Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “triglycerides”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 829 records · Page 46Linked to original sources
PubMed2000

Two subpopulations of intermediate density lipoprotein and their relationship to plasma triglyceride and cholesterol levels.

We observed the appearance of two intermediate density lipoprotein (IDL) subfractions on gradient gel electrophoresis of lipoproteins in the density range 1.006-1.030 g/ml and estimated their approximate concentrations in plasma in subjects with a wide range of lipid levels, from 0.55 to 28.0 mmol/l plasma triglyceride and 3.75-10.0 mmol/l cholesterol. The larger species, IDL-I (31.7 +/- 0.7 nm, mean +/- SD), showed little variation in size in normal and moderate hyperlipidaemic individuals. The estimated concentration of IDL-I was positively related to plasma triglyceride (r = 0.63, P = 0.0004) and low density lipoprotein (LDL) cholesterol (r = 0.68, P = 0.0003). These findings are consistent with the view that IDL-I is a metabolic intermediate between very low density lipoprotein (VLDL) and LDL. The smaller subfraction, IDL-II (25.7 +/- 2.4 nm) was virtually the only true species observed in subjects with plasma triglyceride < 1.0 mmol/l and its estimated concentration fell as plasma triglyceride increased (r = -0.58, P = 0.0002). IDL-II particle size changed in concert with LDL particle size (r = 0.61, P < 0.0001), suggesting that they were influenced by common metabolic factors. These observations provide further support for the hypothesis outlined by Musliner et al. [1] that IDL-I was part of the delipidation chain from VLDL to LDL, whereas IDL-II arose from a separate source, possibly directly released from the liver. Hence the two subpopulations of IDL differ in their relationship to plasma triglyceride and cholesterol levels.

Adult↗
PubMed2000

Intestinal absorption of triglyceride and cholesterol. Dietary and pharmacological inhibition to reduce cardiovascular risk.

Triglycerides and cholesterol are important biological lipids, and their excessive intake in the diet is relevant to the development of two prevalent cardiovascular risk factors, obesity and hypercholesterolemia. Because most lipids are essentially water-insoluble molecules, their transport within and absorption from the aqueous medium of intestinal contents is rather complex. This takes place in a series of orderly and interrelated steps, including emulsification, hydrolysis by specific esterases, micellar transport, mucosal absorption, re-synthesis of parent molecules in enterocytes, and assembly with apolipoproteins and other molecules to form chylomicrons, the secretory product of intestinal cells. Many of these processes, however, are not well characterized at the molecular level. While in health the intestinal absorption of triglycerides is very efficient, the same does not apply to cholesterol absorption. Besides being generally inefficient, cholesterol absorption is highly variable, with a between-subject variability that depends in part on genetic factors and an intra-individual variability, which may be modulated by physiological and dietary conditions. All of the sequential steps in intestinal lipid absorption can be interfered with by dietary components or drugs and thus are potential therapeutic targets for inducing a controlled malabsorption of triglyceride, useful in the treatment of obesity, or for rendering cholesterol absorption even more inefficient in an attempt to lower blood cholesterol levels. Nevertheless, intestinally derived cholesterol available to the liver exerts complex feedback regulation on whole-body cholesterol homeostasis that limits the efficacy of cholesterol absorption inhibitors to lower blood cholesterol. This review focuses first on present knowledge of the physiology of intestinal fat absorption, necessary to understand the ways to manipulate it in order to obtain the desired effects on dietary triglyceride and cholesterol disposition. The second part discusses old, present and future ways, both dietary and pharmacological. of interfering with cholesterol and triglyceride absorption to reduce blood cholesterol and energy acquisition, respectively.

Animals↗
PubMed1996

Effect of the apolipoprotein C-II/C-III1 ratio on the capacity of purified milk lipoprotein lipase to hydrolyse triglycerides in monolayer vesicles.

