Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “LIPIDS”

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 469 records · Page 26Linked to original sources
PubMed1981

Characteristics of a lipid preparation (lipid A) from Haemophilus influenzae type a lipopolysaccharide.

Mild hydrolysis of Haemophilus influenzae type a lipopolysaccharide by ion exchangers yielded a lipid A extracted by chloroform. It contained phosphorus, glucosamine, and fatty acids. Myristic, palmitic, 3-hydroxymyristic, and oleic acids and two other unidentified long-chain fatty acids were found. The free lipid A was not toxic for mice at doses of up to 50 mg/kg and did not provoke a Shwartzman reaction. The Limulus test activity was positive up to 10(-12) g/ml, but the pyrogenicity in rabbits was lower than with the original lipopolysaccharide. However, the lipid A did induced a mitogenic response and polyclonal B-cell activation in mouse spleen cell cultures. Complexing lipid A with bovine serum albumin gave a nontoxic preparation which lost these immunological activities. Immunochemical studies showed that the major reactive determinants of this lipid-protein complex were altered after such a linkage. Consequently, the nontoxic and mitogenic lipid A isolated from H. influenzae type a did not exhibit all of the classical activities of lipid A preparations.

Animals↗
PubMed1983

Immunobiological activities of synthetic lipid A analogs and related compounds as compared with those of bacterial lipopolysaccharide, re-glycolipid, lipid A, and muramyl dipeptide.

Thirteen acylated and phosphorylated derivatives of beta-1,6-linked glucosamine disaccharide (lipid A analogs), which were synthesized after the structural model of Salmonella-type lipid A, and seven similar derivatives of glucosamine monosaccharide (lipid A-related compounds) were studied for their immunobiological activities. These included mitogenicity and polyclonal B cell activation enhancement of migration of monocytes and polymorphonuclear leukocytes derived from human peripheral blood, stimulation of guinea pig peritoneal macrophages, activation of human complement, and stimulation of serum antibody production and induction of delayed-type hypersensitivity against ovalbumin in guinea pigs. Comparisons were made with lipid A, RE-glycolipid, lipopolysaccharide of natural sources, and a well-known synthetic adjuvant, N-acetylmuramyl-L-alanyl-D-isoglutamine. Some of the lipid A analogs were found to manifest the mitogenic, polyclonal B cell-activating macrophage-stimulating, complement-activating, and immunostimulating activities, although the observed activities were generally far less than those of natural products in intensity and efficiency. Other immunobiological effects exhibited by most of the synthetic lipid A analogs were the enhancement of migration of monocytes and polymorphonuclear leukocytes. It is premature to draw definite conclusions on structure-activity relationships, since a few compounds which were active in some assay systems were scarcely active in other assays. However, an indisputable fact was that beta-1,6-glucosamine disaccharide 1 alpha,4'-diphosphate, which carries two amide-bound (R)-3-hydroxytetradecanoyl and three ester-bound tetradecanoyl residues, and thus has the structure most closely resembling natural lipid A among test compounds in this study, was definitely active in all of the present assay systems. However, its potency was generally much less than natural products. Some of glucosamine monosaccharide derivatives, especially N-(R)-3-[(R)-3-hydroxytetradecanoyloxy]tetradecanoyl glucosamine, also exerted all of the in vitro activities described above. This fact suggests that a glucosamine disaccharide structure may not necessarily be a prerequisite as far as the in vitro immunobiological activities tested are concerned.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1984

Mitogenic activities of synthetic lipid A analogs and suppression of mitogenicity of lipid A.

