

Since the relation between serum triglyceride level and coronary heart disease after adjustment for cholesterol and other risk factors remains controversial, the authors have tested the hypothesis that it could be different according to the level of serum cholesterol, i.e., that there may be an interaction between cholesterol and triglyceride level in prediction of coronary heart disease risk. The data of the Paris Prospective Study were used to carry out a survival analysis, by using the Cox model, with coronary heart disease death as the end point and triglyceride and different risk factors as the predictor variables. In this study, during a mean follow-up of 11.4 +/- 2.2 years, 157 coronary heart disease deaths occurred. Serum triglyceride level is not an independent predictor of coronary heart disease death after adjustment for serum cholesterol. However, when cholesterol, triglyceride, and their interaction term are introduced in the regression equation, all variables contribute significantly to the risk. This is also true when other risk factors are taken into account. As a consequence of this interaction, among the 3,585 subjects with a serum cholesterol level lower than 220 mg/100 ml, serum triglyceride level is an independent predictor of risk, even after adjustment for all other risk factors.

Adult↗
PubMed1992

The relation of high density lipoprotein cholesterol and its subfractions to apolipoprotein A-I and fasting triglycerides: the role of environmental factors. The Atherosclerosis Risk in Communities (ARIC) Study.

Cross-sectional analysis of four general representative populations of middle-aged adults in the United States in 1986-1989 provides estimates of the close relation of high density lipoprotein cholesterol (HDL cholesterol) to its major structural apolipoprotein (apolipoprotein A-I) and to fasting plasma triglyceride levels. HDL cholesterol differences of approximately 0.4 mg were associated with 1-mg differences in apolipoprotein A-I; differences of 20% in HDL cholesterol (reductions) were associated with triglyceride doublings. Variation in apolipoprotein A-I and triglyceride concentration together accounted for 66% of the population variance in HDL cholesterol. The uniformity of this pattern in the four race-sex groups studied suggests an important role of triglyceride-cholesterol transfer as a determinant of HDL cholesterol. The fundamental relations observed among HDL cholesterol, apolipoprotein A-I, and triglycerides were unaltered by levels of factors under personal volition. The volitional factors appeared to influence HDL cholesterol indirectly: Obesity and physical activity were affected primarily through their associations with triglycerides, and alcohol use and smoking through associations with apolipoprotein A-I. The association of alcohol use with elevated HDL cholesterol was attenuated in persons with greater body mass.

Aged↗
PubMed1990

The intraindividual variability of fasting triglyceride--a challenge for further standardization.

The extraordinarily high intraindividual variability of fasting triglyceride levels often leads to substantial bias in epidemiologic studies and hinders the use of the former as potential markers of coronary heart disease risk in individual patients. The magnitude of the latter problem is illustrated applying the concept of the intraclass correlation coefficient to repeated fasting triglyceride measurements in 2227 white men aged 20 to 69 in the Lipid Research Clinics Prevalence Study. A one-way random effects analysis of variance model with the natural logarithm of triglycerides as the outcome variable is used to calculate 95% confidence intervals for a person's 'true' or 'steady-state' triglyceride level, depending on the number and results of measurements taken. For example, a 95% confidence interval corresponding to a single triglyceride measurement of 200 mg dl-1 (a commonly used threshold value for hypertriglyceridaemia) would be as wide as 124 to 323 mg dl-1. Although there is a substantial gain in precision if a second triglyceride measurement is available, the confidence intervals remain very large. The gain in precision from each additional measurement becomes progressively smaller and has to be weighed against considerations of costs and inconvenience.

Adult↗
PubMed1994

Serum triglycerides and HDL cholesterol--major predictors of long-term survival after coronary surgery.