The effect of the apolipoprotein C-II/C-III1 ratio on the capacity of purified bovine milk lipoprotein lipase to hydrolyse triglycerides was measured in a controlled model of pyrene-labeled nonanoyltriglycerides (1-2 ditetradecyl 3-pyrene nonanoyl glyceride) monolayer vesicles. Monolayer was composed of triglycerides, a non-hydrolysable phospholipid ether and cholesterol, a model system where the quality of the interface can be controlled. LPL released fatty acids from pyrene-triglycerides which were transferred from the lipoprotein structure to albumin. This transfer induces a decrease in the excimer production and in the excimer fluorescence intensity. Apolipoprotein C-II and C-III0 and C-III1 were purified from apolipoprotein VLDL. The 2 fragments, C-III1 A (peptide 1-40) and C-III1 B (peptide 41-79), were obtained after thrombin cleavage. Apolipoproteins C-III0 and C-III1 had a similar inhibitory effect on LPL. Inhibition with apo C-III0 or apo C-III1 was 85% of full LPL activity without inhibitor: Apo C-III1 B inhibited 62% of basal activity. It was 27% less effective than apo C-III1. Fragment C-III1 A did not inhibit LPL. The effect of change in both apo C-II (0-0.6 microM) and apo C-III1 (0-1.0 microM) on triglyceride hydrolysis shows the importance of the apo C-II/C-III1 ratio for the release of free fatty acids from triglycerides by LPL. The activating effect of apo C-II in the absence of the apo C-III inhibitor was maximal at 0.06 microM. No further activation was obtained between 0.06 and 0.30 microM. Higher concentrations decreased LPL activity. Apo C-III1 (0.1 microM) decreased the maximum activation by apo C-II from 0.0196 to 0.063 nmol/min/nmol LPL. Higher concentrations of apo C-III1 (0.1-0.5 microM) required higher apo C-II concentrations (0.30 microM instead of 0.06 microM) for maximal activation than when apo C-III1 was absent. The activity of the enzyme without apo C-II was decreased by 65% by 0.12 microM apo C-III1. Increasing the apo C-II/apo C-III1 ratio from 0.1 to 1, increased the activation of the enzyme by a given apo C-II concentration. Moreover, for a given apo C-II/C-III1 ratio, the LPL activation increased with the apo C-II concentration (between 0 and 0.010 microM), until a plateau was reached. This is important, as the change in the C-II/C-III1 ratio is not the only factor affecting LPL activity, and inhibition by apo C-III1 also depends on the overall quantity of apolipoproteins. Extrapolation of these results suggests that hyperlipoproteinemia seems to be more likely due to overproduction of VLDL, than to a decrease in lipoprotein lipase activity.

Animals↗
PubMed2000

Effect of LDL+VLDL oxidizability and hyperglycemia on blood cholesterol, phospholipid and triglyceride levels in type-I diabetic patients.

Oxidative modification of low-density lipoproteins has been implicated in impaired lipid metabolism and its deposition in the arterial wall, and atherosclerosis. This study was carried out to determine the relationship between the in vitro oxidizability of low-density lipoprotein (LDL) and very-low-density lipoprotein (VLDL) and the cholesterol, phospholipid and triglyceride (TG) levels in the blood of Type-I diabetic patients. LDL+VLDL was isolated using a micro-affinity column from serum of diabetic patients (n = 34) and age-matched normal individuals (n = 22). The oxidative susceptibility of LDL+VLDL was determined by treatment with 25 microM CuCl(2) for 1.5 h. The levels of total-, LDL-, and HDL-cholesterol, phospholipids and triglycerides, as well as glycated hemoglobin (HbA(t)), were measured in the blood using standard methods. The diabetics had significantly higher levels of triglycerides and phospholipids, but cholesterol levels were similar between Type-I diabetics and age-matched normals. However, among diabetics, there was a significant correlation between the in vitro oxidation of LDL+VLDL at 1.5 h and total cholesterol (r = 0.49, P<0.002), and LDL cholesterol (r = 0.54, P<0.001) and TG (r = 0.34, P<0.05) levels. The level of in vitro oxidizability of LDL+VLDL did not have any correlation with HDL-cholesterol or phospholipid levels. The level of glycemic control (HbA(1)) did not have any correlation with levels of LDL- or HDL-cholesterol or triglycerides, but was significantly correlated with phospholipid levels (r = 0.48, P<0.005). This study suggests that the levels of LDL-cholesterol and triglycerides in the blood are directly related to the degree of in vitro oxidative susceptibility of low-density lipoproteins in Type-1 diabetic patients.

Adolescent↗
PubMed2000

Cilostazol, a selective type III phosphodiesterase inhibitor, decreases triglyceride and increases HDL cholesterol levels by increasing lipoprotein lipase activity in rats.

