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At least 1,369 records · Page 76Linked to original sources
PubMed1976

Effect of insulin on plasma triglyceride concentration in hepatectomized geese.

The effect of insulin on the removal of plasma triglycerides was tested in hepatectomized geese. In this preparation plasma triglyceride concentration decreases exponentially following hepatectomy. Infusion of insulin (0.001 U/kg/min. for 60 minutes) had no significant effect on the rate of disappearance of plasma triglycerides in the hepatectomized animals. The conclusion is, therefore, reached that insulin does not affect the removal of plasma triglycerides by the extrahepatic tissues in the goose.

Adipose Tissue↗
PubMed1998

[Is antihypertensive treatment a risk factor of coronary disease? Therapy-related triglyceride increase nor diabetes increase the risk].

In an observational study designed to determine whether metabolic changes during long-term antihypertensive drug treatment are associated with an increased risk of coronary heart disease (CHD), 686 middle-aged hypertensive men recruited from a random population screening sample were followed up for 15 years. Antihypertensive treatment predominantly consisted of beta-adrenoceptor blockers and/or thiazide diuretics. CHD and diabetes mellitus were checked for at annual examinations. Time-dependent Cox regression analysis was used to determine correlation between the incidence of CHD and entry characteristics, the monitored serum levels of cholesterol and triglyceride concentrations and the development of diabetes mellitus. Univariate analysis showed the presence of diabetes mellitus a entry to the study and increased baseline serum concentrations of cholesterol and of triglycerides each to be a significant predictor of CHD, the respective relative risks (RR) being 2.12, 1.21 and 1.21. However, analysis of monitored levels of metabolic variables during follow-up showed only an increased serum cholesterol concentration to be significantly and independently associated with CHD (RR 1.07). Although serum triglyceride concentrations increased slightly during follow-up, they were unrelated to the incidence of CHD; nor was onset of diabetes mellitus during follow-up significantly associated with an increased risk of CHD (RR 1.48. Thus, the study showed the presence of metabolic disturbances such as diabetes mellitus and hyperlipidaemia before the start of antihypertensive treatment to be of positive predictive value in middle-aged hypertensive men, and an increase in the monitored serum cholesterol level to be an independent predictor of CHD, whereas neither drug-related diabetes nor an increase in the monitored serum triglyceride concentration seemed to be associated with the occurrence of CHD.

Adrenergic beta-Antagonists↗
PubMed1998

Evidence that microsomal triglyceride transfer protein is limiting in the production of apolipoprotein B-containing lipoproteins in hepatic cells.

The microsomal triglyceride transfer protein (MTP) is a heterodimeric lipid transfer protein that is required for the assembly and secretion of apolipoprotein B (apoB)-containing lipoproteins. A key unresolved question is whether the MTP-mediated step is rate limiting. To address this, a unique experimental strategy was used that allowed the in situ modulation and measurement of MTP triglyceride transfer activity. In order to accomplish this, an irreversible photoaffinity inhibitor, BMS-192951, was designed and synthesized. When incubated with purified MTP and irradiated with UV light at 360 nm, BMS-192951 inhibits triglyceride transfer by covalently binding to the protein. HepG2 cells were treated with either increasing concentrations of BMS-192951 (0-15 microM) with 5 min of ultraviolet irradiation, or 3.0 microM BMS-192951 with various lengths (0-15 min) of ultraviolet irradiation. Microsomal extracts were prepared exhaustively dialyzed to remove unbound inhibitor, and assayed for MTP-mediated triglyceride transfer activity. BMS-192951 was shown to reduce MTP activity in both a dose- and UV exposure time-dependent fashion. Measurement of apoB concentration in the media showed that apoB secretion was reduced in proportion to the in situ inhibition of MTP activity, while no change was observed in apoA-I secretion. Experiments performed in McArdle RH-7777 rat hepatoma cells and primary rat hepatocytes gave nearly identical results; the decrease in apoB secretion was proportional to the decrease in MTP activity. These results indicate that MTP-mediated lipid transfer is limiting in the assembly and secretion of apoB-containing lipoproteins in hepatic cells under the conditions tested.

Affinity Labels↗
PubMedDate not supplied

[Effects of adrenalectomy and cortisol administration on the concentration of free fatty acids, triglycerides and total lipids on the liver of rats].

The hepatic concentration of triglycerides, free fatty acids and total lipids was determined in four groups of rats: normals, adrenectomized and normal and adrenectomized previously treated with cortisol, 30 mg. In chronic adrenectomized state, total lipids and hepatic triglycerides are diminished, particularly the triglycerides. Adrenectomy does not appear to have significative effect on the free fatty acids. The administration of cortisol does not change those observations and, when given to normal animals, decreases the hepatic concentrations of free fatty acids, triglycerides and total lipids.