The influence of pre-operative serum lipid levels on late clinical outcome after coronary artery bypass surgery was analysed in 83 patients undergoing coronary bypass surgery for stable angina pectoris. The mean follow-up period for surviving patients was 105 +/- 33 months (range 65-133). Twenty-two patients (27%) had died during follow-up, of whom 14 had sustained a fatal myocardial infarction and four had succumbed to other cardiovascular causes. Thirty-one patients sustained 35 cardiac events, defined as either fatal or non-fatal myocardial infarction, or reoperation, or PTCA during the follow-up period. With univariate analysis, pre-operative serum levels of total cholesterol and triglycerides were significantly related to cardiac events, P < 0.05 and P < 0.05, respectively. In a Cox proportional analysis, cardiac mortality and total mortality were related to serum triglycerides and HDL cholesterol (P < 0.05 and P < 0.01 respectively). Eighty-five percent of the patients with triglycerides < 2.0 mM.l-1 survived for 10 years, while only 48% of patients with triglycerides > 2.0 mM.l-1 remained alive for that period. Figures were similar for subjects with HDL cholesterol > 1.0 mM.l-1 or HDL cholesterol < 1.0 mM.l-1, at 89 and 38%, respectively. Only 28% of the patients with the combination triglycerides > 2.0 mM.l-1 and HDL cholesterol < 1.0 mM.l-1 were alive 10 years after surgery. These data suggest that dyslipidaemia, especially the combination of high serum triglycerides and low HDL cholesterol, is an important factor influencing long-term clinical outcome after coronary bypass surgery.

Angina Pectoris↗
PubMed1976

Dietary control of triglyceride and phospholipid synthesis in rat liver slices.

1. The effect of dietary manipulation on the synthesis of triglycerides and phospholipids was investigated by determining the incorporation of labeled long-chain fatty acid or glycerol into these lipids in liver slices derived from normally fed, fasted, and fat-free refed rats. 2. Triglyceride synthesis was affected markedly by the dietary regime of the animal; the lowest rates were measured with fasted rats, and the highest ones with fat-free refed rats. 3. In contrast to triglyceride synthesis, phospholipid synthesis occured at virtually constant rates regardless of the dietary conditions. 4. Addition of large amounts of fatty acid to the incubation mixture resulted in a marked stimulation of triglyceride synthesis, whereas phospholipid synthesis was affected to a much smaller extent. 5. These results indicate that the synthesis of triglycerides and that of phospholipids are controlled independently, and that the availability of fatty acid in the cell contributes to the control of triglyceride synthesis.

Animals↗
PubMed1993

Relationship between plasma triglycerides and apolipoprotein CII in infants during the first year of life.

Plasma triglyceride and apolipoprotein CII (apo CII) levels were measured in normal full-term infants and low-birth-weight infants at birth (from umbilical cord blood at 0 weeks), as well as at 2, 3, 4, 8, 24, and 48 weeks of age, and the relationship between plasma triglyceride and apo CII levels was studied. In both full-term and low-birth-weight infants, the plasma triglyceride and apoprotein CII levels were very low at birth, but they increased rapidly thereafter in the full-term infants and somewhat more slowly in the low-birth-weight infants. Both triglyceride and apoprotein CII levels became stable from 3 weeks of age in full-term infants and from 8 weeks in low-birth-weight infants. When the logarithmic values of triglyceride and apoprotein CII levels were compared, they showed a close correlation, and slopes of regression lines were 0.62 in full-term infants aged 0-2 weeks, 1.04 in full-term infants aged 3-48 weeks, 0.56 in low-birth-weight infants aged 0-4 weeks, and 1.04 in low-birth-weight infants aged 8-48 weeks. These results suggest that there may be some differences in triglyceride transport between full-term infants aged 0-2 weeks and 3-48 weeks as well as between low-birth-weight infants aged 0-4 weeks and 8-48 weeks.

Apolipoprotein C-II↗
PubMed1989

Regulation of triglyceride mobilization in isolated hepatocytes by dibutyryl cyclic AMP and epinephrine.

