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PubMed1991

Dual pathways for agonist-stimulated arachidonic acid release in pancreatic acini: roles in secretion.

The present experiments were performed to determine pathways responsible for arachidonic acid release stimulated by cholecystokinin (CCK) and phorbol ester, 4 beta-phorbol 12-myristate 13-acetate (PMA), and the roles of pathways in the secretory response in dispersed acini from guinea pig pancreas. Both CCK-octapeptide (CCK-OP) and PMA increased intracellular arachidonic acid. To determine the source of released arachidonic acid, we measured the effects of PMA and CCK-OP on cellular 1,2-diacylglycerol and lysophosphatidylcholine (LPC) and of diglyceride lipase inhibitor RHC 80267 on [3H]arachidonic acid release. Both PMA and CCK-OP increased 1,2-diacylglycerol and LPC. RHC 80267 had no effect on LPC but inhibited the increase in [3H]arachidonic acid release with a concentration of CCK-OP that was maximal for enzyme secretion. The increase in [3H]arachidonic acid release with PMA or a supramaximal concentration of CCK-OP was not inhibited by RHC 80267. In parallel fashion, RHC 80267 inhibited amylase release caused by maximally effective concentrations of CCK-OP but not that caused by PMA or by supramaximally effective concentrations of CCK-OP. Arachidonic acid stimulated amylase release. Exogenous addition of phospholipase A2 caused increases in [3H]arachidonic acid release, LPC formation, and amylase release. The results indicate that there are at least two pathways responsible for the increase in free cellular arachidonic acid stimulated by pancreatic agonists. One is sequential action of phospholipase C and diglyceride lipase on phosphatidylinositol. The other is a phospholipase A action on phosphatidylcholine. The results also suggest a stimulatory role for both pathways in the secretory response.

Amylases↗
PubMed1985

Effects of vasopressin on phosphoinositides and prostaglandin production in cultured mesangial cells.

We studied the effects of vasopressin on phospholipid metabolism in mesangial cells and the temporal relationship of these changes to prostaglandin production. The changes included: 1) increased breakdown of phosphatidylinositol (PI), 2) increased breakdown of diphosphoinositide (PI-P) and triphosphoinositide (PI-P2), 3) an increase in the mass of diglyceride and phosphatidic acid, 4) increased synthesis, first of PI-P and PI-P2, then phosphatidic acid, and, finally, PI, and 5) increased water-soluble inositol phosphates. Vasopressin treatment resulted in a significant increase (90%) in the mass of phosphatidic acid and a smaller (13%) decline in the mass of PI. Changes in diglyceride were seen following 45 s of treatment with vasopressin. Alterations of phosphoinositide metabolism were seen as early as 45 s and continued for up to 5 h following hormone exposure. By contrast, prostaglandin production declined after 30 min. These observations on vasopressin-stimulated metabolism in cultured mesangial cells may provide a basis for an understanding of the functional changes that follow hormone exposure.

Animals↗
PubMed1994

Effects of glucose on sorbitol pathway activation, cellular redox, and metabolism of myo-inositol, phosphoinositide, and diacylglycerol in cultured human retinal pigment epithelial cells.

Sorbitol (aldose reductase) pathway flux in diabetes perturbs intracellular metabolism by two putative mechanisms: reciprocal osmoregulatory depletion of other organic osmolytes e.g., myo-inositol, and alterations in NADPH/NADP+ and/or NADH/NAD+. The "osmolyte" and "redox" hypotheses predict secondary elevations in CDP-diglyceride, the rate-limiting precursor for phosphatidylinositol synthesis, but through different mechanisms: the "osmolyte" hypothesis via depletion of intracellular myo-inositol (the cosubstrate for phosphatidylinositol-synthase) and the "redox" hypothesis through enhanced de novo synthesis from triose phosphates. The osmolyte hypothesis predicts diminished phosphoinositide-derived arachidonyl-diacylglycerol, while the redox hypothesis predicts increased total diacylglycerol and phosphatidic acid. In high aldose reductase expressing retinal pigment epithelial cells, glucose-induced, aldose reductase inhibitor-sensitive CDP-diglyceride accumulation and inhibition of 32P-incorporation into phosphatidylinositol paralleled myo-inositol depletion (but not cytoplasmic redox, that was unaffected by glucose) and depletion of arachidonyl-diacylglycerol. 3 mM pyruvate added to the culture medium left cellular redox unaltered, but stimulated Na(+)-dependent myo-inositol uptake, accumulation, and incorporation into phosphatidylinositol. These results favor myo-inositol depletion rather than altered redox as the primary cause of glucose-induced aldose reductase-related defects in phospholipid metabolism in cultured retinal pigment epithelial cells.