Cilostazol, a selective type III phosphodiesterase inhibitor, has antiplatelet and vasodilating effects. In this study, the effects of cilostazol on lipid metabolism and lipoprotein lipase (LPL) activity were studied in rats. Cilostazol was administered orally at doses of 30 or 100 mg/kg twice a day for 1-2 weeks to rats. Cilostazol decreased the serum triglyceride level in normolipidemic rats. The serum triglyceride level was reduced and HDL cholesterol level was increased by cilostazol in streptozotocin (STZ)-induced diabetic rats. The disappearance of exogenous triglyceride was accelerated by cilostazol in normolipidemic rats. Cilostazol increased post-heparin plasma LPL activity but had no effect on hepatic triglyceride lipase activity in STZ-induced diabetic rats. Cilostazol also increased LPL activity in the heart in STZ-induced diabetic rats. These findings suggest that an increase in LPL activity is responsible for the serum triglyceride lowering and HDL cholesterol elevating effects of cilostazol in rats.

Animals↗
PubMed1988

Densitometric identification of triglycerides separated by reversed-phase thin-layer chromatography.

A method to identify triglycerides, separated by reversed-phase thin-layer chromatography on silanized Kieselguhr G layers using densitometric data only, is described. Different triglyceride mixtures, containing components with partition numbers in the range 44-56, have been scanned. A linear relationship between the partition numbers of the zones and the maximum-to-maximum distances of the corresponding peaks, relative to the peak of the zones with partition number 48, has been found. The validity of this equation has been confirmed experimentally for triglycerides with partition numbers in the range 30-46. The method allows the identification of the triglyceride components of a mixture by their partition numbers, provided only one partition number is known or can be determined independently. An example concerning sunflower oil triglycerides is presented.

Chromatography, Gas↗
PubMed1988

Comparison of retention mechanisms of homologous series and triglycerides in non-aqueous reversed-phase liquid chromatography.

The retention behaviour of saturated homogeneous triglycerides was compared to that of single chain homologous compounds in reversed-phase liquid chromatography on silica-based octadecyl bonded phases with non-aqueous binary eluents containing chloroform. For both series, in all eluents and at all investigated temperatures, a discontinuity (1-6% slope change) in log k' vs. the carbon atom number, nc, of each solute hydrocarbonaceous chain was observed for a given critical number of carbon atoms, nc,crit approximately 12-13. Similar discontinuities were observed in delta H degrees and delta S degrees vs. nc for the same nc,crit value. These and other phenomena (existence of two convergence points for log k' vs. nc plotted at different eluent compositions; existence of two convergence temperatures in log k' vs. 1/T plotted for several members of a given solute series) reflect the mechanism of penetration of the solute aliphatic chains into the bonded layer. The eluotropic strength of acetonitrile-chloroform mobile phases was determined and seen to have a larger rate of variation with the solvent composition than that of some other non-aqueous binary eluents. The ratio of the slope of plots of log k' vs. nc curves for triglycerides and single chain homologous series is not a whole number but has a value lying between 2 and 3. This explains why triglyceride retentions cannot be predicted from retention data for the fatty acid methyl esters. More importantly, this indicates that the triglycerides may interact with the stationary phase using various conformations, one, two or three chains penetrating into the bonded layer. These conformations, in dynamic equilibrium with each other, contribute differently to the retention. This offers, in principle, the possibility to separate unsaturated triglycerides having the same number of carbon atoms and of double bonds but differing in the distribution of the unsaturations along the chains, if the double bonds located in a non-penetrating chain can selectively interact with a mobile phase component.

Chromatography, Liquid↗
PubMed2003

R219K polymorphism of the ABCA1 gene and its modulation of the variations in serum high-density lipoprotein cholesterol and triglycerides related to age and adiposity in white versus black young adults. The Bogalusa heart study.