Regulation of the mobilization of endogenous fatty acids from lipid droplet triglyceride was investigated in isolated hepatocytes from normal-fed rats. Mobilized fatty acid was entirely accounted for in oxidation products (CO2 plus acid-soluble products). Dibutyryl cyclic AMP (DBcAMP) stimulated the mobilization of endogenous fatty acids by over 50% although no change in free fatty acid (FFA) levels was observed. In the presence of tetradecyglycidic acid (TDGA), a specific inhibitor of mitochondrial fatty acid oxidation, DBcAMP was unable to promote endogenous fatty acid oxidation; instead, the nucleotide increased the FFA level. This effect was blocked by the lysosomal inhibitor, chloroquine, supporting the concept that a lysosomal lipase is involved in the degradation of endogenous triglyceride. These findings suggest that cyclic AMP stimulates lysosomal lipolysis by a mechanism that is independent of changes in fatty acid oxidation. Epinephrine alone slightly suppressed triglyceride mobilization. Epinephrine plus doxazosin slightly increased lipid mobilization. Epinephrine plus propranolol suppressed endogenous fatty acid oxidation to a level significantly below that induced by epinephrine plus doxazosin. These results suggest that alpha 1-adrenoceptor activation suppresses hepatic triglyceride mobilization. The weak stimulatory effects of beta-adrenoceptor activation on hepatocyte triglyceride mobilization compared with the potent stimulation by DBcAMP is probably attributable to the relatively low level of beta-adrenoceptors in hepatocytes from the mature male rats used in these studies. Further characterization of a possible mutually antagonistic interaction between alpha 1- and beta 2-adrenoceptors in the regulation of hepatic triglyceride mobilization might be better accomplished in a species with hepatocytes that have a higher proportion of beta-adrenoceptors, e.g., guinea pig, rabbit, and dog.

Adrenergic alpha-Antagonists↗
PubMed1997

Recent advances in elucidating the role of the microsomal triglyceride transfer protein in apolipoprotein B lipoprotein assembly.

The microsomal triglyceride transfer protein is necessary for the assembly and secretion of lipoproteins containing apolipoprotein B. During the past year, significant progress has been made towards understanding the role of microsomal triglyceride transfer protein in lipoprotein assembly at both a cellular and molecular level. Studies carried out in a variety of heterologous expression systems, as well as the use of microsomal triglyceride transfer protein inhibitors in hepatoma cell lines, have been critical to this progress. It has been shown that microsomal triglyceride transfer protein plays a key role in the early stages of lipoprotein assembly, most likely by transferring lipid to nascent apolipoprotein B as it enters the lumen of the endoplasmic reticulum. The evidence indicates that microsomal triglyceride transfer protein does not play a major role in addition of bulk core lipid in the late stages of apolipoprotein B48 lipoprotein assembly. Thus, microsomal triglyceride transfer protein appears to control the number of apolipoprotein B lipoprotein particles secreted but not the lipid composition.

Animals↗
PubMed2005

Effect of fenofibrate on lipoprotein(a) in hypertriglyceridemic patients: impact of change in triglyceride level and liver function.

We investigated the effect of fenofibrate on lipoprotein(a)levels in hypertriglyceridemic patients and the parameters relating to its effect. Patients with a triglyceride level >/=300 mg/dL or with a triglyceride level >/=200 mg/dL and a high density lipoprotein cholesterol level </=40 mg/dL were treated either with 200 mg of fenofibrate(Fenofibrate group, n = 56) or with general measures (Control group,n = 56). Lipid and lipoprotein levels were measured at baseline and 2 months. Baseline lipoprotein(a) levels were negatively correlated with triglyceride (r = 20.30, P = 0.001) and alanine aminotransferase levels (r = 20.24, P = 0.012). Fenofibrate therapy increased lipoprotein(a) level from 9.4 6 10.6 to 15.6 6 17.5 mg/dL (P = 0.000). The more triglyceride levels decreased, the more lipoprotein(a) levels increased in all subjects (r = 20.46, P = 0.000) and in Control (r =20.35, P = 0.008) and Fenofibrate groups (r = 20.35, P = 0.008). Fenofibrate elevated lipoprotein(a) level greater in patients with a normal liver function. When Fenofibrate group was divided into two subgroups according to the degree of percentage change in lipoprotein(a) level, change in triglyceride level and alanine aminotransferase level were independent predictors by forward logistic regression analysis. In summary, fenofibrate therapy increases lipoprotein(a) level,and this elevation is associated with change in triglyceride level and liver function.

Aged↗
PubMed2006

Assessment of intramuscular triglycerides: contribution to metabolic abnormalities.