The effect of synthetic lipid A analogs on murine spleen cells was studied. The preparations represented D-glucosamine and D-glucosaminyl-beta 1,6-D-glucosamine disaccharide derivatives substituted in different combinations by ester- and amide-bound fatty acids and by phosphate groups. Significant mitogenic activity was demonstrated with a number of synthetic disaccharide preparations; however, their potency was lower than that of lipid A. The synthetic preparations were not mitogenic for spleen cells from C3H/HeJ mice. Furthermore, the mitogenicity of the synthetic preparations was abolished after binding with polymyxin B. The results indicate that for expression of mitogenicity, a phosphate group at position 1 of the reducing glucosamine and amide-bound acyloxyacyl residues are important factors. Some of the synthetic preparations containing the diglucosamine backbone and expressing relatively low mitogenicity suppressed B-cell mitogenicity of lipid A. Although these preparations were lytic for erythrocytes, they did not affect the viability of the splenic lymphocytes. Suppression was seen when the synthetic preparations were added simultaneously with or after the lipid A mitogen, but optimal suppression was expressed when the preparations were added to the system 3 h before lipid A. Washing of the cells before the addition of lipid A did not affect the results. The suppression was not due to the induction of suppressor cells by the synthetic preparations. The disaccharide preparations did not inhibit T-cell mitogenicity of concanavalin A. In contrast to the disaccharide preparations, the monosaccharide preparations suppressed mitogenicity of both lipid A and concanavalin A, probably because of their direct toxicity for lymphocytes.

Animals↗
PubMed1985

Synthetic lipid A with endotoxic and related biological activities comparable to those of a natural lipid A from an Escherichia coli re-mutant.

A synthetic compound (506), beta (1-6) D-glucosamine disaccharide 1,4'-bisphosphate, which is acylated at 2'-amino and 3'-hydroxyl groups with (R)-3-dodecanoyloxytetradecanoyl and (R)-3-tetradecanoyloxytetradecanoyl groups, respectively, and has (R)-3-hydroxytetradecanoyl groups at 2-amino and 3-hydroxyl groups, exhibited full endotoxic activities identical to or sometimes stronger than those of a reference lipid A from an Escherichia coli Re-mutant (strain F515). Endotoxic activities tested include pyrogenicity and leukopenia-inducing activity in rabbits, body weight-decreasing toxicity in normal mice, lethal toxicity in galactosamine-sensitized mice and chicken embryos, and the preparation and provocation of the local Shwartzman reaction in rabbits. Compound 406, a synthetic counterpart of a biosynthetic precursor of lipid A molecule, showed by contrast only weak activities in all of the above assay systems except for the lethality in galactosamine-loaded mice. This finding strongly suggests that the presence of acyloxyacyl groups at the C-2' and C-3' positions of the disaccharide backbone is one of the most important determinant structures of the lipid A molecule for exhibition of strong biological activities characteristic of lipopolysaccharide and its lipid A moiety. The activities of the corresponding 4'-monophosphate (compound 504) and 1-monophosphate (505) analogs were considerably less than those of the parent molecule 506 and the reference F515 lipid A. Regarding other biological activities, not only compound 506 but also compounds 504, 505, and 406 showed definite activities, sometimes comparable to those of F515 lipid A and other reference natural products. These are the activation of Tachypleus tridentatus amoebocyte clotting enzyme cascade and human complement via the classical pathway, mitogenic and polyclonal B-cell activation of murine splenocytes, stimulation of peritoneal macrophages in a guinea pig, enhancement of migration of human blood polymorphonuclear leukocytes, and induction of a serum factor that is cytostatic and cytocidal to L-929 cells in Mycobacterium bovis BCG-primed mice. Relative potencies of test synthetic compounds depended on the assay systems and varied from one system to another. Dephospho-compound 503 lacked most of the biological activities that were definitely observed with phosphorylated compounds, probably because of its insolubility. This study demonstrates the successful chemical synthesis of an E. coli-type lipid A.

Adjuvants, Immunologic↗
PubMed1999

Lipid extract of Mycoplasma penetrans proteinase K-digested lipid-associated membrane proteins rapidly activates NF-kappaB and activator protein 1.