Aldehyde Reductase↗
PubMed1982

Fine-structural changes in rat liver microsomes treated with phospholipase C.

Phospholipase C hydrolyses 50% of the phospholipids of rat liver microsomes. Our previous observations suggest that the hydrolysis is of the outer leaflet of the membrane bilayer. In the present investigation the products of hydrolysis and effect of phospholipase C treatment on the morphology of total, rough and smooth microsomes were investigated. The only product of phospholipase C treatment of microsomes was diglyceride. After hydrolysis of half the phospholipid, the microsomes retained their vesicular structure; however, the average diameter of total and smooth microsomes was reduced by approximately half, and that of rough microsomes by a third. Profiles were observed that suggested that small vesicles may form by pinching off from large vesicles. About 10-15% of the phospholipase-treated microsomes had associated with them an amorphous droplet yielding a 'signet-ring'-like structure. The rest of the vesicle membrane retained a bilayer structure. About 10-15% of the treated vesicles adhered in groups of two or three. In these groups the shared membrane was trilaminar. Freeze-fracture replicas of phospholipase C-treated microsomes exhibited a similar morphology to untreated microsomes having both concave and convex surfaces, the former exhibiting a greater density of intramembranous particles. These observations suggest that microsomal vesicles remain closed after treatment with phospholipase C and that the bilayer structure is retained. However, there are morphological changes that are possibly related to maintaining the stability of the membranes in which the outer leaflet consists essentially of diglyceride.

Animals↗
PubMedDate not supplied

Binding of antibodies onto the thylakoid membrane. I. Maximal antibody binding and adsorption of antibodies to lipids.

The binding of antibodies onto the lamellar system of Antirrhinum majus was determined in dependence on the serum addition. The unspecific adsorption of serum proteins was taken into account or eliminated. The binding of antibodies as a function of the amount of serum added is seem from a saturation curve. From an antiserum obtained by hyperimmunization with stroma-freed chloroplasts, the chloroplasts bind maximally 1 gram antibodies per gram stroma-freed chloroplasts. From an antiserum to the proteins of the thylakoid membrane prepared in the same way an equal amount of antibodies is adsorbed. It is assumed that with this amount the surfaces of the lamellar system accessible to antibodies is completely covered by antibodies. For an antiserum to monogalactosyl diglyceride a maximal antibody binding of 0.16 g, for sulphoquinovosyl diglyceride 0.12 g and for phosphatidyl glycerol 0.13 of antibodies per gram stroma-freed chloroplasts are obtained. The significance of these results with respect to the molecular surface structure of the thylakoid membrane is discussed.

Agglutination↗
PubMed1980

[Effect of lipid normalizers (clofibrate and procetofene) on chylomicron metabolism in rats].

Clofibrate (250 mg/kg/day) and Procetofene (100 mg/kg/day) feedings determine a significant increase of the rat liver weight. After intravenous injection in treated and control rats of doubly labelled chylomicrons ([14C] glycerol and [3H] oleic acid) an enhancement of radioactive triglyceride hydrolysis was observed in the treated groups. The oxidation of exogenous oleic acid was increased by both drug feeding. Alterations of liver and blood lipids (especially large amounts of labelled diglycerides in the blood) could be probably related to the inhibition of the diglyceride acyltransferase in the liver.