PURPOSE OF REVIEW: The purpose of this review is to highlight recent methodological advances that have helped us to understand the role of intramuscular triglycerides in human health as well as prevention and treatment of disease. In addition to both invasive (muscle biopsy) and noninvasive methods, techniques to assess other lipids within muscle will be reviewed. RECENT FINDINGS: In addition to intramuscular triglycerides, other lipids contained within skeletal muscle such as diacylglycerol and ceramides may have an important role in human metabolic disease. Both ex-vivo and in-vivo methods to obtain serial measurements of these muscle lipids as a result of experimental perturbation have recently provided unique insight into their respective roles in human metabolism. SUMMARY: Triglyceride accumulation within skeletal muscle has received considerable interest due to its potential role in insulin resistance and fatty acid metabolism of obesity, aging and type 2 diabetes. Observations that triglycerides themselves may be used as a fuel source for exercising muscle, and thus may not be detrimental in all circumstances, has in part prompted the development and implementation of analytical methods to quantify the fatty acid composition of muscle triglycerides as well as other lipid species within muscle, e.g. diacylglycerol and ceramides. In addition, noninvasive computed tomography, magnetic resonance spectroscopy and magnetic resonance imaging methods have been applied to examine the serial effects of intervention on muscle triglycerides.

Absorptiometry, Photon↗
PubMed1994

Gemfibrozil treatment of the high triglyceride-low high-density lipoprotein cholesterol trait in men with established atherosclerosis.

OBJECTIVE: To study the short-term efficacy, tolerability and safety of the treatment with gemfibrozil 600 mg twice daily or placebo in male patients with established atherosclerosis, with a lipid profile matching the 'high triglyceride-low high-density lipoprotein (HDL) cholesterol trait'. DESIGN: Double-blind randomized placebo controlled prospective trial. SETTING: Amsterdam Lipid Research Clinic at the Academic Medical Centre of the University of Amsterdam and the Slotervaart Training Hospital affiliated to the University of Amsterdam, Amsterdam, the Netherlands. SUBJECTS: Thirty-five male patients, age 30-70, with established atherosclerosis and the high triglyceride-low HDL cholesterol trait. MAIN OUTCOME MEASURES: Plasma total cholesterol, triglycerides, lipoproteins, apolipoproteins A1 and B100, clinical and laboratory safety parameters. RESULTS: Seventeen patients in the gemfibrozil group and 16 patients in the placebo group completed the study period. Compliance was considered adequate. Mean (+/- standard deviation) plasma HDL cholesterol levels increased 20.3% (+/- 12.22) from 0.82 to 0.99 mmol L-1 in the gemfibrozil group against 9.9% (+/- 18.31) from 0.79 to 0.87 mmol L-1 in the placebo group (P = 0.001). Mean plasma triglyceride level fell 49.5% (+/- 14.27) from 3.65 to 1.82 mmol L-1 in the gemfibrozil group against an increase of 13.6% (+/- 40.31) from 3.62 to 4.01 mmol L-1 in the placebo group (P < 0.001). Although plasma HDL cholesterol and triglyceride levels improved in all patients, normalization of these lipoproteins was only observed in approximately half of them. Plasma total and low-density lipoprotein (LDL) cholesterol levels, as well as plasma levels of apolipoprotein (apo) A1, B100 and lipoprotein [Lp(a)], did not show significant alterations compared to the placebo. All safety parameters were comparable between the two groups and remained within the reference limits. Gemfibrozil was well tolerated during treatment. Minor inconveniences were equally distributed between the two treatment groups. CONCLUSIONS: Gemfibrozil is an effective and safe drug in patients with coronary heart disease (CHD) and the high triglyceride-low HDL cholesterol trait.

Adult↗
PubMed1980

Intrafamilial associations of cholesterol and triglyceride among related and unrelated household members.

The purpose of this report was to assess intrafamilial associations of lipids between related and unrelated household members seen in the course of a population-based survey of lipids in schoolchildren and their parents. Fasting plasma total cholesterol and triglyceride levels were measured in 6,857 and 3,079 adults. Age effects were removed for each sex-race group using a third-degree polynomial regression of lipid on age; the residuals were then used as observations in the analyses. For both cholesterol and triglyceride, significant positive correlations existed between father and son, father and daughter, mother and son, and mother and daughter. For both cholesterol and triglyceride, although the mother-child correlations were stronger than those for father-child, they were not significantly different. There were no significant correlations between step, foster, or adoptive parents and children. For cholesterol in sibships of size two, intrasibship correlations for fully related siblings were 0.333, for half-sibs 0.164, and for unrelated sibs, 0.085. Consistently closer intrafamilial cholesterol and triglyceride associations between related than unrelated family members, and the strong parental effects on cholesterol and triglyceride indicate, in aggregate, that a considerable proportion of the variation of cholesterol and triglyceride can be explained by genetic factors.