Lipid-associated membrane proteins (LAMPs) of Mycoplasma penetrans rapidly induced macrophages to produce proinflammatory cytokines such as tumor necrosis factor alpha (TNF-alpha). Our analysis showed that the macrophage-stimulating activity of TNF-alpha production was mainly attributable to a lipid extractable component(s) in the LAMP preparation. Since induction of gene expression is normally preceded by activation of transcriptional factors that bind to their specific recognition elements located in the upstream promoter region, we examined the activity of transcriptional factors, namely, NF-kappaB and activator protein 1 (AP-1), in thioglycolate exudate peritoneal (TEP) macrophages treated with M. penetrans lipid extract of proteinase K (PK)-digested LAMPs. Initially, in the nuclei of unstimulated TEP cells, there was only a low basal level of active AP-1, and the active form of NF-kappaB could not be detected. M. penetrans lipid extract of PK-digested LAMPs activated both NF-kappaB and AP-1 in TEP macrophages within 15 min. The markedly increased activities of both factors gradually declined and dissipated after 2 h. Parallel to the rapid increase of NF-kappaB and AP-1, the TNF-alpha transcript also increased significantly 15 min after the stimulation. The high-level expression of TNF-alpha persisted over 2 h. Dexamethasone blocked the activation of both NF-kappaB and AP-1 and suppressed the production of TNF-alpha in TEP macrophages stimulated by M. penetrans lipid extract of PK-digested LAMPs. Our study demonstrates that the M. penetrans lipid extract of PK-digested LAMP is a potent activator for NF-kappaB and AP-1 in murine TEP macrophages. Our results also suggest that high-level expression of TNF-alpha in cells induced by M. penetrans lipid extract of PK-digested LAMPs is associated with rapid activation of transcriptional factors NF-kappaB and AP-1.

Animals↗
PubMed1980

Intermolecular hydrogen bonding between lipids: influence on organization and function of lipids in membranes.

Biological membranes have unique lipid compositions suggesting a specific role for many lipids. Evidence is reviewed concerning the intermolecular forces between glycero- and sphingolipids and cholesterol, the dependence of many of these interactions on the state of ionization of lipids, pH, ionic strength, and divalent cation concentration. The effect of intermolecular interactions between certain lipids on lipid clustering, interaction with cholesterol, on the conformation of proteins, and on transitions to the hexagonal phase is considered. Other forces which cause lipids phase separation or clustering are discussed. It is concluded that lipids are in dynamic equilibrium with their environment and can act as receptors for certain intra- or extra-cellular stimuli, which they can translate into a response by undergoing changes in fluidity, phase transitions, or phase separation.

Animals↗
PubMed2002

ADRP stimulates lipid accumulation and lipid droplet formation in murine fibroblasts.

Adipose differentiation-related protein (ADRP) is a lipid droplet-associated protein that is expressed early during adipose differentiation. The present study was undertaken to reveal the role of ADRP in adipose differentiation. In murine fibroblasts infected with green fluorescent protein (GFP)-ADRP fusion protein expression adenovirus vector, confocal microscopic analysis showed the number and size of lipid droplets apparently increased comparing with those of control cells. Overexpressed GFP-ADRP were mainly located at the surface of lipid droplets and appeared to be "ring-shaped." Triacylglycerol content was also significantly (P < 0.001) increased in GFP-ADRP-overexpressed cells compared with control cells. ADRP-induced lipid accumulation did not depend on adipocyte-specific gene induction, such as peroxisome proliferator-activated receptor-gamma, lipoprotein lipase, or other lipogenic genes, including acyl-CoA synthetase, fatty acid-binding protein, and fatty acid transporter. In conclusion, ADRP stimulated lipid accumulation and lipid droplet formation without induction of other adipocyte-specific genes or other lipogenic genes in murine fibroblasts. The detailed molecular mechanisms of ADRP on lipid accumulation remain to be elucidated.

3T3 Cells↗
PubMed1985

Assessment of lipid peroxidation in newborn infants and rabbits by measurements of expired ethane and pentane: influence of parenteral lipid infusion.