Animals↗
PubMed1976

[Structure, amount and composition of sulfuric, sulfonic and phosphoric esters of glycosyldiglycerides of three fucacea].

The mono and polyester glycosyl sulfates or phosphate diglycerides account for a group of polar lipids which is found in large amounts in the three fucacae that are studied: Pelvetia canaliculata (L) Deen and Thur, Fucus vesiculosus (L), Fucus serratus (L). These polar lipids have been shown to have complex structures, most of them are unknown in the present nomenclature. Both quantity and composition of these polar lipids are species characteristics, forming the equipment of polar lipids for every species of algae. Glycosyl ester sulfate and phosphate diglycerides are very unstable substances when pure, moreover photolabile and thremodegradable. This extreme fragility caused many difficulties in the determination of molecular structures which require a very high purity of isolated substances, The determination of the structures, studies of quantities and composition cytological localization of these polar lipids should allow to define clearly their physiological function and importance from the biochemical and ecological point of view.

Diglycerides↗
PubMedDate not supplied

[Fatty acid composition of polar lipid fractions of ripening wheat].

By thin-layer chromatography on silica gel L (Czechoslovakia) monoglycerides, diglycerides, free fatty acids and triglycerides were isolated from free lipids of ripeining wheat. The composition of free fatty acids of these fractions was studied by gas-liquid chromatography. The following fatty acids were identified and quantified: C10:0; C12:0; 14:0; C14:1; X15:0; C16:0; C17:0; C18:1; C18:2; C18:3; C20:09 Linoleic, palmitnic, oleic, stearic and linolenic acids accured in large quantities. The wheat ripeinig was followed by a decrease in the sum total of saturated and an increase of the sum total of unsaturated fatty acids. During ripening the content of biologically important linoleic acid increased: in monoglycerides from 42.6 to 19.5%, diglycerides from 51.0 to 62.4%, in free fatty acids from 48.8 to 51.0% and in triglycerides from 54.5 to 61.1%, whereas the content of palmitinic and linolenic acids diminished.

Chromatography, Thin Layer↗
PubMed2006

Preclinical investigations of a medium-chain triglyceride:fish oil emulsion. I. Effects of bovine milk lipoprotein lipase on lipid composition.

The bolus intravenous injection of a novel medium-chain triglyceride:fish oil emulsion (MCT:FO, 8:2, w:w) was recently found to increase within 60 min the leucocyte and platelet phospholipid content of long-chain polyunsaturated omega3 fatty acids. The present report deals with the effects of bovine milk lipoprotein lipase on the lipid composition of this emulsion. The results are compared to those obtained with either a pure fish oil emulsion or a medium-chain triglyceride: long-chain triglyceride:fish oil emulsion (MLF, 5:4:1). Emphasis is placed on i) differences in the fate of distinct fatty acids initially present in the triglycerides, di glycerides and phospholipids, ii) the generation of unesterified fatty acids relative to their initial content in each emulsion, and iii) the time course for these various events. The comparison between the three emulsions under consideration also provides information relevant to their respective sensitivity to lipoprotein lipase and suitability in terms of the generation of distinct unesterified fatty acids, including long-chain polyunsaturated omega3 fatty acids. Furthermore, attention is drawn to the greater efficiency for the hydrolysis of fatty acids from diglycerides as compared to triglycerides and a transient increase in the paired C8:0/C10:0 ratio in the diglycerides generated from the MCT:FO or MLF emulsion. The present study thus affords novel information relevant to the possible use of the MCT:FO emulsion in human subjects.

Animals↗
PubMed1991

Tumor necrosis factor alpha priming of phospholipase D in human neutrophils. Correlation between phosphatidic acid production and superoxide generation.