Adult↗
PubMed2005

Interaction of the G182C polymorphism in the APOA5 gene and fasting plasma glucose on plasma triglycerides in Type 2 diabetic subjects.

AIM: Apolipoprotein AV (APOA5) is an important determinant of plasma triglyceride concentration. This study aimed to investigate the relationship of an amino acid substitution at position 182 (G182C) of the apolipoprotein AV (APOA5) gene with triglyceride concentration in a Taiwanese population. METHODS: This study enrolled two cohorts: non-diabetic subjects (112 males and 89 females) aged 50.3+/-11.0 years (mean+/-sd) and diabetic subjects (106 males and 96 females) aged 62.1+/-10.3 years. The relationship between the G182C polymorphism (rs 2075291) and plasma triglycerides was examined. Demographic and metabolic parameters including age, sex, body mass index, fasting plasma glucose and total cholesterol were also obtained. RESULTS: The G182C polymorphism was a determinant of plasma triglycerides in both non-diabetic (P=0.022) and diabetic (P=0.003) groups, independent of age, gender, fasting plasma glucose, body mass index and total cholesterol. In the diabetic group, this genetic polymorphism interacts significantly (P=0.032) with fasting plasma glucose concentration on plasma triglycerides after adjustment for age, sex, body mass index and total cholesterol. CONCLUSIONS: In conclusion, the G182C polymorphism of the APOA5 gene affects plasma triglycerides in both non-diabetic and diabetic populations. The observed interaction of gene and glycaemic control further indicates a multifactorial nature of clinical phenotypes in subjects with Type 2 diabetes.

Adult↗
PubMed1979

Plasma HDL cholesterol in epileptics with elevated triglyceride and cholesterol.

Due to the metabolic changes induced, e.g. in the liver by anti-epileptic drugs, the significance of high serum triglyceride and cholesterol in epileptics was studied and the plasma HDL cholesterol level was compared in 190 epileptic patients with elevated or normal triglyceride and cholesterol, with the corresponding values in 43 healthy subjects. One-third of the epileptic patients showed elevated plasma HDL cholesterol levels. Female epileptics had higher plasma HDL cholesterol than the normolipidemic healthy subjects. Epileptics with elevated triglyceride or a combination of elevated triglyceride and cholesterol had a lower plasma HDL cholesterol level than normolipidemic patients with epilepsy. HDL cholesterol level in epileptics with high serum cholesterol did not diverge from the level in epileptics with normal serum triglyceride and cholesterol. The results show significant differences of plasma HDL cholesterol between epileptic patients and normolipidemic healthy controls on one hand, and between epileptics with altered and epileptics with normal serum lipid levels on the other. The findings suggest that the increase of plasma HDL cholesterol level in epileptics undergoing anticonvulsant treatment is influenced by endogenous triglyceride metabolism.

Adolescent↗
PubMed1988

Neonatal parenteral nutrition with a fat emulsion containing medium chain triglycerides.

Fifty-one newborn infants requiring parenteral nutrition were randomly assigned to receive a 50% medium chain triglyceride/50% long chain triglyceride lipid emulsion or the conventional 100% long chain triglyceride emulsion. Fat was administered daily for 20 hours, to a maximum of 3 g/kg/day. Plasma triglycerides, cholesterol, free fatty acids, ketones, glucose and capillary blood gases were monitored daily up to the sixth day of fat infusion. There were no significant differences in mean plasma triglycerides and free fatty acids between the two groups. No cases of hyperketonaemia were detected in the infants studied. Hyperglycaemic episodes were detected with similar frequency in both groups. The group who received the emulsion containing medium chain triglycerides had significantly lower mean plasma cholesterol values during the study. After 6 days of intravenous fat administration mean plasma cholesterol was more than 100% higher in the group which received the conventional emulsion. Differences in cholesterol content between the emulsions and a cholesterol lowering effect of medium chain triglycerides are possible explanations for these findings.