Peroxidation of the unsaturated fatty acid constituents of tissue is one proposed mechanism of in vivo oxidant damage. Products of unsaturated fatty acid peroxidation include the volatile hydrocarbons ethane and pentane. These volatile hydrocarbons are eliminated in expired air and reflect in vivo lipid peroxidation. Newborn infants excrete 16 pmol of ethane per kilogram body weight per minute and 15 pmol of pentane per kilogram body weight per minute. This compares with 1.4 pmol of ethane per kilogram body weight per minute and 1.3 pmol of pentane per kilogram body weight per minute in healthy adult men. Infants receiving total parenteral nutrition including intravenous lipid emulsion excrete more than 100 pmol of pentane per kilogram body weight per minute. Newborn rabbits, delivered at term, also excrete more pentane while receiving lipid emulsion infusion. In the newborn rabbit, the amount of pentane exhaled increases linearly with the dose of lipid emulsion. Blood and tissue thiobarbituric acid reactants are also increased in newborn rabbits after administration of lipid emulsion. These results indicate that lipid peroxidation is quantitatively greater in infants than in adult humans and can be significantly increased by parenteral administration of lipid emulsion.

Adult↗
PubMed2005

Inositol-lipid binding motifs: signal integrators through protein-lipid and protein-protein interactions.

Inositol lipids have emerged as universal lipid regulators of protein signaling complexes in defined membrane compartments. The number of protein modules that are known to recognise these membrane lipids is rapidly increasing. Pleckstrin homology domains, FYVE domains, PX domains, ENTH domains, CALM domains, PDZ domains, PTB domains and FERM domains are all inositide-recognition modules. The latest additions to this list are members of the clathrin adaptor protein and arrestin families. Initially, inositol lipids were believed to recruit signaling molecules to specific membrane compartments, but many of the domains clearly do not possess high enough affinity to act alone as localisation signals. Another important notion is that some (and probably most) of these protein modules also have protein binding partners, and their protein- and lipid-binding activities might influence one another through allosteric mechanisms. Comparison of the structural features of these domains not only reveals a high degree of conservation of their lipid interaction sites but also highlights their evolutionary link to protein modules known for protein-protein interactions. Protein-protein interactions involving lipid-binding domains could serve as the basis for phosphoinositide-induced conformational regulation of target proteins at biological membranes. Therefore, these modules function as crucially important signal integrators, which explains their involvement in a broad range of regulatory functions in eukaryotic cells.

Adaptor Proteins, Signal Transducing↗
PubMed1975

Replacement time for alveolar lipid removed by pulmonary lavage: effects of multiple lavage on lung lipids.

Daily washing in vivo of the lung with 0.15 M saline did not deplete the Beagle dog lung of surfactant lipids, but rather increased the quantity of surfactant lipid in the tissue. Replacement time for the lung lipids removed by the lavage was approximately 5 hours. This rate is one indication of the time required for movement of surfactant lipid from storage areas to the surface of the alveoli. The increase in tissue surfactant lipid following multiple lavage suggests that the rate of surfactant lipid synthesis is controlled in part by the level of surfactant lipid in the alveoli.

Animals↗
PubMed1999

The relationship between nuclear magnetic resonance-visible lipids, lipid droplets, and cell proliferation in cultured C6 cells.

