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Pea fiber lowers fasting and postprandial blood triglyceride concentrations in humans.

The effect of a pea cell wall fiber preparation with a high content of soluble fiber on fasting and postprandial blood lipids was investigated in young healthy subjects. Inclusion of 33 g pea fiber product/10 MJ (20 g dietary fiber) in a low fiber diet was tested in five men and six women (mean age 23 y) in a strictly controlled randomized cross-over intervention study over 2 wk separated by a 2-wk period of habitual diet consumption. No significant differences in fasting concentrations of total cholesterol, LDL cholesterol or HDL cholesterol were observed, whereas total and VLDL triglyceride concentrations were lower when subjects consumed the pea fiber diet compared with the low fiber diet (P < 0.05). Postprandial response to pea fiber was studied in eight men. Addition of 12 g pea fiber product/ 10 MJ to a breakfast meal and 15 g/10 MJ to the following lunch meal resulted in significantly lower total triglyceride (P = 0.01), chylomicron triglyceride (P = 0.03) and insulin (P = 0.003) concentrations after the lunch meal compared with results following the same meal without pea fiber. No differences were observed in glycemic response. In conclusion, this source of dietary fiber lowered fasting and postprandial triglyceride concentrations but did not change fasting cholesterol concentrations.

Adult↗

Fatty acids modulate lecithin:cholesterol acyltransferase secretion independently of effects on triglyceride secretion in primary rat hepatocytes.

The regulation of plasma lecithin:cholesterol acyltransferase (LCAT) expression is not well understood. Although oleic acid increases both the secretion of triglycerides and LCAT by primary rat hepatocytes, the effect of other fatty acids (FA) on LCAT secretion is not known. This study was designed to examine the effect of FA on the hepatic secretion of LCAT, triglyceride and apolipoprotein A-1 (apoA-1). Primary rat hepatocytes were incubated with serum-free medium, supplemented with individual FA (0-1 mmol/L) for 22-24 h. Preliminary studies indicated a linear secretion of LCAT up to 24 h in both control and FA-treated cells. When hepatocytes were incubated with 1 mmol/L FA, the LCAT secretion increased 50-100% (P < 0.01) in the presence of the 18-carbon FA (stearic, oleic, elaidic and linoleic acids), whereas the presence of butyric, lauric and palmitic acids had no significant effect. LCAT secretion decreased (P < 0.01) in the presence of docosahexaenoic acid (DHA). All FA (except DHA) significantly enhanced triglyceride secretion; however, only the 18 carbon FA significantly stimulated the synthesis and secretion of apoA-1 and secretion of LCAT. The secretion of LCAT correlated with apoA-1 secretion (r = 0.88, P = 0.004) but not with triglyceride secretion (r = 0.55, P = 0.12). Treatment with oleic acid resulted in a 1.5-fold increase in hepatocyte LCAT mRNA accumulation, whereas butyrate and palmitate had no effect. These data indicate that FA that promote the apparent synthesis and secretion of apoA-1 also stimulate the secretion of LCAT in vitro, suggesting a coordinate regulatory mechanism for apoA-1 and LCAT expression.

Animals↗

Triglyceride-rich HDL3 from patients with familial hypercholesterolemia are less able to inhibit cytokine release or to promote cholesterol efflux.

Familial hypercholesterolemia (FH) is associated with heterogeneity of the onset and severity of coronary heart disease (CHD). In this study, we investigated different low-grade proinflammatory markers and the atheroprotective function of the HDL3 subfraction in FH-patients (n = 13) with identical LDL-receptor mutations and in age- and sex-matched healthy controls (n = 11). Compared with healthy controls, FH-patients had greater gene expressions of the proatherogenic mediators TNF-alpha and IL-8 in circulating peripheral blood mononuclear cells. In addition, they had a higher serum concentration of intercellular adhesion molecule-1 (ICAM-1) and a lower net antioxidant capacity. FH-derived HDL3 with a high level of triglycerides had a reduced capacity to inhibit the release of IL-8 from TNF-alpha-stimulated human umbilical vein endothelial cells (HUVEC) [1.864 mg/L (1.461-2.208 mg/L) vs. 1.466 mg/L (1.225-1.643 mg/L); P < 0.05; median (range)], and a reduced capacity to promote cholesterol efflux from lipid-loaded macrophages [12% (12-14%) vs. 15% (14-18%); P < 0.05; median (range)] compared with HDL3 with a lower triglyceride content. Notably, the degree of inhibition of IL-8 release from HUVEC by HDL3 was correlated with the ability of HDL3 to promote cholesterol efflux (r = -0.80, P = 0.03). In conclusion, compared with healthy controls, FH-patients are characterized by higher levels of low-grade proinflammatory markers, and FH-derived HDL3 with high triglyceride content may be more proatherogenic. These triglyceride rich-HDL3 might be partly responsible for the phenotypic variation among FH-patients with identical LDL-receptor mutations.

