Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Diglycerides”

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 1,405 records · Page 78Linked to original sources
PubMed1988

[Hepatic lipid overload in 2 cases of cholestasis associated with parenteral feeding].

The authors report 2 cases of patients with ileal stenosis who developed progressive jaundice while receiving total parenteral nutrition including lipids (Intralipid). In both cases the histologic and histochemical study of the liver demonstrated lipid overload in Kupffer cells and to a lesser extent hepatocytes. Biochemical study established that linoleic acid, a component of Intralipid, associated with a digalactosyl-diglyceride from vegetal origin were the main components of the hepatic overload. The authors hypothesize that two associated mechanisms were responsible for jaundice in their patients: Kupffer cell dysfunction due, at least in part, to lipid overload and intestinal bacterial overgrowth leading to endotoxinemia.

Adult↗
PubMed1988

[Lipid metabolic indices in patients with the gastrointestinal form of food poisoning].

The serum concentration of some substances of lipid nature was studied in 103 patients with food toxinfections with relation to the severity of a course and period of the disease. The levels of cholesterol, triglycerides, diglycerides, nonesterified fatty acids (NEFA), and phospholipids were determined using thin-layer chromatography. A mild course of the disease was characterized by a slight rise of lipid concentration. Moderately severe courses were characterized by hyperlipidemia with an increase in the level of NEFA, lysophosphatidylcholine (LPC), phosphatidylcholine. Patients with a severe course demonstrated a decrease in the concentration of most lipid fractions with an increase in the amount of LPC and NEFA. All disorders were observed on the 1st-2nd day of the disease and disappeared against a background of routine rehydration therapy by the 5th-7th day of disease, in patients with a severe course of the disease by the 10th day.

Acute Disease↗
PubMed1977

Localization of a phosphoglycolipid in Mycoplasma membranes using specific anti-lipid-antibodies.

A phosphoglycolipid, presumably identical to glyceryl-phosphoryldiglycosyl diglyceride, is the main component of the membrane glycolipids of Mycoplasma mycoides subsp. capri. It is immunologically active. Anti-phosphoglycolipid antibodies were induced in rabbits by intravenous injection of the flocculated complexes of methylated bovine serum albumin with a mixture of the phosphoglycolipid and the auxiliary lipids, phosphatidyl-choline and cholesterol. The specificities of the antibodies directed against the phosphoglycolipid, are due to both the phosphate and carbohydrate moieties of the lipid molecule. Anti-phosphoglycolipid antibodies were detected in the sera of rabbits intravenously immunized with intact M. mycoides subsp. capri. The intravenous method of immunization was chosen in order to select for a response to surface antigenic determinants. Anti-phosphoglycolipid antibodies specifically reacted with intact organisms and isolated membranes of M. mycoides subsp. capri, as shown by complement fixation and agglutination tests. The antigenic determinants of the phosphoglycolipid are mainly located on the outer membrane surface. It is concluded that the antigenic determinants of the phosphoglycolipid in intact M. mycoides subsp. capri significantly contribute to the surface architecture of mycoplasma membranes.

Acholeplasma laidlawii↗
PubMed1987

Intestinal apoB synthesis, lipids, and lipoproteins in chylomicron retention disease.

Chylomicron retention disease is characterized by fat malabsorption, hypocholesterolemia, normal fasting triglycerides, and marked intestinal steatosis despite the presence of both plasma and intestinal apoprotein B. The defect remains unknown but presumably involves the synthesis or secretion of chylomicrons. The present investigation examines this hypothesis by studying the biosynthesis of chylomicrons in cultured jejunal explants and by defining the quantitative and qualitative abnormalities of plasma lipids and of circulating lipoproteins. Following 2-3 years of a low fat diet supplemented with medium chain triglycerides, six patients with chylomicron retention disease had significantly higher triglyceride (TG) levels coupled with a decrease in both free (FC) and esterified cholesterol (EC) as well as in essential fatty acids and phospholipids (PL) when compared to healthy controls. The low total plasma cholesterol was largely accounted for by low levels of both low density (LDL) and high density lipoprotein (HDL) cholesterol. VLDL and LDL were characterized by a diminished percentage of CE with an increase of TG while HDL contained relatively more FC as well as PL and less CE. The diameter of VLDL was larger whereas those of LDL and HDL were smaller than in normal controls. Jejunal explants, when incubated with [14C]palmitate, were capable of normal biosynthesis of TG, diglycerides, PL, and CE. These lipids, however, except for PL, were retained in the tissue and could not be secreted into the culture medium. Incubation of intestinal biopsies with [3H]leucine and [14C]mannose resulted in normal protein synthesis and reduced glycosylation. The presence of intestinal apoB-48 was confirmed by immunoblot using 2D8 antibodies. These data suggest that the intestinal defect in this disease results from a disorder of the final assembly of chylomicrons or in the mechanism of their exocytosis.