Mutations in adenosine triphosphate (ATP)-binding cassette transporter 1 (ABCA1) gene have been established as the molecular defect in Tangier disease and familial hypoalphalipoproteinemia, uncommon genetic disorders characterized by deficient or depressed high-density lipoprotein (HDL) cholesterol and increased triglycerides. However, information regarding the frequency of common variants, including Arg219Lys (R219K) within the coding region of the ABCA1 gene and their effect on these phenotypes in the general population is limited. This study examined the frequency and phenotypic effect of R219K variant in a community-based sample of 887 white and 390 black young adults aged 20 to 38 years. The frequency of the variant allele (K219) was higher in blacks than in whites (0.595 v 0.262, P<.001), with carriers (KK+RK) representing 83.8% of blacks versus 44.2% of whites. After adjusting for age, body mass index (BMI), and sex, the genotype effect on HDL cholesterol and natural logarithm of triglycerides was not apparent in whites or blacks. However, significant interaction effects of genotype and age on HDL cholesterol (P<.001) and genotype and BMI on triglycerides (P=.029) were found in whites. Carriers (KK+RK), unlike noncarriers (RR) showed a positive relationship between age and HDL cholesterol (regression coefficient beta=0.28, P=.029 for carriers v beta=-0.18, P=.112 for noncarriers). In addition, the variant allele attenuated the adverse positive relationship between BMI and triglycerides (beta=0.032, P<.001 for carriers v beta=0.046, P<.001 for noncarriers). These results indicate that the K219 allele frequency differs markedly between blacks and whites, and that the variant-allele modulates the association between age and HDL cholesterol, as well as body fatness and triglycerides in a beneficial manner only in whites.

ATP Binding Cassette Transporter 1↗
PubMed1996

The relation of plasma triglyceride, apolipoprotein B, and high-density lipoprotein cholesterol to postheparin lipoprotein lipase activity is dependent on apolipoprotien E polymorphism.

Postheparin plasma (PH)-lipoprotein lipase (LPL) activity has been reported to be a significant correlate of plasma triglyceride and high-density lipoprotein cholesterol (HDL-C) levels. However, some studies have failed to observe these associations. In this regard, apolipoprotein (apo) E polymorphism may play an important role, since the apo E2 isoform has unfavorable effects on the catabolism of triglyceride-rich lipoprotein particles. We have thus examined the relationships between PH-LPL activity and plasma lipoprotein-lipid levels within groups of men classified on the basis of apo E phenotypes, to verify whether apo E polymorphism could alter these associations. In men carrying the apo E2 isoform (n = 12), PH-LPL activity showed a strong negative correlation with plasma triglyceride (r = -.72, P < .01), very-low-density lipoprotein (VLDL) triglyceride ([VLDL-TG] r = -.83, P < .001), and VLDL cholesterol ([VLDL-C] r = -.57, P < .05) levels and a positive correlation with plasma HDL-C (r = .87, P < .001) and HDL2-C (r=.90, P < .001) concentrations. These correlations were also noted for plasma apo B levels (r = -.65, P < .05), VLDL-apo B concentrations (r= -.76, P < .01), and the HDL-C to cholesterol ratio (r = .85, P < .001). In contrast, none of these associations were found in men carrying the apo E4 isoform (n = 11). In men homozygous for the apo E3 isoform (n = 29), PH-LPL activity was only significantly correlated with plasma HDL2-C levels (r = .46, P < .01). Results of the present study indicate that PH-LPL activity is related to plasma triglyceride, VLDL-TG, VLDL-C, VLDL-apo B, apo B, and HDL-C levels and the HDL-C to cholesterol ratio in men carrying the apo E2 isoform, but not in men homozygous for the apo E3 isoform or among apo E4 carriers. Thus, apo E polymorphism appears to modulate the effect of variation in PH-LPL activity on the plasma lipoprotein profile.

Adult↗
PubMed1998

The relationship between smoking and triglyceride-rich lipoproteins is modulated by genetic variation in the glycoprotein IIIa gene.