Adult↗

Fiber intakes and anthropometric measures are predictors of circulating hormone, triglyceride, and cholesterol concentrations in the women's health trial.

The unhealthy eating patterns and obesity among women in the U.S. are indicated by changes in biomarkers, such as insulin, lipoproteins, and estradiol, that are risk factors for breast cancer and cardiovascular diseases. This article models the inter-relations among diet, serum insulin, estradiol, and sex hormone binding globulin (SHBG) concentrations, plasma LDL and HDL cholesterol, and net triglyceride concentrations, using the data at baseline and 12 mo on 379 and 615 postmenopausal women in the Control and Intervention groups, respectively, of the Women's Health Trial: Feasibility Study in Minority Populations. Subjects in the Intervention group received detailed advice over a period of 1 y for reducing fat intakes and increasing the consumption of whole grains and fruits and vegetables. The main findings were that there were significant differences between the Control and Intervention groups in the changes from baseline to 12 mo in LDL and HDL cholesterol and SHBG concentrations. Second, using a comprehensive random effects modeling framework, the ratio of fiber to energy intake was significantly associated (P < 0.05) with lower insulin and triglyceride levels, and with a higher HDL cholesterol concentration in the Intervention group. Third, the subjects' waist-to-hip ratio and BMI were significantly associated with insulin, SHBG, LDL and HDL cholesterol, and triglyceride concentrations. Fourth, insulin levels were significantly negatively associated with SHBG and HDL cholesterol, and positively associated with LDL cholesterol, triglyceride, and estradiol concentrations. Overall, weight loss, especially around the waist, and increased fiber intakes are likely to be beneficial for lipid, cholesterol, and hormone profiles of U.S. women.

Aged↗

Effect of bezafibrate on lipoprotein (a) and triglyceride-rich lipoproteins, including intermediate-density lipoproteins, in patients with chronic renal failure receiving haemodialysis.

The effect of bezafibrate, at doses of 200 mg three times weekly throughout a period of 10 weeks, on lipoprotein (a) and triglyceride-rich lipoproteins including intermediate-density lipoproteins (IDL) has been studied in 12 patients with chronic renal failure receiving haemodialysis. No side-effects were observed, and serum creatine phosphate kinase values remained within normal limits throughout the duration of the study. Serum cholesterol, triglycerides and apoprotein (apo) B significantly decreased after bezafibrate, whereas apo A-I increased significantly. Serum lipoprotein (a) decreased after bezafibrate, although differences reached no statistical significance. The very-low-density lipoproteins (VLDL) cholesterol and the VLDL triglycerides decreased from 0.93 +/- 0.45 mmol/l (Mean +/- SD) to 0.54 +/- 0.27 mmol/l (P less than 0.05) and from 1.50 +/- 0.58 mmol/l to 0.91 +/- 0.35 mmol/l (P less than 0.01) respectively. The IDL cholesterol and IDL triglycerides decreased from 0.44 +/- 0.35 mmol/l to 0.20 +/- 0.18 mmol/l (P = NS) and from 0.46 +/- 0.35 mmol/l to 0.17 +/- 0.12 mmol/l (P less than 0.05) respectively. These data, with a substantial improvement of the lipoprotein profile in patients with chronic renal failure on haemodialysis after treatment with bezafibrate, suggest a decrease in the coronary heart disease risk.

Adult↗

Retest reliability of plasma cholesterol and triglyceride. The Lipid Research Clinics Prevalence Study.