Adrenalectomy↗
PubMed1976

Evaluation of three commercially available menual "kit" methods for triglycerides in serum.

We compared three commercially available kits for use in determining triglycerides (triacylglycerols) in serum, by different methods, for accuracy and precision, with use of pooled sera of low, normal, and high triglyceride concentrations. Accuracy varied from -17% to +16% of the independently determined value, depending on the method and triglyceride concentration. In general, the Calbiochem method was the most nearly accurate, and only it met Center for Disease Control criteria for precision at all three triglyceride concentrations. The relationships of mean values to the suggested normal range for each method varied, some significant differences being found. Our data demonstrate the importance of a correlation between the independently determined value and the normal range for the method used and stresses the need for normal-range values to accompany all patients' reports.

Evaluation Studies as Topic↗
PubMed1987

Stimulation of myocardial neutral triglyceride lipase activity by adenosine-3':5'-monophosphate: involvement of glycogenolysis.

Endogenous lipolysis can be influenced by various hormones. Hormonal stimulation of endogenous lipolysis in the Langendorff heart was diminished by inhibition of glycogenolysis. Therefore we studied the influence of glycogenolysis on the cAMP-dependent activation of the neutral triglyceride lipase activity using a 40,000 X g post mitochondrial supernatant fraction from rat heart homogenates. In the presence of cAMP and ATP neutral triglyceride lipase activity was stimulated by 40%. This stimulation could not be detected in supernatants from which glycogen was removed after incubation in the presence of amyloglucosidase. Addition of glycogen overcomes this loss of stimulation. The activation of neutral triglyceride lipase by cAMP and ATP was mimicked by glucose plus ATP as well as by glycerol-3-phosphate but not by glyceraldehyde-3-phosphate. Moreover, the cAMP stimulation of neutral triglyceride lipase activity was suppressed by low amounts of palmitoyl-CoA indicating product inhibition of lipase activity. These results indicate that the level of intracellular precursors of fatty acid re-esterification, by determining the removal rate of product fatty acids, may be the major determinant of the stimulation of lipolysis by cAMP.

Animals↗
PubMed1977

Hepatic triglyceride lipase deficiency in liver disease.

The activity of post-heparin lipases in patients with alcoholic hepatitis and viral hepatitis was evaluated. Lipoprotein lipase and hepatic triglyceride lipase were differentiated by assay under high and low salt conditions and also by separation on heparin-agarose affinity chromatography columns. The mean activity of hepatic triglyceride lipase in the sera of liver disease patients was only 21-24% of the mean of controls, but lipoprotein lipase in patients' sera was not different from normal levels. Hepatic triglyceride lipase deficiency may partially account for the accumulation of a triglyceride-rich low density lipoprotein in liver disease.

Alcoholism↗
PubMedDate not supplied

A comparative study of human tissue and post-heparin plasma triglyceride lipases.

Human post-heparin plasma contains at least two different triglyceride lipases (TGL). The plasma lipolytic activity has been attributed to extra-hepatic and hepatic origin. Both post-heparin triglyceride lipases were partially purified and characterized. With heparin-Sepharose 4 B affinity chromatography it was possible to partially purify human adipose tissue lipoprotein lipase (LPL) as well as a lipase from human liver. The effects of NaCl, pre-heparin plasma, pH and temperature on these two tissue lipases and plasma lipases were studied in parallel. Antibodies were produced against plasma hepatic triglyceride lipase (plasma H-TGL) that did not cross react with LPL. TGL activity of human liver was completely inhibited by antibodies against plasma H-TGL. From these results it appears that human post-heparin plasma contains two triglyceride lipase activities which originate from liver and extra-hepatic tissues such as adipose tissue.

Adipose Tissue↗
PubMed2000

Evidence that triglycerides are an independent coronary heart disease risk factor.