Apolipoproteins B↗
PubMed1987

Variability in the composition of human skin surface lipids in tropical climates.

Skin surface lipid samples were collected by the hexane sponge technique from the foreheads of 180 male and 131 female Saudi subjects living in the Jeddah-Makkah area (summer temperatures up to 47 degrees C). The lipid samples were analyzed by densitometric thin layer chromatography. Seven major lipid classes were determined. The percentages for squalene, cholesterol esters, wax esters, triglycerides, free fatty acids, cholesterol and diglycerides were determined. When these parameters were compared to the corresponding values reported for subjects living in the much cooler climates of Europe and N. America, most of the values for Saudi females were found very similar to the values of these subjects, while for Saudi males squalene and wax esters were 2.8-5.1% higher and the triglycerides/free fatty acids were 3-5% lower. The possible reasons for the observed variability between both sexes, their relation to European and N. American subjects, as well as the role of hot climates in inducing these variations are discussed.

Adolescent↗
PubMed1987

Effect of lipid-free milk on prostaglandin synthesis and lipid esterification in the young rabbit aorta.

The effect of lipid-free human milk on prostaglandin synthesis and lipid esterification by [14C]-arachidonic acid was examined in one week-old rabbit aortas, in vitro. In the presence of albumin, lipid-free milk increased arachidonic acid incorporation into aortic phospholipids, cholesterol esters and triglycerides but not into mono- and diglycerides. Lipid-free milk also increased the conversion of arachidonic acid into aortic 6-keto-PGF1 alpha, but not into PGF2 alpha or PGE2.

Animals↗
PubMed1987

Fatty acid modification of C3H 10T 1/2 fibroblast cells: changes in benzo(a)pyrene metabolism and phorbol ester binding.

The mouse embryo fibroblast cell line, C3H 10T 1/2 Cl8, was studied as an in vitro experimental model to investigate the mechanism and specificity behind the modulation of carcinogenesis by dietary lipid. The cells were grown in medium supplemented with 95 microM stearate, linoleate, or palmitate as fatty acid/albumin complexes, during which time they maintained normal growth and morphology characteristics. After 5 days of supplementation total cellular lipid fatty acid was enriched in the supplemented fatty acid. By Day 40, however, fatty acid profiles of all groups were the same. Cellular uptake and utilization of 14C-radiolabeled fatty acids were measured. Within 24 h of supplementation, label was incorporated into cholesterol and diglycerides, cholesterol ester, alkyldiacylglycerols, and phospholipids. Approximately half of the radiolabel was found in phosphatidylcholine. Supplementation significantly increased the rate of benzo(a)pyrene metabolism, but did not affect DNA modification by benzo(a)pyrene. Phorbol dibutyrate binding to C3H 10T 1/2 cells at 4 degrees C was modified by lipid supplementation. At 37 degrees C and 23 degrees C, phorbol dibutyrate binding was characterized by both high- and low-affinity sites for linoleate- and stearate-supplemented cells. At 4 degrees C high-affinity binding was absent in stearate- and palmitate-supplemented cells, but was maintained in linoleate-supplemented cells. These studies suggest that the unsaturated fatty acid content of the diet may not significantly affect the initiation stage of benzo(a)pyrene carcinogenesis, but may instead affect promotion. One possible mechanism for this could involve changes in the lipid microenvironment of membrane receptors involved in tumor promotion.

Animals↗
PubMed1987

Metabolic fate of radiolabeled palmitate in ischemic canine myocardium: implications for positron emission tomography.

Interpretation of dynamic and integrated myocardial tomograms requires elucidation of the biochemical fate of the tracer and characterization of its tissue distribution and rate of efflux. The fate of [1-11C] and [1-14C]palmitate was studied in 13 open-chest dogs during control or ischemic extracorporeal perfusion of the left circumflex coronary artery. Residue detection of myocardial radioactivity, and radio-biochemical analyses of sequential transmural biopsies and arterial and coronary venous effluent were performed for 30 min after intracoronary bolus administration of tracer. In control hearts, 10.3% of initially extracted tracer was retained in tissue (2.9% in triglyceride, 3.5% in phospholipid, and 3.9% in other lipid and aqueous fractions), 73.7% was oxidized, and 16.1% back-diffused unaltered. With ischemia (pump flow 10% of normal), 28.1% was retained (18% in triglyceride, 6.0% in phospholipid, and 4.1% in other lipid and aqueous fractions), 27.2% was oxidized, and 44.4% back diffused (p less than 0.05 compared to control). Throughout the 30-min study interval, triglyceride, diglyceride, and nonesterified fatty acid comprised a significantly greater fraction of initially extracted radioactivity in ischemic than in control hearts. Thus, during ischemia externally detected clearance rates cannot be used as a direct measure of fatty acid metabolism because of marked influences on efflux of nonmetabolized radiolabeled palmitate and the distribution of tracer retained in tissue. Quantitative measurements of specific metabolic processes by tomography will require development and validation of tracers confined to individual metabolic pathways or pools.