Tumor necrosis factor alpha (TNF) primes human neutrophils (PMN) for enhanced superoxide (O2-) production if cells are subsequently stimulated with the chemotactic peptide, n-formyl-Met-Leu-Phe (fMLP). fMLP activates phospholipase D to form phosphatidic acid (PA), and a correlation may exist between PA production and O2- generation in PMN. Therefore, we assessed the ability of TNF to prime phospholipase D activation in PMN stimulated with fMLP. TNF (100 units/ml) pretreatment primed enhanced PA production in PMN challenged with 1 microM fMLP, in the absence of cytochalasin B, as demonstrated by increased production of tritiated PA from PMN label with 1-O-[9',10'-3H]hexadecyl-2-lyso-sn-glycero-3-phosphocholine ([3H]LPAF) and by increased PA mass. PA was formed via activation of phospholipase D and occurred with minimal production of diglycerides. Production of O2- was also enhanced in identically treated cells, and we demonstrated a direct correlation between enhanced PA formation and O2- production. Conversely, ethanol inhibition of PA formation led to a comparable reduction in O2- generation. This report of priming of phospholipase D by physiological agonists is the only natural system where enhanced PA formation has been dissociated from diglyceride formation. Our results suggest a link between PA production and NADPH oxidase activation in human PMN.

Cytochalasin B↗
PubMed1991

Elevated cytosolic Ca2+ activates phospholipase D in human platelets.

We have examined the activation of phospholipase D in human platelets treated with alpha-thrombin. When incubated with 1-O-[9,10-3H2]hexadecyl-2-lysophosphatidylcholine (PtdCho) and 1-alkyl-[32P]lysoPtdCho for 2 h, platelets formed 3H/32P-labeled PtdCho in a ratio of 11:1. After incubation of such labeled platelets with alpha-thrombin for 5 min, increased accumulation of 3H/32P-labeled phosphatidic acid (PtdOH) was detected in the same ratio, indicating the action of phospholipase D. The Ca2+ ionophore A23187 and alpha-thrombin each stimulated the formation of labeled PtdOH as above in a time- and concentration-dependent manner, with only minor changes in labeled diglyceride. A23187 was able to cause increases in labeled PtdOH comparable to those observed with alpha-thrombin. beta-Phorbol 12,13-dibutyrate, an activator of protein kinase C, only slightly stimulated the accumulation of labeled PtOH. The protein kinase C inhibitor, staurosporine, totally blocked these changes but only slightly inhibited the increases in labeled PtdOH promoted by alpha-thrombin. These results suggest that an increase in intracellular Ca2+, rather than protein kinase C activity, is a major factor regulating phospholipase D in platelets exposed to alpha-thrombin. We have also examined the relative contributions of phospholipase D and diglyceride kinase (following phospholipase C action) to PtdOH accumulation in [32P]Pi-labeled platelets by comparing the 32P-specific radioactivities of PtdOH, PtdCho, and metabolic gamma-ATP in control and alpha-thrombin-exposed platelets. Based on these determinations, we conclude that 13 and 87% of incremental PtdOH in human platelets exposed to alpha-thrombin arises via phospholipase D acting on PtdCho and phospholipase C/diglyceride kinase, respectively.

Alkaloids↗
PubMed1990

Stereoselectivity of lipases. I. Hydrolysis of enantiomeric glyceride analogues by gastric and pancreatic lipases, a kinetic study using the monomolecular film technique.