Cholesterol↗
PubMed2006

Adipophilin increases triglyceride storage in human macrophages by stimulation of biosynthesis and inhibition of beta-oxidation.

Lipid accumulation alters macrophage biology and contributes to lipid retention within the vessel wall. In this study, we investigated the role of adipophilin on triglyceride accumulation and lipid-droplet formation in THP-1-derived macrophages (THP-1 macrophages). In the presence of acetylated low-density lipoprotein, macrophages infected with an adenovirus expressing human adipophilin showed a 31% increase in triglyceride content and a greater number of lipid droplets compared with control cells. Incubation of macrophages with very low-density lipoprotein (VLDL) dramatically increased cellular triglyceride content similarly in control and adipophilin-overexpressing cells. By itself, VLDL increased adipophilin expression, which explains the lack of effect of adipophilin overexpression on cellular triglyceride content in macrophages loaded with VLDL. The lipid-droplet content of macrophages was increased by overexpression of adipophilin and/or loading with VLDL. In contrast, inhibition of adipophilin expression using siRNA prevented lipid-droplet formation and significantly reduced intracellular triglyceride content. Using inhibitors of beta-oxidation and acyl-coenzyme A synthetase, results were obtained which suggest that adipophilin elevates cellular lipids by inhibition of beta-oxidation and stimulation of long-chain fatty acid incorporation into triglycerides. Adipophilin expression in THP-1 macrophages altered the cellular content of different lipids and enhanced the size of lipid droplets, consistent with a role for adipophilin in human foam cell formation.

Base Sequence↗
PubMed1967

The effect of a non-ionic detergent (Triton WR 1339) on the removal of triglyceride fatty acids from the blood of the rat.

1. The initial rate of removal from the circulation of injected [(14)C] labelled chylomicron triglyceride is much slower in rats that have been injected with the non-ionic detergent, Triton WR 1339, than in normal animals. Pre-incubation of the lipid with Triton before its injection causes a further reduction in removal rate.2. After the injection of [(14)C]labelled chyle triglyceride into animals given Triton, the rate of disappearance of radioactivity falls markedly as the percentage of the labelled material remaining in the blood declines.3. A much smaller decrease in the rate of removal of injected chylomicron triglyceride occurs with increase in the size of the injected dose and with increase in the time interval between Triton and chylomicron triglyceride injections.4. Serum triglycerides labelled with (14)C are removed from the circulation of rats that have been given Triton at a much slower rate than [(14)C] labelled chylomicron triglycerides.

Animals↗
PubMed1993

Non-fasting serum triglyceride concentration and mortality from coronary heart disease and any cause in middle aged Norwegian women.

OBJECTIVE: To study the association between non-fasting serum triglyceride concentrations and mortality in women from coronary and cardiovascular disease and all causes. DESIGN: Follow up by ambulatory teams of men and women who underwent cardiovascular screening for a mean of 14.6 years. SETTING: National health screening service in Norway. SUBJECTS: 25,058 men and 24,535 women aged 35-49 years. MAIN OUTCOME MEASURE: Predictive value of non-fasting serum triglyceride concentrations. RESULTS: At initial screening total serum cholesterol concentration, serum triglyceride concentration, blood pressure, height, and weight were measured, and self reported information about smoking habits, physical activity, and time since last meal were recorded. During subsequent follow up 108 women died from coronary heart disease, 238 from cardiovascular diseases, and 931 from all causes. In women mortality increased steadily with increasing triglyceride concentration for all three causes of death. With the proportional hazards model and adjustment for age, systolic blood pressure, total cholesterol concentration, time since last meal, and number of cigarettes a day the relative risk between triglyceride concentration > or = 3.5 mmol/l and < 1.5 mmol/l was 4.7 (95% confidence interval 2.5 to 8.9) for deaths from coronary heart disease, 3.0 (1.9 to 4.8) for deaths from cardiovascular disease, 2.3 (1.8 to 2.9) for total deaths in all women. CONCLUSIONS: A raised non-fasting concentration of triglycerides is an independent risk factor for mortality from coronary heart disease, cardiovascular disease, and any cause mortality among middle aged Norwegian women in contrast to what is seen in men.

Adult↗