Animals↗
PubMed1986

Effect of the diabetic environment on the lipid metabolism of Ehrlich ascites cells.

One strain of Ehrlich ascites cells lacking of insulin receptors, was grown into control and diabetic mice and cells harvested from diabetic mice reimplanted into control mice. The fatty acid composition of neutral and polar lipids was analyzed and several parameters calculated. Results showed that it is possible to produce similar changes in the lipid fatty acid unsaturation of Ehrlich cells to those observed in the liver of the diabetic bearing mice. These changes may be reverted by growing these cells into control mice. The diabetic environment also promoted a relative increase in the radioactivity from incorporated in vitro into neutral lipids of Ehrlich cells. This metabolic adjustment, probably due to an induction of the enzyme diglyceride acyltransferase, was completely reverted by transplanting these cells in control mice. The metabolic adaptation of Ehrlich ascites cells to the diabetic environment did not modify their biological behaviour as pointed out by their mean generation time. The evidence presented here, showing relatively normal growth of Ehrlich cells in association with changes in the lipid fatty acid pattern and in lipid metabolism, indicates the adaptation of these cells, lacking of insulin receptors, to the environment provided by the diabetic mice.

Animals↗
PubMed1979

Increased synthesis of phosphatidylserine decarboxylase in a strain of Escherichia coli bearing a hybrid plasmid. Altered association of enzyme with the membrane.

A strain of Escherichia coli bearing a hybrid plasmid containing the psd gene, starved for isoleucine by the addition of valine, produces amounts of phosphatidyl-serine decarboxylase, a membrane-bound enzyme, about 40-fold higher than wild type. At least 98% of the enzyme from cells with high levels of decarboxylase is isolated in the inner, cytoplasmic membrane fraction if the cells are broken by osmotic lysis of spheroplasts following treatment with lysozyme/EDTA. In contrast, if cells containing these large amounts of enzyme are disrupted by sonication, 40 to 45% of the activity is recovered in the 100,000 times g supernatant fraction, whereas with wild type cells, only 5 to 10% is recovered in this fraction. About half of the decarboxylase in membranes saturated with the enzyme is thus only loosely bound, and readily removed by sonication, but not by osmotic lysis. This apparent saturation of the membrane with decarboxylase seems specific, since two other membrane-bound enzymes, phosphatidyl-glycerophosphate synthetase, and CDP-diglyceride synthetase, are not displaced into the supernatant fraction upon sonication. Fractionation on columns of agarose and by centrifugation through gradients of sucrose revealed that the decarboxylase in the supernatant is associated with lipid, in a complex with an apparent molecular weight of at least 5 times 10(6).

Carboxy-Lyases↗
PubMed1986

Release of pyrazolone derivatives from suppositories formulated with hydrophilic and hydrophobic bases.

The release and dissolution of aminophenazone and propyphenazone from suppositories prepared with Witepsol (H 15 and S 55), Suppocire (BM and AS 2), and macrogols 400 and 4000 placed in a small volume of water enclosed within a semipermeable wall, were followed by measuring the concentrations of dissolved drug that crossed the wall into an outside aqueous compartment. The rates of appearance of drugs in the outside compartment depended on their "affinities" to the bases, ascertained by determining the lipid/water partition coefficients. Propyphenazone had more "affinity" to less hydrophobic bases and was more slowly liberated from these; the opposite is true for aminophenazone. A higher proportion of mono- and diglycerides in Witepsol S 55 and Suppocire AS 2 influences the solubility of propyphenazone which was thereby liberated more easily than from Witepsol H 15 and Suppocire BM. The presence of polyethylene glycols in an aqueous solvent increased the solubilities of both drugs. On the other hand, marked solubilities in the bases cause slower liberation. With the macrogols, mixtures with a larger proportion of higher-molecular components turned out as better bases for propyphenazone suppositories, those with a smaller proportion of these components were more suitable for aminophenazone suppositories.

Aminopyrine↗
PubMed1985

[Intranuclear lipids in the late oocytes of the common frog].