In the past, the relation between hypertriglyceridemia and coronary heart disease (CHD) has been uncertain. However, a recent multivariate analysis of 8-year follow-up data from the large-scale Prospective Cardiovascular Münster study found hypertriglyceridemia to be an independent risk factor for major coronary events after controlling for low-density lipoprotein (LDL) and high-density lipoprotein (HDL) cholesterol. Hypertriglyceridemia combined with elevated LDL cholesterol and high LDL:HDL cholesterol ratio (>5) increased the CHD event risk by approximately sixfold. Similarly, a large meta-analysis of 17 prospective trials reported hypertriglyceridemia to be an independent risk factor for cardiovascular disease. In this study, an 88 mg/dl (1.0 mmol/L) increase in plasma triglyceride levels significantly increased the relative risk of cardiovascular disease by approximately 30% in men and 75% in women; the corresponding rates were somewhat lower (14% and 37%) but still statistically significant after adjustment for HDL cholesterol level. These data and observations from patients in the Helsinki Heart Study and the Stockholm Ischemic Heart study, that the greatest coronary benefit during lipid-lowering drug therapy occurred among hypertriglyceridemic patients, argue strongly for an independent role for hypertriglyceridemia in CHD risk. In the recent Veterans Affairs Cooperative Studies Program High-Density Lipoprotein Cholesterol Intervention Trial, the use of gemfibrozil to raise HDL cholesterol levels and lower levels of triglycerides without lowering LDL cholesterol levels reduced coronary events in men with established CHD, whereas preliminary results from the Bezafibrate Infarction Prevention Trial indicate a reduction in coronary end points in patients with elevated baseline triglyceride levels. To achieve the greatest possible reduction in CHD risk, antihyperlipidemic treatment strategies should also be aimed at reducing elevated triglycerides.

Adult↗
PubMed2002

Differential effects of dietary flaxseed protein and soy protein on plasma triglyceride and uric acid levels in animal models.

The effect of dietary soy protein and flaxseed meal on metabolic parameters was studied in two animal models, F344 rats with normal lipid levels and obese SHR/N-cp rats with elevated levels of cholesterol and triglyceride. The rats were fed AIN 93 diet differing only in the source of protein. The rats were fed either 20% casein, 20% soy protein or 20% flaxseed meal. Plasma was analyzed for cholesterol, triglyceride, uric acid, blood urea nitrogen (BUN), creatinine and total protein. In both strains of rats, flaxseed meal significantly decreased plasma cholesterol and triglyceride concentrations. The effect of soy protein on lipids was not as striking as that of flaxseed meal. Flaxseed meal also lowered uric acid in F344 rats and BUN in SHR/N-cp rats. Since cholesterol, triglyceride and uric acid are independent risk factors for cardiovascular disorders, our data show that both flaxseed meal and soy protein may have beneficial effects. Which chemical constituent(s) of flaxseed meal or soybean is (are) responsible for the beneficial effects need to be identified.

Journal Article↗
PubMed1984

Thermal behavior of cores of human serum triglyceride-rich lipoproteins: a study of induced circular dichroism of beta-carotene.

Induced circular dichroism (CD) of beta-carotene has been used to study the physical state in the cores of three classes of triglyceride-rich lipoproteins from human serum: intermediate-density lipoproteins (IDL) (1.006 less than d less than 1.019 g/mL) and subfractions of the d less than 1.006 g/mL lipoproteins of beta and pre-beta electrophoretic mobility. Effects on the physical state in the cores attributable to the ratio of triglycerides to cholesteryl esters and particle diameters were assessed by comparing the temperature-dependent CD spectra of beta-carotene with those of low-density lipoproteins (LDL). Lipoproteins were prepared from serum by sequential ultracentrifugation after the donors were given supplemental dietary beta-carotene (60 mg/day) for 2 weeks. The beta- and pre-beta-migrating d less than 1.006 g/mL lipoproteins were separated by starch block electrophoresis and were then individually separated into subfractions by agarose gel filtration chromatography. Between 7 and 30 degrees C, four subfractions of the beta-migrating d less than 1.006 g/mL lipoproteins and IDL exhibited reversible, temperature-dependent induced CD of beta-carotene, with contours similar to those of LDL but with smaller magnitudes and much broader transitions of the CD bands than those of LDL. In contrast, subfractions of the pre-beta-migrating d less than 1.006 g/mL lipoproteins showed no detectable induced CD of beta-carotene. These results show that the cores of triglyceride-rich lipoproteins can exist in some ordered state between 7 and 30 degrees C if they have a relatively low ratio of triglycerides to cholesteryl esters (mass ratio less than 1.6) and relatively small particle diameter (less than 60 nm).

Carotenoids↗
PubMed1995

COOH-terminal disruption of lipoprotein lipase in mice is lethal in homozygotes, but heterozygotes have elevated triglycerides and impaired enzyme activity.