Retest reliability for plasma cholesterol and triglyceride is important diagnostically and in the planning of studies. Coefficients of variation of about 8% for cholesterol and 25% for triglyceride are reported here during Visits 1 and 2 of the Lipid Research Clinics Prevalence Study in 1972-1975. Retest reliability showed little or no dependence on other factors studied. It would not be unusual to observe apparent cholesterol changes of 50 mg/dl and occasionally 100 mg/dl with no obvious explanation. Apparent random triglyceride changes may be as high as several hundred mg/dl. It is of clinical importance that two thirds of persons in the upper quintile of cholesterol and/or triglyceride at first measurement remain in this rank and one third rank lower on retest. Multiple observations of these lipid values are recommended both for clinical use and for establishment of study baselines.

Adult↗

Boys from populations with high-carbohydrate intake have higher fasting triglyceride levels than boys from populations with high-fat intake.

Experimentally, high-carbohydrate diets have been shown to elevate triglycerides, but it has not been established whether this rise is permanent or transient. The authors approached this question by studying 719 boys from worldwide populations with marked differences in long-term carbohydrate intake. Fasting serum triglycerides, total cholesterol and high density lipoprotein (HDL) cholesterol concentrations were measured in boys aged 8 and 9 years from 12 countries--eight in Europe, three in Africa, and one in Asia. A standardized protocol was used for obtaining fasting blood and for the preparation, storage and transport of serum, and all measurements were made in one laboratory. Published values were used for the United States. Mean values for lipid levels per country were compared with the percentage of daily energy intake consumed as carbohydrate or fat, as determined by survey. Boys from populations with higher carbohydrate and lower fat intake had lower low density lipoprotein (LDL) cholesterol levels (univariate regression coefficient (+/- standard error, -0.028 +/- 0.009 mmol/liter for each percent of energy from carbohydrate; p less than 0.01, n = 13), but they also had higher fasting triglycerides (0.010 +/- 0.002 mmol/liter for each percent of energy from carbohydrate; p less than 0.01, n = 13) and lower HDL cholesterol levels (-0.022 +/- 0.003 mmol/liter for each percent of energy from carbohydrate; p less than 0.001, n = 13). These trends agree with results from epidemiologic studies within populations and from controlled dietary trials, and suggest that in normolipidemic healthy subjects, high-carbohydrate, low-fat diets cause higher triglyceride levels than diets that are higher in fats and oils.

Africa↗

Safflower oil emulsion administration during parenteral nutrition in the preterm infant. 2. Effect on triglyceride and free fatty acid levels.

During a study to evaluate the effect of a safflower oil emulsion on essential fatty acid status during parenteral nutrition, we also measured plasma triglycerides and plasma free fatty acids (FFA) in a group of preterm infants. Subjects received 0.34 g/kg (group 1) or 0.68 g/kg (group 2) of lipid daily for 5 days. Essential fatty acid status remained normal in both groups, but the changes in plasma triglycerides were greater (p less than 0.025), and hypertriglyceridemia was somewhat more common (p = 0.06) in group 2 than in group 1. Plasma FFA did not differ in either treatment group. However, postinfusion FFA were greater (p less than 0.05) and FFA uptake was less (p less than 0.05) in infants at less than 32 than at 32-34 weeks gestation, but in no instance did postinfusion FFA exceed an FFA/albumin ratio of 6:1. In addition, triglyceride and FFA uptake did not improve during the study, but the changes in plasma triglycerides and FFA were greater (p less than 0.05) at the end than at the beginning of the study.

Emulsions↗

Intraduodenal lipase activity in celiac disease assessed by means of 13C mixed-triglyceride breath test.