In the last year, several studies have reported conflicting results concerning an association between the PI(A2) allele of the PI(A1/A2) polymorphism of platelet glycoprotein IIIa and the risk of myocardial infarction. In the present study, we analyzed the hypothesis of whether glycoprotein IIIa genotypes have any association with lipids and lipoproteins as classical cardiovascular risk factors. Smoking, associated with changes in triglyceride-rich lipoprotein (TRL) concentrations and with both hypercoagulability and reduced fibrinolysis, was also analyzed as an environmental factor. Blood samples were obtained from 170 subjects (83 men and 87 women; mean age, 57 years; SD 15) recruited by random sampling from the census of Girona, Spain. Subjects were classified as current smokers (n=41) and nonsmokers or exsmokers (n=129). Whereas no differences were found in lipid and lipoprotein concentrations between smokers and nonsmokers in subjects with the PI(A1/A1) genotype, smokers with the PI(A1/A2) or PI(A2/A2) genotypes showed significantly higher triglyceride and very-low-density lipoprotein (VLDL) triglyceride concentrations than nonsmokers or exsmokers with the same genotypes. Similarly, the VLDL triglyceride/HDL cholesterol ratio was significantly different in subjects with the PI(A1/A2) or PI(A2/A2) genotypes stratified according to smoking status. Further analysis revealed a significant interaction between smoking and genotype when those homozygous for the allele PI(A1) were compared with one or two PI(A2) alleles for the three lipidic parameters. The observed effects appear to show links between smoking, triglyceride metabolism, and a glycoprotein involved in platelet aggregation. It is likely that the pI(A) polymorphism is in linkage disequilibrium with other functional mutations that might influence triglyceride metabolism under some environmental factors such as smoking. This finding may provide a new perspective in the complex relationship between glycoprotein IIIa gene, environment, and their interactions.

Adult↗
PubMed2001

Maternal serum triglyceride at 24--32 weeks' gestation and newborn weight in nondiabetic women with positive diabetic screens.

OBJECTIVE: To determine whether elevated midpregnancy maternal serum lipid levels predict newborn weight at term and the risk of large for gestational age (LGA) infants in women with positive diabetic screen but normal glucose tolerance test. METHODS: Japanese gravidas who had positive diabetic screens and normal 75-g oral glucose tolerance tests (GTT) at 24--32 weeks were enrolled. Subjects with complications, including diabetes, hypertension, or fetal anomalies were excluded, as were women with multifetal gestations. Fasting serum triglyceride, free fatty acids, and total cholesterol levels were measured at the time of GTT. We tested the association between maternal variables and birth weight by univariable analysis. We used multivariable analysis to test whether the association between fasting lipids and birth weight was independent of prepregnant maternal body mass index (BMI), maternal weight gain during pregnancy, and plasma glucose levels at GTT. We also used multiple logistic regression analysis to determine whether maternal hyperlipidemia, defined as more than the 75th percentile of each lipid, is a risk factor for having an LGA infant. RESULTS: We enrolled 146 subjects. Among measured maternal lipids, only triglyceride levels correlated with birth weight in univariable analysis (r = 0.22, P =.009). Birth weight also was correlated with prepregnant maternal BMI (r = 0.18, P =.04) and fasting plasma glucose levels (r = 0.17, P =.04). The association between maternal fasting triglyceride level and birth weight remained significant after adjusting for prepregnant BMI, maternal weight gain, fasting plasma glucose levels, fetal gender, and gestational age at birth (P =.01). Logistic regression analysis showed that fasting maternal hypertriglyceridemia (over 259 mg/dL) was the significant predictor of LGA infants, independent of prepregnant BMI, maternal weight gain, and maternal plasma glucose levels (odds ratio 11.6; 95% confidence interval 1.1, 122; P =.04). CONCLUSION: In women with positive diabetic screens but normal GTTs, fasting triglyceride levels at 24-32 weeks correlated positively with newborn weight at term, independent of maternal plasma glucose levels and obesity. Maternal fasting serum triglyceride levels in midpregnancy might be an independent predictor of fetal macrosomia in those women.

Adult↗
PubMed1998

Age-dependent changes and interrelations of number of cells and biochemical parameters (glucose, triglycerides, TBARS, calcium, phosphorus) in cultured human vein endothelial cells.

The aim of this study is to assess in human vein endothelial cells cultures the variations related to aging in: number of cells, glucose, triglycerides, thiobarbituric acid reactive substances (TBARS), calcium, phosphorus, cholesterol, total protein and urea and to analyze the relation of these parameters between themselves. Eight parallel flasks were subjected to the natural aging process, one of them without cells, analyzed at eight chronological stages. The determinations of biochemical parameters were performed in culture medium when it was changed. The number of cells, glucose, triglycerides and TBARS show significant variations during the aging process (P < 0.001). The glucose uptake per cell is maintained relatively constant in time (0.9 ng/cell day). A high linear correlation between glucose and the number of cells (r=0.935), triglycerides and the number of cells (r=0.505), triglycerides and decrease in number of cells (r=0.805) is observed. The measurement of glucose uptake seems to be an excellent method for the assessment of energetic cellular metabolism and, in certain conditions, can be used to estimate the number of cells. In the latest stages of aged cells a slight increase in glucose uptake has been observed. There is an increase of triglycerides and thiobarbituric acid reactive substances release during aging process.