There is an ongoing controversy about the subcellular origin of the fatty acyl chains that give rise to the NMR visible mobile lipids (MLs) resonance at approximately 1.24 ppm in the 1H spectra of cells and solid tumors. Some groups have been supporting the hypothesis that triglycerides originating MLs are isotropically tumbling in small membrane microdomains, whereas other authors back the proposal that they are inside cytosolic or extracellular (necrotic areas) lipid droplets. Furthermore, MLs are frequently present in in vivo spectra recorded from human brain tumors, but the meaning of this detection is not fully clear. We have addressed the possible contribution of intracellular droplets to the ML pattern recorded from human brain tumors in vivo by studying cultured C6 rat glioma cells as a model system for astrocytic tumors. We show here that cultured C6 cells display ML resonances in high field (9.4 T) 1H NMR spectra recorded at 136 ms echo time when grown at saturation density conditions, but no MLs are visible for log-phase cells. Fluorescence microscopy analysis of cells stained with the lipophylic dye Nile red shows intracellular spherical yellow-gold droplets containing neutral lipids; cells at saturation density present lipid droplets of diameters about 1.6 microm in most cells (85%), whereas they are almost absent in log-phase cells (only 6% of the cells contain them). Furthermore, log-phase cells can be induced to display MLs and accumulate Nile red-positive droplets by culturing them for 24 h at pH 6.2. This acid pH effect can be fully reversed by 24 h of standard media incubation. Lipid droplet volume calculated from fluorescence microscopy preparations in an average cell is different for both culture conditions (2.2 times higher volume for saturation density than for pH-stressed cells). This difference in lipid droplet volume is reflected by a different ML peak height at 1.24 ppm (about 2 times higher for saturation density than for pH-stressed cells). Flow cytometry analysis shows that both culture conditions result in a slowing down of the proliferation rate of the cells. The fact that MLs are found to originate in lipid droplets inside cells that are growth compromised but still viable suggests that changes in the proliferative state of tumor cells, in the absence of necrosis, may be detected non invasively by in vivo NMR spectroscopy.

Animals↗
PubMedDate not supplied

Lipid microdomains, lipid translocation and the organization of intracellular membrane transport (Review).

Eukaryotic cells contain hundreds of different lipid species that are not uniformly distributed among their membranes. For example, sphingolipids and sterols form gradients along the secretory pathway with the highest levels in the plasma membrane and the lowest in the endoplasmic reticulum. Moreover, lipids in late secretory organelles display asymmetric transbilayer arrangements with the aminophospholipids concentrated in the cytoplasmic leaflet. This lipid heterogeneity can be viewed as a manifestation of the fact that cells exploit the structural diversity of lipids in organizing intracellular membrane transport. Lipid immiscibility and the generation of phase-separated lipid domains provide a molecular basis for sorting membrane proteins into specific vesicular pathways. At the same time, energy-driven aminophospholipid transporters participate in membrane deformation during vesicle biogenesis. This review will focus on how selective membrane transport relies on a dynamic interplay between membrane lipids and proteins.

Animals↗
PubMed1975

A method for microdetermination of major neutral lipids and an application of the procedure to tissue lipids.

Cholesterol, cholesteryl esters, triglycerides and fatty acids as major neutral lipids and phospholipids were examined in quantitative analysis. The method consisted of three steps: (1) separation of lipids by one-dimensional thin-layer chromatography on silica gel plates; (2) elution of neutral lipids from scraped silica gel with chloroform-methanol (4:1); and (3) colorimetric determination of individual neutral lipids in eluates and phospholipids in silica gel. The conditions were modified for chromotropic acid reaction for determining triglycerides. Laurell's method for determining fatty acids was also modified to apply to quantitative thin-layer chromatography. The accuracy of the modified methods was well-defined as the absorbance values were on a linear curve. A quantitative study was made of the recovery of triglycerides and fatty acids after chromatography. Combining these modified methods and colorimetry for determination of cholesterol cholesteryl esters and phospholipids, the author established a micromethod for determining the major neutral lipids and phospholipids by thin-layer chromatography. Lipids from HeLa, S-3 cells were analyzed to examine the applicability of this method to tissues. The results indicated that the new method permitted a reliable estimation of the major neutral lipids and phospholipids from small amounts of tissues.

Cholesterol↗
PubMed1992

Lipid peroxidation in rod outer segments. Role of hydroxyl radical and lipid hydroperoxides.