The role of the enzyme lipoprotein lipase (LPL) in atherosclerosis is uncertain. To generate an animal model of LPL deficiency, we targeted the LPL gene in embryonic stem cells with a vector designed to disrupt the COOH terminus of the protein and used these cells to generate LPL-deficient mice. Germ line transmission of the disrupted LPL allele was achieved with two chimeric males, and offspring from each of these animals were phenotypically identical. Pups homozygous (-/-) for LPL deficiency died within 48 h of birth with extreme elevations of serum triglycerides (13,327 mg/dl) associated with essentially absent LPL enzyme activity in heart and carcass. Newborn heterozygous (+/-) LPL-deficient pups had lower LPL enzyme activity and higher triglycerides (370 versus 121 mg/dl) than wild type (+/+) littermates. Adult heterozygotes had higher triglycerides than wild type mice with ad libitum feeding (236 mg/dl for +/- versus 88 mg/dl for +/+) and after fasting for 4 h (98 mg/dl for +/- versus 51 for +/+) or 12 h (109 mg/dl for +/- versus 56 mg/dl for +/+). Triglycerides were present as very low density lipoprotein particles and chylomicrons, but high density lipoprotein cholesterol levels were not decreased in +/- animals. Plasma heparin-releasable LPL activity was 43% lower in +/- versus +/+ adult animals. LPL activity, mRNA, and protein were lower in the tissues of +/- versus +/+ mice. Homozygous LPL deficiency caused by disruption of the COOH terminus of the enzyme is lethal in mice. Heterozygous LPL deficiency caused by this mutation is associated with mild to moderate hypertriglyceridemia without affecting static HDL cholesterol levels. Heterozygous LPL-deficient mice could be useful for determining if hypertriglyceridemia, independently or in combination with other discrete defects, influences atherosclerosis.

Animals↗
PubMed2000

A mechanism of membrane neutral lipid acquisition by the microsomal triglyceride transfer protein.

The microsomal triglyceride transfer protein (MTP) and apolipoprotein B (apoB) belong to the vitellogenin (VTG) family of lipid transfer proteins. MTP is essential for the intracellular assembly and secretion of apoB-containing lipoproteins, the key intravascular lipid transport proteins in vertebrates. We report the predicted three-dimensional structure of the C-terminal lipid binding cavity of MTP, modeled on the crystal structure of the lamprey VTG gene product, lipovitellin. The cavity in MTP resembles those found in the intracellular lipid-binding proteins and bactericidal/permeability-increasing protein. Two conserved helices, designated A and B, at the entrance to the MTP cavity mediate lipid acquisition and binding. Helix A (amino acids 725-736) interacts with membranes in a manner similar to viral fusion peptides. Mutation of helix A blocks the interaction of MTP with phospholipid vesicles containing triglyceride and impairs triglyceride binding. Mutations of helix B (amino acids 781-786) and of N780Y, which causes abetalipoproteinemia, have no impact on the interaction of MTP with phospholipid vesicles but impair triglyceride binding. We propose that insertion of helix A into lipid membranes is necessary for the acquisition of neutral lipids and that helix B is required for their transfer to the lipid binding cavity of MTP.

Amino Acid Sequence↗
PubMed1990

Lipoprotein electrophoresis differentiation of chylous and nonchylous pleural effusions in dogs and cats and its correlation with pleural effusion triglyceride concentration.

Pleural effusions from 23 dogs and 25 cats hospitalized between November 1986 and April 1987 at the Veterinary Hospital of the University of Pennsylvania (VHUP) were classified as chylous (chylomicrons present) or nonchylous (chylomicrons absent) by the presence or absence, respectively, of a chylomicron band on lipoprotein electrophoresis gels of the effusions. Triglyceride concentrations, cholesterol concentrations, and cholesterol/triglyceride (C/T) ratios were compared between the chylous and nonchylous groups in each species. Cholesterol concentrations were not significantly different between chylous and nonchylous effusions in both dogs and cats. Cholesterol/triglyceride ratios of less than 1 were present in all dogs and cats with chylous effusions; however, 12% of dogs with nonchylous effusions and 50% of cats with nonchylous effusions also had a C/T ratio less than 1. Triglyceride concentrations accurately classified all effusions as chylous or nonchylous in both dogs and cats. Pleural effusions with triglyceride concentrations greater than l00 mg/dl were chylous in all cases, whereas, effusions with triglyceride concentrations less than l00 mg/dl were nonchylous in all cases.

Journal Article↗
PubMed1984

Bioconversion of xylan to triglycerides by oil-rich yeasts.