Biological Transport, Active↗
PubMed1996

Triglyceride expression.

Current epidemiologic reports claim an important role for triglycerides in coronary artery disease (CAD). By cross-sectional data analysis, the role of triglycerides was assessed in 1726 consecutive patients investigated for chest pain, 1119 with CAD and 607 with normal coronaries. Besides study of male and female patients as separate groups, the males were divided into age groups of below 40 years, 41 to 50 years, 51 to 60 years and over 61 years. The female patients were divided into those below 50 years and over 51 years because of smaller numbers. Using the mean value for cholesterol, triglyceride, HDL cholesterol, LDL cholesterol and body mass index for normals as the demarcation line, logistic regression analysis was carried out to study their association in the patients with CAD and normals. Results showed that while the odds ratio for total cholesterol were higher for the younger age groups, the odds ratio for triglycerides were consistently higher for the groups over 51 years both male and female. It is speculated that there may be a difference in the relative importance of lipid fractions with reference to age in the development of atherosclerotic plaque with cholesterol playing a more important role in younger people and triglycerides being equally or more important in older people, on the basis of metabolic handling of lipid fractions.

Adult↗
PubMedDate not supplied

Triglyceride levels affect cognitive function in noninsulin-dependent diabetics.

Noninsulin-dependent diabetes mellitus (NIDDM) is associated with decrements in several cognitive functions. Among the variables that apparently contribute to the decline in cognitive performance is poor glucose control, as measured by hemoglobin A1c. Elevated levels of triglycerides in diabetics may also contribute to this cognitive decline through the increased incidence of atherosclerosis in these patients. The authors examined the relationship between triglycerides and cognitive performance in 246 NIDDM outpatients, aged 55-74 years. The relationship between triglyceride levels and performance on three cognitive tasks and on a test of reaction time was measured. Elevated levels of triglycerides were associated with significant decrements in performance on the digit symbol substitution test, digit span (backward) test, and on a reaction time measure. High levels of triglycerides, independent of chronic glucose control, appear to contribute to the decreased ability to perform short-term memory tasks in NIDDM.

Blood Glucose↗
PubMed2003

Examination of oral absorption and lymphatic transport of halofantrine in a triple-cannulated canine model after administration in self-microemulsifying drug delivery systems (SMEDDS) containing structured triglycerides.

The potential for lipidic self-microemulsifying drug delivery systems (SMEDDS) containing triglycerides with a defined structure, where the different fatty acids on the glycerol backbone exhibit different metabolic fate, to improve the lymphatic transport and the portal absorption of a poorly water-soluble drug, halofantrine, were investigated in fasted lymph cannulated canines. Two different structured triglycerides were incorporated into the SMEDDS; 1,3-dioctanoyl-2-linoleyl-sn-glycerol (C8:0-C18:2-C8:0) (MLM) and 1,3-dilinoyl-2-octanoyl-sn-glycerol (C18:2-C8:0-C18:2) (LML). A previously optimised SMEDDS formulation for halofantrine, comprising of triglyceride, Cremophor EL, Maisine 35-1 and ethanol was selected for bioavailability assessment. The extent of lymphatic transport via the thoracic duct was 17.9% of the dose for the animals dosed with the MLM SMEDDS and 27.4% for LML. Also the plasma availability was affected by the triglyceride incorporated into the multi-component delivery system and availabilities of 56.9% (MLM) and 37.2% (LML) were found. These data indicate that the pharmaceutical scientist can use the structure of the lipid to affect the relative contribution of the two absorption pathways. The MLM formulation produced a total bioavailability of 74.9%, which is higher than the total absorption previously observed after post-prandial administration. This could indicate the utility of disperse lipid-base formulations based on structured triglycerides for the oral delivery of halofantrine, and potentially other lipophilic drugs.