Lipid peroxidation of rod outer segment (ROS) membranes has been implicated in the pathogenesis of numerous ocular disease processes. The hydroxyl radical might be involved in initiating the reaction. An in vitro system was developed to study lipid peroxidation of the ROS and the role of the hydroxyl radical. Bovine ROS were suspended in various concentrations of ferrous sulfate, incubated for 10 min at 37 degrees C, treated with diethylenetriamine pentaacetic acid to chelate the iron, and subjected to a thiobarbituric acid assay for malondialdehyde. A predictable increase in lipid peroxidation occurred in the presence of Fe+2. No effect was seen in the presence of Fe+3. Adding hydrogen peroxide, which would form the hydroxyl radical by reacting with Fe+2, had no effect at low concentrations. At higher concentrations, lipid peroxidation was inhibited, presumably from the oxidation of Fe+2 to Fe+3. Ethanol, a known hydroxyl radical scavenger, had no inhibitory effect in concentrations up to 0.50 mol/l. Conversely, cumene hydroperoxide and linoleic acid hydroperoxide, which form hydrophobic radicals, stimulated lipid peroxidation in the presence of Fe+2. These findings suggest that, under these experimental conditions, the hydroxyl radical is not an initiator of lipid peroxidation in ROS. They provide evidence that endogenous lipid radicals may initiate the reaction.

Animals↗
PubMed2006

[Assessment of malonyldialdehyde concentration as a product of lipid peroxidation and lipid metabolism in patients on chronic dialysis].

UNLABELLED: Chronic hemodialysis in patients with renal insufficiency is a factor significantly intensifying oxidative stress, resulting in increased lipid and lipoprotein peroxidation. It intensifies atherosclerotic activity. Malonyldialdehyde (MDA) concentration in serum, and isolated fraction of low density lipoprotein is indicators of lipid peroxidation intensification and therefore arteriosclerosis development. THE AIM OF THE STUDY: Assessment of MDA concentration as a product of lipid peroxidation and lipid metabolism in patients on chronic dialysis. MATERIALS AND METHODS: The study included 48 dialyzed patients, age 22-68 undergoing chronic dialysis for, on average, 56 months. On account of dialysis period the patients were included into 3 subgroups: group 1 (n = 17) dialysis period 2 years, group 2 (n = 13) dialysis period 2-5 years and group 3 (n = 18) dialysis period longer than 5 years. Control group consisted of 30 healthy subjects. We assessed: malonyldialdehyde in serum and isolated fraction of low density lipids (LDL) and high density lipid (HDL) and cholesterol (CH) and triglycerides (TG), phospholipids (PL) in serum and isolated lipoprotein fractions. RESULTS: Significantly decreased levels of HDL, LDL fractions and increased triglicerides and elevated levels of MDA in serum and isolated LDL fraction were found in patients on chronic dialysis in comparison to control group (p < 0.05). CONCLUSION: Our results indicate apparent normalization of lipid metabolism in patients on chronic dialysis and suggest that MDA assessment is better marker for arteriosclerosis risk estimation in long-term dialyzed patients.

Adult↗
PubMed1991

Structure and function of lamellar bodies, lipid-protein complexes involved in storage and secretion of cellular lipids.

This review article attempts to present an overview of the occurrence and function of lipid storage and secretory organelles: the lamellar bodies. Morphologically these organelles vary considerably in size (100 nm to 2400 nm); they are surrounded by a membrane and contain multilamellar lipid membranes. Lamellar bodies may also contain apolipoproteins and lytic enzymes and have an acidic pH, which confers on them a lysosomal character. Under normal physiological conditions, the main function of lamellar bodies is the supply of extracellular domains with specialized lipid components related to a specialized function. The lamellar bodies of the lung epithelium are best investigated in their functional and structural features and are the storage form of the lung surfactant. They provide a monomolecular lipid film of dipalmitoyl phosphatidylcholine (DPPC) on the surface of lung alveoli to lower surface tension necessary for optimal gas exchange and a hydrophobic protective lining against environmental influences. Additional cells of the respiratory system such as the mucosa of the human nose and the bronchi contain lamellar bodies. Lamellar bodies are also found in the gastrointestinal tract, in tongue papillae, oral epithelium, and mucosa cells of the stomach. The major phospholipid of lamellar bodies in mucosa cells of the stomach is DPPC, providing a hydrophobic protective lipid film against the tissue-damaging activities of gastric juice. The hydrophobic water-protective barrier of the skin, which consists mainly of neutral lipids, however, also originates from lamellar bodies secreted by epithelial cells. Lamellar bodies, mainly consisting of DPPC, also occur in mesodermal cell layers of sliding surfaces to provide the lubrication of joints, of the peritoneum, pericardium, and pleural mesothelium. In certain pathological conditions, such as atherosclerosis, Niemann-Pick disease, lecithin:cholesterol acyltransferase (LCAT) deficiency, cholestasis, degeneration of nerves and brain, and regeneration of nerves and wound healing, lipid-containing lamellar bodies have been observed in various cells, the function of which still remains to be elucidated. In early and late lesions of atherosclerotic plaques, lamellar bodies, consisting of unesterified cholesterol and phospholipids, are associated with the extracellular matrix of the intima. During regression of fatty streaks, lamellar bodies are seen intracellularly in macrophages and smooth muscle cells. Inherited metabolic disorders, such as Niemann-Pick disease type I and type II, result in the excessive accumulation of lamellar body-containing cells, for example in bone marrow, spleen, and lymphoid tissue. Type I is a deficiency in sphingomyelinase and type II is a defect in intracellular trafficking of lipoprotein-derived cholesterol.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1989