BACKGROUND: In patients with celiac disease, the occurrence of exocrine pancreatic insufficiency has been related to an impairment of the gut-mediated stimulatory effect of the meal on the pancreas. The purpose of this study was to assess the intraduodenal lipase activity in patients with celiac disease by means of the 13C mixed-triglyceride breath test and to monitor pancreatic function after the institution of a gluten-free diet. METHODS: Seventeen untreated patients with celiac disease (mean age, 17.4 +/- 10.5 years) were studied. After an overnight fast, patients were given a standard test meal consisting of 100 g of white bread and 0.25 g of butter per kilogram of body weight, to which 16 mg di-stearyl-13C-octanoyl-glyceride (mixed triglyceride) had been added. Breath samples were taken twice at baseline and at 30-minute intervals for 6 hours after the meal. 13C enrichment in breath was determined by means of Isotope Ratio Mass Spectrometer (IRMS) (ANCA-NT; Europa Scientific, Crewe, UK). Results were expressed as the maximum percentage of 13C recovery per hour at any time, the time to reach peak excretion of 13C, and the percentage of 13C cumulative dose over 6 hours. RESULTS: Mixed-triglyceride breath test results were pathologic in three patients and at the lower limit of the normal range in another patient. In the remaining 13 patients, the results were within normal values. At the 6- and 12-month follow-ups, all patients showed normal intraduodenal lipase activity. CONCLUSIONS: In approximately 24% of patients with celiac disease, the intraduodenal pancreatic lipolytic activity is impaired. The mixed-triglyceride breath test could be used to assess fat maldigestion and to monitor the need for enzyme replacement therapy in such patients.

Adolescent↗

Role of muscle in triglyceride metabolism.

It has long been recognized that skeletal muscle can contain modest stores of triglyceride and that this depot of fuel can make a major contribution to energy production during exercise. More recently, an adverse effect of muscle triglyceride has begun to be defined within the context of insulin resistance. Animal and clinical investigations have revealed a significant relation between increased muscle triglyceride and insulin resistance, at least among mostly sedentary individuals. These observations have stimulated the development, or at least the refinement, of new methodologies to assess this aspect of 'regional' fat deposition. In parallel, there has also been important new work designed to enable better understanding of the factors that regulate muscle triglyceride and to determine whether fatty acids taken up by skeletal muscle are oxidized or stored, and how these pathways might be either altered by the presence of insulin resistance or, in turn, contribute to the pathogenesis of insulin resistance.

Animals↗

Relevance of the reduction of triglycerides in the prevention of coronary heart disease.

Triglyceride metabolism is complex and still poorly understood. Hypertriglyceridemia seems to enhance the risk for the development of coronary heart disease, but it cannot be regarded as a counterpart of hypercholesterolemia as a risk factor. The relevance of reduction of triglycerides in the prevention of coronary heart disease is still unclear. This is related to a number of problems, such as the lack of adequate clinical trials, heterogeneity in the abnormalities of triglyceride metabolism and unknown atherogenic threshold levels for serum triglycerides.

Clinical Trials as Topic↗

Elevated triglyceride and decreased high density lipoprotein level in carbon disulfide workers in Taiwan.

Carbon disulfide (CS2) is a man-made product utilized primarily in the manufacture of viscose rayon. Overexposure to CS2 has been associated with an increase in coronary heart disease. The aims of this study were to examine the dose-response relationship of CS2 exposure and elevated lipid profile tests among CS2-exposed workers in Taiwan. A total of 132 workers were recruited from two viscose rayon plants. Air sampling was performed to determine the CS2 exposure of workers. Demographic data and work history were gathered by a standard self-administered questionnaire. Lipid profile tests were also performed by routine methods. The average CS2 exposure concentration was 50.6 +/- 25.6 ppm (range: 24-127 ppm) in the high-exposure group, 12.9 +/- 5 ppm (range: 5.2-22.3 ppm) in the mid-exposure group, and 3.5 +/- 1.2 ppm (range 0.97-5.2 ppm) in the low-exposure group. There were 21 out of 33 (63.7%) elevated triglyceride levels among high-CS2-exposure workers, 27 out of 64 (42.2%) among the middle-CS2-exposure, and 14 out of 35 (40%) among low-CS2-exposure workers, respectively. Compared to the low-CS2-exposure workers, the age- and weight-adjusted odds ratios (and 95% confidence intervals) of the prevalence of elevated triglyceride value were 1.12 (0.5, 2.7) for middle-CS2-exposure workers, and 2.81 (1.02, 7.8) for high-CS2-exposure workers. There was a significant linear trend between CS2 exposure and the prevalence of elevated triglyceride value (P = 0.046) after adjusting for other factors. There was also a lower prevalence of elevated HDL level in high-CS2-exposure workers than low-CS2-exposure workers (15.2% versus 31.4%). Compared to the low-CS2-exposure workers, the age- and weight-adjusted odds ratio (and 95% confidence intervals) of elevated HDL level were 0.34 (0.1, 1.18) for high-CS2-exposure workers, which was borderline significant. In conclusion, this study suggests that elevated triglyceride level and decreased HDL level are associated with CS2 exposure. The study also suggests that exposure to CS2 (concentration > 23.2 ppm, which was above the current TLV-TWA of 10 ppm) are significantly associated with increased risk and decreased protective effect for coronary heart disease.