In the present study, porcine pancreatic lipase, rabbit gastric lipase, and human gastric lipase stereospecificity toward enantiomeric glyceride derivatives was kinetically investigated using the monomolecular film technique. Pseudoglycerides such as enantiomeric 1(3)-alkyl-2,3(1,2)-diacyl-sn-glycerol, enantiomeric 1(3)-alkyl-2-acyl-sn-glycerol, or enantiomeric 1(3)-acyl-2-acylamino-2-deoxy-sn-glycerol were synthesized in order to assess the lipase stereoselectivity during the hydrolysis of either the primary or the secondary ester position of these glycerides analogues. The cleaved acyl moiety was the same in both enantiomers, thereby excluding the possibility of effects occurring due to fatty acid specificity. We observed a porcine pancreatic lipase sn-3 stereoselectivity when using the enantiomeric 1(3)-alkyl-2-acylamino-2-deoxy-sn-glycerol (diglyceride analogue) which contrasted with the lack of stereoselectivity observed when using the enantiomeric 1(3)-alkyl-2,3(1,2)-diacyl-sn-glycerol (triglyceride analogue). The gastric lipases, in contrast to the pancreatic lipase, preferentially catalyze the hydrolysis of the primary sn-3 ester bond of the enantiomeric monoakyl-diacyl pair tested. From these kinetic data, high hydrolysis rates and no chiral discrimination were observed in the case of rabbit gastric lipase, whereas low rates and a clear chiral discrimination was noticed in the case of human gastric lipase during hydrolysis of the acyl chain from the secondary ester bond of 1(3)-alkyl-2-acyl enantiomers. It is particularly obvious that in the case of human gastric lipase decreasing the lipid packing increases the lipase sn-3 stereopreference during hydrolysis of the primary ester bond of the enantiomeric 2-acylamino derivatives (diglyceride analogue).

Animals↗
PubMed1986

Differences in glycerolipid synthesis and insulin regulation in rat hepatocytes and adipocytes.

Glycerolipid synthesis was studied by determining radioactive incorporation from either [1-14C] acetate or [U-14C] palmitate. Glycerolipid synthesis in adipocytes, mainly from exogenous palmitate, was preferentially directed to the formation of triacylglycerols, whereas in hepatocytes triacylglycerols and phospholipids were synthesized at similar rates. Insulin stimulated glycerolipid synthesis from acetate in both types of cells, being triacylglycerols more significantly increased than phospholipids. The most relevant difference was the finding that in adipocytes insulin strongly stimulated the formation of diglycerides, apparently from phosphatidate, whereas in hepatocytes insulin only slightly increased diglyceride levels. A possible role of diacylglycerol in insulin action in adipocytes, but not in hepatocytes, is also discussed.

Acetates↗
PubMed1985

Trypanosoma brucei variant surface glycoprotein has a sn-1,2-dimyristyl glycerol membrane anchor at its COOH terminus.

The membrane form of Trypanosoma brucei variant surface glycoprotein (mfVSG) is acylated with ester-linked tetradecanoic (myristic) acid (Ferguson, M. A. J., and Cross, G. A. M. (1984) J. Biol. Chem. 259, 3011-3015). Comparative analysis of Pronase peptides from mfVSG and soluble VSG localizes the site of mfVSG acylation to a COOH-terminal oligosaccharide structure. Chemical and enzymatic treatment of the acylated Pronase mfVSG fragment revealed that the myristic acid is present as a diglyceride (sn-1,2-dimyristin) that is probably linked to the COOH-terminal oligosaccharide via a phosphodiester bond between the sn-3-glycerol hydroxyl and a sugar hydroxyl group. The endogenous membrane-associated enzyme, which quantitatively cleaves myristic acid from mfVSG to produce soluble VSG, releases diglyceride, as would be expected of a phospholipase C.

Acylation↗
PubMed1985

The effects of 1-oleoyl-2-acetylglycerol on platelet protein phosphorylation and platelet ultrastructure.

1-oleoyl-2-acetylglycerol (OAG), an activator of protein kinase C and a synthetic diglyceride, was used in an investigation of the role of diglycerides in platelet stimulus-activation coupling. OAG (20-100 micrograms/ml) added to platelets resulted in rapid phosphorylation of the 47,000-dalton protein as well as a gradual dose dependent disappearance of alpha granules and dense bodies and the appearance of vacuolar structures containing remnants of granule matrix material. These morphologic changes occurred more slowly than the phosphorylation of 47K, which suggests that if these are related the phosphorylated 47K serves to activate some other mechanism, which is ultimately responsible for the changes observed. These results are most consistent with the role for the phosphorylation of 47K to promote granule labilization. Myosin light chain (MLC) phosphorylation also occurred. An absence of granule centralization suggests that MLC phosphorylation by protein kinase C may not trigger effective actin-myosin contraction.