A series of lipid-accumulating yeasts was examined for their potential to saccharify xylan and accumulate triglyceride. Of the genera tested, including Candida, Cryptococcus, Lipomyces, Rhodosporidium, Rhodotorula, and Trichosporon, only Cryptococcus and Trichosporon isolates saccharified xylan. All of the strains could assimilate xylose and accumuate triglyceride under nitrogen-limiting conditions. Strains of Cryptococcus albidus were found to be especially useful for a one-step saccharification of xylan coupled to triglyceride synthesis. Cryptococcus terricolus, a strain constitutive for lipid accumulation, lacked extracellular xylanase, but did assimilate xylose and xylobiose and was able to continuously convert xylan to triglyceride if the culture medium was supplemented with xylanase.

Journal Article↗
PubMed1986

Secretion of triglyceride lipase from rat hepatocytes in culture: modulation by insulin and phenobarbital.

Hepatic triglyceride lipase (HTGL) was measured in primary rat hepatocytes maintained for 3 days under three different culture conditions: basal medium, basal medium plus insulin, and basal medium plus insulin and phenobarbital. The activity of HTGL secreted by these cells was measured by treating intact cells with heparin; intracellular enzyme was subsequently measured in cell homogenates. Insulin stimulated intracellular triglyceride lipase activity by 48% and extracellular lipase by 30%. Phenobarbital, an enzyme-inducing drug, caused a further 15% increase in extracellular hepatic triglyceride lipase; whereas, the intracellular activity was reduced. The presence of insulin greatly stimulated the rate of enzyme secretion, and this rate was not notably affected by the presence of phenobarbital. After 3 days in culture, the short term (2-8 h) synthesis and secretion of enzyme from cultures treated with insulin or insulin plus phenobarbital were equally inhibited by cycloheximide. Monensin also inhibited enzyme secretion in both cultures and caused a similar increase in intracellular lipase activities. Insulin did not significantly affect the proportion of intracellular enzyme (17.7% basal vs. 15.8% insulin). On the other hand phenobarbital produced a 20-30% reduction in the proportion of intracellular enzyme (12.5 vs. 17.7% basal or 15.8% insulin). These findings suggest a drug-induced redistribution of triglyceride lipase.

Animals↗
PubMed1976

Lipoprotein lipase and uptake of chylomicron triglyceride by skeletal muscle of rats.

Uptake of chylomicron triglyceride and lipoprotein lipase was studied in red and white skeletal muscles, heart, and adipose tissue of rats. Retention of triglyceride fatty acids 10 min after injection was 1.6%/g in heart and adipose tissue, 0.2-0.4%/g in red (soleus and diaphragm) muscles, and 0.1%/g in white (psoas minor) muscles of fed rats. Fasting (24 h) increased retention two- to fourfold in red skeletal muscles and heart, had no effect in white muscles, and decreased retention greater than 75% in adipose tissue. Lipoprotein lipase activity in fed rats was lowest in white muscles and in certain red (posterior belly of digastric and medial head of triceps brachii) musclws, intermediate in soleus and diaphragm muscles and adipose tissue, and highest in heart. Fasting doubled lipoprotein lipase activity in all red skeletal muscles and heart, had no effect in white muscles, and decreased activity 60% in adipose tissue. The findings indicate that triglyceride uptake is related to lipoprotein lipase activity in skeletal muscle and the changes in enzyme activity during fasting divert blood triglyceride to red skeletal muscles.

Animals↗
PubMedDate not supplied

Neutral triglyceride lipase in macrophages.

High levels of neutral triglyceride lipase activity have been demonstrated in several types of macrophages (J774 cells, human monocyte/macrophages, rabbit alveolar macrophages, and resident mouse peritoneal macrophages). The pH optima ranged from 6.5 to 7.4 depending upon the buffer and the conditions of incubation. The addition of bovine serum albumin stimulated activity at low concentrations, as expected for a fatty acid-releasing reaction, but strongly inhibited at higher concentrations; maximal activity was observed in the presence of 0.625 mg/ml of bovine serum albumin. The enzyme was remarkably thermostable, showing no apparent loss of activity at 50 degrees C for as long as 6 hours. The lipase was inhibited 80% by 0.1 M NaCl. Assayed under optimal conditions, the specific activity of the neutral triglyceride lipase from J774 cells was more than 100-fold greater than the activity of lipoprotein lipase or neutral cholesterol esterase from those cells; this activity was 10-fold greater than the levels of hormone-sensitive lipase from 3T3-L1 adipocytes. This neutral triglyceride lipase may play an important role in the degradation and mobilization of cytosolic triglyceride in macrophage-derived foam cells.

Animals↗