Studies on the purified, lipid-reconstituted (Na+ + Mg2+)-ATPase from Acholeplasma laidlawii B membranes. Dependence of enzyme activity on lipid headgroup and hydrocarbon chain structure.

The purified (Na+ + Mg2+)-ATPase from Acholeplasma laidlawii B membranes was successfully reconstituted with a number of different phospho- and glycolipids, and the ability of these lipids to support the function of this enzyme was evaluated by their ability to increase the specific activity of the purified enzyme and by their ability to restore its lipid-phase state-dependent properties which were lost during purification. The incorporation of this ATPase into liposomes composed of the endogenous membrane lipids of the organism, or of zwitterionic phospholipids such as phosphatidylcholine or phosphatidylethanolamine, results in a full reconstitution of its activity and its lipid-phase state-dependent properties. In contrast, anionic phospholipids alone, or in combination with zwitterionic phospholipids at concentrations higher than 10 mol % of the anionic phospholipid, cause an irreversible inhibition of this ATPase. However, when combined with neutral glycolipids, larger amounts of anionic phospholipid can be tolerated without enzyme inhibition. Phosphatidylcholines with acyl chains of 14-24 linear carbon atoms and varying degrees of branching and unsaturation successfully reconstitute the enzyme, in marked contrast to the shorter chain homologues, which were ineffective. Our results indicate that the full expression of the activity of the A. laidlawii B ATPase requires a host lipid bilayer membrane of low to moderate negative surface charge which is predominantly liquid-crystalline and of a minimal bilayer thickness. Once such requirements are met, the enzyme exhibits considerable flexibility regarding the nature of the lipids which can effectively support its function. In particular, the activity of the A. laidlawii B ATPase is not very sensitive to lipid "fluidity" in the liquid-crystalline state.

Acholeplasma laidlawii↗
PubMed1989

An insect lipid transfer particle promotes lipid loading from fat body to lipoprotein.

The role of Manduca sexta lipid transfer particle (LTP) in the transport of lipid from fat body to lipophorin was investigated in vitro. Fat body that contained radiolabeled lipid was incubated with either high density lipophorin or low density lipophorin, and it was shown that lipid was transferred from fat body to lipophorins. The transfer of diacylglycerol was blocked by preincubating fat body with LTP antibody. Furthermore, transfer was restored by the addition of LTP, indicating that LTP promotes the transfer of lipid from fat body to lipophorins. Using lipophorins radio-labeled in their lipid moiety, transfer of lipid from lipophorin to fat body was demonstrated. This transfer was not mediated by LTP. The adipokinetic hormone induced diacylglycerol mobilization from the fat body and the concomitant interconversion of high density lipophorin to low density lipophorin were performed in vitro and were shown to require the presence of LTP.

Animals↗