Carbon Disulfide↗

Effects of medium-chain triglyceride (MCT) application to SHR on cardiac function, hypertrophy and expression of endothelin-1 mRNA and other genes.

In spontaneously hypertensive rats a decrease occurs in myocardial energy supply from long-chain triglyceride (LCT) by CD36 gene mutation-induced dysfunction. We investigated whether long-term intake of medium-chain triglyceride, which enters into cells without CD36, upregulates fatty acid metabolic capacity in the heart of spontaneously hypertensive rats, and whether this upregulation improves cardiac hypertrophy and molecular markers. Male 4-week-old spontaneously hypertensive rats were given medium-chain triglyceride (SHR-MCT) or LCT (SHR-LCT) for 16 weeks. After hemodynamic measurement, we determined myocardial fatty acid metabolic enzyme activity and mRNA expression of molecular markers (endothelin-1, alpha-skeletal actin, angiotensin-converting enzyme and brain natriuretic peptide) for cardiac hypertrophy. We used Wistar-Kyoto rats (WKY-MCT and WKY-LCT) as controls. When compared with SHR-LCT rats, SHRMCT rats showed an increase in myocardial fatty acid metabolic enzyme activity and improvement in cardiac function (left ventricular end-diastolic pressure and +dP/dt/P) and cardiac hypertrophy. Blood pressure did not differ between them. The mRNA expression of endothelin-1, alpha-skeletal actin, angiotensin-converting enzyme and brain natriuretic peptide in the heart was significantly higher in SHR-LCT than in WKY-MCT and WKYLCT rats, and there was no significant difference between SHRLCT and SHR-MCT. These findings suggest that medium-chain triglyceride application to spontaneously hypertensive rats improves decreased cardiac function and cardiac hypertrophy without affecting blood pressure and myocardial mRNA expression of molecular markers. Because mechanical stress to the heart is similar between SHR-LCT and SHR-MCT, this may be a reason for the lack of difference in expression of molecular markers.

3-Hydroxyacyl CoA Dehydrogenases↗

Peroxisome proliferator-activated receptor-gamma coactivator 1alpha (PGC-1alpha) regulates triglyceride metabolism by activation of the nuclear receptor FXR.

Peroxisome proliferator-activated receptor-gamma coactivator 1alpha (PGC-1alpha) has been shown to regulate adaptive thermogenesis and glucose metabolism. Here we show that PGC-1alpha regulates triglyceride metabolism through both farnesoid X receptor (FXR)-dependent and -independent pathways. PGC-1alpha increases FXR activity through two pathways: (1) it increases FXR mRNA levels by coactivation of PPARgamma and HNF4alpha to enhance FXR gene transcription; and (2) it interacts with the DNA-binding domain of FXR to enhance the transcription of FXR target genes. Ectopic expression of PGC-1alpha in murine primary hepatocytes reduces triglyceride secretion by a process that is dependent on the presence of FXR. Consistent with these in vitro studies, we demonstrate that fasting induces hepatic expression of PGC-1alpha and FXR and results in decreased plasma triglyceride levels in wild-type but not in FXR-null mice. Our data suggest that PGC-1alpha plays an important physiological role in maintaining energy homeostasis during fasting by decreasing triglyceride production/secretion while it increases fatty acid beta-oxidation to meet energy needs.

Animals↗

Characterization of wax esters, triglycerides, and free fatty acids of follicular casts.