Blood Platelets↗
PubMed1983

The influence of polyunsaturated phosphatidylcholine on brain lipid synthesis during aging.

The synthesis of choline phosphoglycerides and ethanolamine phosphoglycerides is noticeably decreased in brain microsomal membranes of aged rats as compared to that of two-month-old rats. Experimental evidence is presented that shows that the addition of a diglyceride preparation obtained from a polyunsaturated phosphatidylcholine to microsomes of aged rats practically restores the decreased synthesizing activity of both choline and ethanolamine phosphoglycerides. It is proposed that adding diglycerides to aged membranes affects the properties of the membranes and probably enzyme-lipid interactions.

Aging↗
PubMed1983

Biosynthesis of molecular species of inositol, choline, serine, and ethanolamine glycerophospholipids in the bovine retina.

The distribution of radioactivity among molecular species of inositol, choline, serine, and ethanolamine glycerophospholipids was studied in whole bovine retinas and in microsomes from retinas incubated with [3H]glycerol, [3H]inositol, or [3H]serine, in the presence and absence of propranolol. Most of the labeled glycerol was incorporated into docosahexaenoate-containing molecular species (hexaenes and dipolyunsaturates), which suggests that they are synthesized de novo. The largest accumulation of label in these species occurred in phosphatidylinositol, although they were only a minor component of this phospholipid. At short incubation times, these species, as well as monoenes and saturates, incorporated higher percentages of both [3H]glycerol and [3H]inositol than did the tetraenes. Labeling of tetraenes increased thereafter, suggesting that they are produced by acyl-exchange reactions from less unsaturated species. Propranolol was shown to stimulate phosphatidylinositol and polyphosphoinositide synthesis by preferentially enhancing first the labeling of monoenoic and saturated phosphatidylinositols, and subsequently tetraenes. Labeled glycerol was not redistributed among species of phosphatidylcholine with time. Propranolol inhibited the synthesis of monoenes and saturates to a greater extent than other species of phosphatidylcholine. The labeling of diglycerides was first inhibited, and then stimulated by propranolol; tetraenoic diglycerides were the major product accumulated. Propranolol stimulated [3H]serine incorporation into phosphatidylserine and phosphatidylethanolamine, with no alteration in distribution of radioactivity among species; [3H]glycerol incorporation in phosphatidylethanolamine was inhibited, and its incorporation into phosphatidylserine was stimulated. Labeled serine and glycerol were concentrated largely in docosahexaenoate-containing species of phosphatidylethanolamine and phosphatidylserine.

Animals↗
PubMed1980

Activation of calcium and phospholipid-dependent protein kinase by diacylglycerol, its possible relation to phosphatidylinositol turnover.

Ca2+-activated, phospholipid-dependent protein kinase from various mammalian tissues (Takai, Y., Kishimoto, A., Iwasa, Y., Kawahara, Y., Mori, T., and Nishizuka, Y (1979) J. Biol. Chem. 254, 3692-3695) was greatly stimulated by the addition of diacylglycerol at less than 5% (w/w) the concentration of phospholipid. This stimulation was due to an increase in the apparent affinity of enzyme for phospholipid and to a concomitant decrease in the Ka value for Ca2+ from about 1 x 10(-4) M to the micromolar range. Diacylglycerol alone showed little or no effect on enzymatic activity over a wide range of Ca2+ concentrations. This effect was greatest for diacylglycerol which contained unsaturated fatty acid at least at position 2. The active diacylglycerols so far tested included diolein, dilinolein, diarachidonin, 1-stearoyl-2-oleoyl diglyceride, and 1-stearoyl-2-linoleoyl diglyceride. In contrast, diacylglycerols containing saturated fatty acids such as dipalmitin and distearin were far less effective. Triacyl- and monoacylglycerols were totally ineffective, irrespective of the fatty acyl moieties. Cholesterol and free fatty acids were also ineffective. Based on these observations, a possible coupling is proposed between the protein kinase activation and phosphatidylinositol turnover which can be provoked by various extracellular messengers.

Animals↗