The complex of chromosomes and nucleoli, constituting the karyosphere with a capsule, was removed micro-surgically from the late oocyte nuclei of Rana temporaria. Lipids of nuclei and of karyosphere were investigated using biochemical and autoradiographical methods in hormone-stimulated maturing oocytes in vitro. Neutral lipids (triglyceride, diglyceride, cholesterol ester) were found in the karyosphere substance by thin-layer chromatography. During oocyte maturation the incorporation of a precursor (3H-glycerol) into triglyceride was seen to increase much more than into lecithin. The autoradiography on the sectioned oocytes showed that the intranuclear level of 3H-glycerol was more densely distributed in the nucleolar zone over the material of a fibrous component of the karyosphere capsule. The level was also detected over the central part of the karyosphere in close proximity to the chromosomes. The involvement of lipids in organization of the complicated intranuclear complex of the karyosphere with a capsule is discussed. It is suggested that lipid accumulation in the area of the karyosphere fibrous component may reflect their functional relation with the oocyte nuclear matrix.

Animals↗
PubMed1985

Interaction of lipid vesicles with an heptoseless strain of Escherichia coli.

The conditions for uptake of lipid vesicles by the deep rough mutant of Escherichia coli, strain D21F2, and the parent strain, K12 were studied. A variety of lipids including phosphatidylcholine, phosphatidylethanolamine, diglyceride, cholesterol and palmitic acid were taken up much more readily by the deep rough mutant than the K12 strain. The uptake of lipid in the mutant strain was enhanced by Ca2+ at an optimal concentration of 2 mM, by alkaline pH and by growth of the cells up to the late exponential phase. With K12 cells, cholesterol and phosphatidylethanolamine were taken up from equimolar mixtures at similar rates thus suggesting the involvement of a fusion process. With D21F2 cells, the endogenous lipids of which had been labelled by growth in [3H] acetate, the uptake of exogenous [32P] phosphatidylethanolamine and [32P] lysophosphatidylethanolamine was not accompanied by a loss of endogenous lipid to the incubation medium. This precluded the involvement of an exchange mechanism. The absorbed exogenous lipid and the endogenous lipids of D21F2 cells displayed the same susceptibility to hydrolysis by added phospholipase C. This indicated that the exogenous lipid is inserted into lipid core of the membrane rather than adsorbed at the cell surface.

Calcium↗
PubMed1985

[Cell membrane and phospholipids].

After a short review of the structure of phospholipids, the authors describe the organisation of these compounds in the cell membrane and the metabolic pathways responsible for their degradation. The latter involve the phospholipases C and A2. The first enzyme is the key to practically all cellular activation because the specific hydrolysis of phosphatidylinositol--4,5-biphosphate generates two intracellular messengers, diglycerides and inositol--1,4,5-triphosphate which activate, respectively, a specific kinase and mobilise the calcium. This mobilisation of calcium is essential for the activation of the phospholipase A2 which regulates the liberation of arachidonic acid and lysophosphatidylcholine, precursors of different lipid mediators (prostaglandins, thromboxanes, leukotrienes, platelet activating factor or PAF-acether...). The production of these derivatives represents a system of amplification and recruitment outside the cell, explaining the possible involvement of these metabolic pathways in the physiological and pharmacological regulation of the different cells of the cardiovascular system (platelets, endothelial cells, smooth muscle cells...).

Arachidonic Acid↗
PubMed1986

Gentamicin-induced alterations in pig kidney epithelial (LLC-PK1) cells in culture.

The effect of gentamicin exposure was investigated in LLC-PK1 cells in culture. Gentamicin (0.5-2.0 mM) was added to the medium of cells which had been grown to confluency in the absence of antibiotics and antimycotics. Exposure to gentamicin (1-4 days) did not effect total cellular protein or DNA levels, total cell number or the release of various marker enzymes to the medium. ATP levels in gentamicin-treated cells did not differ from control cells; however, medium from the gentamicin-treated cells contained significantly lower lactic acid levels. Morphological examination by electron microscopy revealed gentamicin-elicited myeloid body formation. Furthermore, total phospholipid level was elevated markedly in gentamicin-treated cells. Analysis of specific phospholipid classes showed only phosphatidylcholine, phosphatidylinositol and polyphosphoinositide phospholipid levels increased in a time-dependent manner. Phosphatidylinositol showed the highest percentage of increase. Raising the normal medium calcium concentration (0.2 mg/ml) 1.5-, 2.0- or 3.0-fold did not alter gentamicin-induced elevation in cellular phosphatidylinositol and phosphatidylcholine. Gentamicin exposure also resulted in a concentration-dependent increase in the turnover of LLC-PK1 cell-free fatty acids, monoglyceride, diglyceride and nonesterified cholesterol and a decrease in triglyceride turnover. Calcium transport into and through the cell monolayer was inhibited markedly by gentamicin despite the fact that 45Ca++ binding to gentamicin-treated cells was greater. These results demonstrate that manifestations of gentamicin toxicity in LLC-PK1 cells parallel those reported in the whole animal thus making the LLC-PK1 cell in culture a valid system for elucidating the mechanism of gentamicin-elicited alterations in renal epithelium.