The abnormal impactation of a sebaceous follicle (the follicular cast) has been implicated as the preclinical lesion of acne vulgaris. We have characterized the lipid composition of these structures in the first of a series of studies aimed at the identification of sebaceous lipids that may be associated and/or responsible for the initiation of clinical lesions. The lipid composition of follicular casts was analyzed using thin-layer chromatography, gas chromatography, and mass spectrometry. The mean wet weight of the casts was 24.7 +/- 8.6 micrograms and 7.2 +/- 5.6 micrograms (29.4 +/- 13.5%) was lipid. Cholesterol (3.8 +/- 1.8%) and cholesterol esters (2.0 +/- 2.7%), wax esters (25.3 +/- 6.0%), squalene (19.9 +/- 6.6%), triglycerides (16.1 +/- 7.8%), and free fatty acids (33.0 +/- 10.0%) were all present in cast lipid. Fatty acids of the free fatty acid and triglyceride fraction ranged from C12 to C22. The major components of the free fatty acids were C14:0, C15:0, C16:1, C16:0, 2-me-C17:0, and C18:1. In the triglyceride fraction C14:0, C15:0, C16:0, C18:1, and C18:0 dominated. The free fatty acids were composed of normal saturated (50.6%), normal unsaturated (32.8%), and monomethyl branched (16.6%) acids; the triglyceride fraction contained (86.3%) normal saturated (10.8%), normal unsaturated, and (3.0%) monomethyl branched fatty acids. Wax esters of follicular casts included esters ranging from C26:1 to C38:0. Saturated esters predominated and both odd- and even-numbered esters were present. The most abundant fatty acid moieties of these esters were C16:0 and C15:0, whereas C14:0, C17:0, and C20:0 were the most frequently detected alcohol moieties.

Acne Vulgaris↗

Changes in serum triglyceride and cholesterol levels during long-term phenytoin treatment for epilepsy.

The effect of long-term phenytoin therapy on serum triglyceride and cholesterol levels in 20 patients with epilepsy was investigated. In patients followed up for six years, phenytoin treatment was associated with an increase in serum triglyceride and cholesterol levels. The most significant increases in lipid levels were measured during the first months of therapy, whereafter values generally tended to decrease. The elevation in serum triglyceride concentration was relatively greater than that in serum cholesterol level. Cholesterol concentrations, however, remained high for a longer period. The results demonstrate that phenytoin therapy for epilepsy is associated with a rise in serum triglyceride and cholesterol levels, the degree of which seems to be related to the duration of the treatment. The changes presumably reflect phenytoin effects on hepatic lipid metabolism.

Adolescent↗

Serum lipids with special reference to HDL cholesterol and triglycerides in young male survivors of acute myocardial infarction.

Serum cholesterol, triglycerides and high-density lipoprotein (HDL) cholesterol were determined in 56 male survivors of myocardial infarction (MI), suffered 6--20 months earlier, and in 82 healthy age- and sex-matched controls. The mean age of both groups was 39 years. Total serum cholesterol was within normal limits in both groups, whereas HDL cholesterol was considerably lower and triglycerides remarkably elevated in MI patients compared with the controls. Judging from previous and present data, low HDL cholesterol seems to be a coronary risk factor as such. This study indicates that low HDL cholesterol, and especially a low HDL cholesterol/total cholesterol ratio, may be stronger coronary risk factors than total serum cholesterol alone. Because HDL cholesterol and triglycerides were inversely correlated, these results also emphasize the importance of serum triglycerides as a risk factor for coronary heart disease.

Adult↗

The relation between the levels of HDL cholesterol and the capacity for removal of triglycerides.

In twenty-two men with "normal" findings clinically, by exercise ECG and laboratory tests, we performed an i.v. fat tolerance test, measurement of LCAT activity and the activities of post-heparin triglyceride lipases, and estimated serum lipids. HDL cholesterol was positively correlated to lipoprotein lipase (r=0.50, p < 0.05) and to the fractional removal rate of exogenous fat (r=0.59, p < 0.01), and negatively to the fasting levels of triglycerides (r=-0.65, p < 0.01). LCAT was neither correlated to HDL cholesterol nor to the fat removal rate. Our reseults confirm that a high triglyceride removal capacity is closely correlated to a high level of HDL. The association between the catabolism of triglyceride-rich lipoproteins and HDL was thus further substantiated.

Cholesterol↗