Administration, Oral↗
PubMed1987

Enzymes involved in triglyceride hydrolysis.

The lipolytic enzymes LPL and HL play important roles in the metabolism of lipoproteins and participate in lipoprotein interconversions. LPL was originally recognized to be the key enzyme in the hydrolysis of chylomicrons and triglyceride, but it also turned out to be one determinant of HDL concentration in plasma. When LPL activity is high, chylomicrons and VLDL are rapidly removed from circulation and a concomitant rise of the HDL2 occurs. In contrast, low LPL activity impedes the removal of triglyceride-rich particles, resulting in the elevation of serum triglycerides and a decrease of HDL (HDL2). Concordant changes of this kind in LPL and HDL2 are induced by many physiological and pathological perturbations. Finally, the operation of LPL is also essential for the conversion of VLDL to LDL. This apparently clear-cut role of LPL in lipoprotein interconversions is contrasted with the enigmatic actions of HL. The enzyme was originally thought to participate in the catalyses of chylomicron and VLDL remnants generated in the LPL reaction. However, substantial in vitro and in vivo data indicate that HL is a key enzyme in the degradation of plasma HDL (HDL2) in a manner which opposes LPL. A scheme is presented for the complementary actions of the two enzymes in plasma HDL metabolism. In addition, recent studies have attributed a role to HL in the catabolism of triglyceride-rich lipoproteins, particularly those containing apo E. However, this function becomes clinically important only under conditions where the capacity of the LPL-mediated removal system is exceeded. Such a situation may arise when the input of triglyceride-rich particles (chylomicrons and/or VLDL) is excessive or LPL activity is decreased or absent.

Animals↗
PubMed2003

Contribution of hepatic de novo lipogenesis and reesterification of plasma non esterified fatty acids to plasma triglyceride synthesis during non-alcoholic fatty liver disease.

BACKGROUND: Non-alcoholic fatty liver disease (NAFLD) is frequently observed in insulin-resistant subjects and can lead to liver fibrosis and cirrhosis. The abnormalities of lipid metabolism behind this development of excess hepatic TG stores are poorly understood. METHODS: To clarify these mechanisms we measured triglyceride secretion rate and the contributions of hepatic lipogenesis and reesterification of non-esterified fatty acids (NEFA) to this secretion in healthy subjects and in patients with clear evidence of NAFLD. All subjects were studied in the post-absorptive state. Hepatic lipogenesis was measured with deuterated water. NEFA turnover rate, triglyceride secretion rate and the contribution of NEFA reesterification to this secretion were determined with [1-(13)C] palmitate infusion. RESULTS: NAFLD patients had higher NEFA concentrations (p<0.05) but normal NEFA turnover rates (5.23 +/- 0.80 vs 5.91 +/- 0.97 micromol.kg(-1).min(-1) in control subjects, ns). Despite a trend for higher plasma triglyceride levels in patients (p<0.10), triglyceride turnover rates were not increased (0.11 +/- 0.01 micromol.kg(-1).min(-1) in patients vs 0.14 +/- 0.01 in controls, ns). However the contribution of hepatic lipogenesis to triglyceride secretion was largely increased in patients (14.9 +/- 2.7 vs 4.6 +/- 1.1% p<0.01) while that of NEFA reesterification was reduced (25.1 +/- 2.9 vs 52.8 +/- 6.2% p<0.01). CONCLUSION: Enhanced lipogenesis appears as a major abnormality of hepatic fatty metabolism in subjects with NAFLD. Therapeutic measures aimed at decreasing hepatic lipogenesis would therefore be the most appropriate in order to reduce hepatic TG synthesis and content in such patients.

Adult↗
PubMed1990

HPLC and GLC analysis of the triglyceride composition of bovine, ovine and caprine milk fat.

A total of 116 molecular species of triglycerides were identified in milk fat using a combination of HPLC and GLC. Triglyceride composition was predicted from the random composition, which was calculated on the basis of the mole fractions of the main fatty acids making up the total triglyceride fraction. The qualitative composition of the milk fat was similar in cows', ewes' and goats' milk. In all three milks the partition number of the main triglycerides was 46, but the proportions of the triglycerides with partition numbers of 34, 38, 42, and 48 exhibited substantial differences among the milks of the three species.

Animals↗