Animals↗
PubMed1986

The phospholipase A1 of Trypanosoma brucei does not release myristate from the variant surface glycoprotein.

[3H]Myristoyl-labeled variant surface glycoprotein (VSG) has been isolated from Trypanosoma brucei by reverse phase high performance liquid chromatography and used as substrate for the conversion by trypanosomal enzymes of membrane-form VSG to soluble VSG. Conversion is detected by the release of myristoyl-containing lipids. The major lipolytic enzyme of T. brucei, phospholipase A1, is effective for the hydrolysis of myristoyl esters of p-nitrophenol, in a colorimetric assay. However, the phospholipase is unable to cleave the myristoyl ester linkage of VSG. The phospholipase can be separated from the myristoyl-releasing activity of trypanosome homogenate by centrifugation, affinity chromatography, and anion-exchange chromatography. Elution profiles on anion-exchange high performance liquid chromatography also indicate that the phospholipase is inactive against VSG. A small amount of myristoyl-releasing activity associated with the purified phospholipase is probably due to contamination with a phosphodiesterase which releases myristoyl-containing diglyceride from VSG.

Animals↗
PubMed1985

Mechanism of autophosphorylation of the multifunctional Ca2+/calmodulin-dependent protein kinase.

The multifunctional Ca2+/calmodulin-dependent protein kinase purified from rat brain cytosol undergoes a self-phosphorylation or autophosphorylation reaction. Our conclusion that this reaction is autocatalytic is based on the following lines of evidence: The autophosphorylation reaction and the protein kinase activity toward other substrates are absolutely dependent on the presence of both Ca2+ and calmodulin; autophosphorylation and phosvitin kinase activity show a similar time course and indistinguishable heat lability; the reaction is a consistent property of every preparation of rat brain kinase; the reaction is present in both crude and highly purified preparations of similar kinases or isozymes from rat lung, spleen, heart, bovine brain, and a neuronal tissue from Aplysia californica, a marine mollusk; phosphorylation of the kinase subunits is not mimicked by addition of cAMP, cGMP, Ca2+ plus diglyceride, or addition of the cAMP-dependent protein kinase, and is not blocked by the heat-stable inhibitor protein of the cAMP-dependent protein kinase; and the reaction is intramolecular. Autophosphorylation results in the stoichiometric incorporation of phosphate into both the 51,000- and 60,000-dalton subunits.

Animals↗
PubMed1985

Metabolic fate of liposomal phosphatidylinositol in murine tumor cells: implications for the mechanism of tumor cell cytotoxicity.

The mechanism of the previously reported cytotoxicity of liposomes containing plant phosphatidylinositol (PI) against numerous tumor cell lines was examined in detail by using liposomes containing synthetic PI specifically labeled either with radioactive myo-inositol, or in the sn-2 position with radioactive linoleic acid, oleic acid, or arachidonic acid. The uptake of liposomal PI by N4TG1 neuroblastoma cells increased with time and was dependent on the nature of the fatty acids. Uptake was highest with liposomal PI containing linoleic acid followed by arachidonic acid and then by oleic acid. The cellular fate of liposomal PI was determined by analysis of radioactive metabolites present in extracts of tumor cell lipids. Appearance of liposomal PI metabolic products in the tumor cells was correlated with thymidine uptake as a measure of viability. After 3 h incubation of cells with PI liposomes it was found that the release of both radioactive liposomal fatty acids (and probably also lyso-Pl) and radioactive diglycerides was correlated inversely with the cellular uptake of [methyl-3H]thymidine and uptake of [3H]myoinositol. An experiment in which liposomes were prepared both from animal Pl which contained predominantly saturated fatty acids in the sn-2 position and an increasing mole fraction of a synthetic Pl containing radioactive linoleic acid in the sn-2 position established that the amount of Pl containing linoleic acid in the sn-2 position could be correlated with a decrease in the amount of thymidine uptake by tumor cells. The above results clearly established that phospholipases A2 and C in the tumor cells were responsible for the formation of metabolites of liposomal Pl, and these metabolic products might have been responsible for cytotoxicity and cell death.

Animals↗