Mobilization and utilization of lipids after trauma: relation to caloric homeostasis. In: Energy metabolism in trauma.
Explore the source record for details and available documents.
Adipose Tissue↗
SEARCH · Search PubMed
Results for “Lipid Mobilization”
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.
Lateral mobility of proteins and lipids of cell surface membranes during aging: do the data support 'The Membrane Hypothesis of Aging'?
Many previous studies regarding the change with age in surface membrane fluidity of different cell types, including hepatocytes, as determined by the fluorescence anisotropy method, are in conflict, demonstrating decreased, unchanged or even increased fluidity with age. In contrast, the results of our series of works using the fluorescence recovery after photobleaching (FRAP) technique, which measures protein lateral diffusion coefficients of hepatocyte surface membranes (Dp), have demonstrated that Dp generally declines in a linear fashion with age in hepatocytes of all animal strains and species examined. The major coworker (I. Zs.-Nagy) of these studies insists that our observations support his original hypothesis, 'The Membrane Hypothesis of Aging' (MHA), the primary assumption of which is that changes in cell surface membranes with age cause a general decline in intracellular enzyme activities. However, while it seems clear that cell surface membrane changes do occur with age, a number of past observations including those from the laboratory of this author, provide strong evidence that intracellular enzyme activities do not generally decline with age. This paper presents the data in detail, along with the author's view that the results do not support the main assumption of the MHA, but are more likely related to alterations in membrane functions with age.
Aging↗
Mobility of bacteriorhodopsin in lipid vesicles.
Explore the source record for details and available documents.
Bacteriorhodopsins↗
Brown adipose cells: spontaneous mobilization of endogenously synthesized lipid.
Isolated brown adipose cell devoid of a basement membrane, readily synthesized a variety of lipids from radioctive acetate, a reactionaugmented by glucose and insulin. A large proportion of the newly formed fatty acids passed into the incubation medium. In intact brown adipose slices and isolated white adipose cells, most of the synthesized lipid was retained as glyceride esters. The date suggest that the rapid turnover of endogenously synthesized lipid in brown adipose cells is almost totally obscured in studies with intact tissue slices because of interstitial barriers to the egress of fatty acid.
Acetates↗
TLR2 is mobilized into an apical lipid raft receptor complex to signal infection in airway epithelial cells.
Toll-like receptors (TLRs) mediate host responses to bacterial gene products. As the airway epithelium is potentially exposed to many diverse inhaled bacteria, TLRs involved in defense of the airways must be broadly responsive, available at the exposed apical surface of the cells, and highly regulated to prevent activation following trivial encounters with bacteria. We demonstrate that TLR2 is enriched in caveolin-1-associated lipid raft microdomains presented on the apical surface of airway epithelial cells after bacterial infection. These receptor complexes include myeloid differentiation protein (MyD88), interleukin-1 receptor-activated kinase-1, and TNF receptor-associated factor 6. The signaling capabilities of TLR2 are amplified through its association with the asialoganglioside gangliotetraosylceramide (Gal beta 1,2GalNAc beta 1,4Gal beta 1,4Glc beta 1,1Cer), which has receptor function itself for many pulmonary pathogens. Ligation of either TLR2 or asialoGM1 by ligands with specificity for either receptor, by Pseudomonas aeruginosa, or by Staphylococcus aureus stimulates IL-8 production through activation of NF-kappa B, as mediated by TLR2 and MyD88. Thus, TLR2 in association with asialo-glycolipids presented within the context of lipid rafts provides a broadly responsive signaling complex at the apical surfaces of airway cells to initiate the host response to potential bacterial infection.
Adaptor Proteins, Signal Transducing↗
Lateral mobility of plasma membrane lipids in bull spermatozoa: heterogeneity between surface domains and rigidification following cell death.
Compartmentalization of surface membrane antigens into discrete regions or domains is a characteristic feature of differentiated cells. In mammalian spermatozoa at least 5 surface domains are known, implying the presence of barriers or boundaries within the plasma membrane. Using the technique of fluorescence recovery after photobleaching (FRAP) to measure diffusibility of fluorescent lipid analogues 1,1'-dihexadecyl-3,3,3'3'-tetramethylindocarbocyanine (DiIC[16]) and 5-(N-octa-decanoyl) aminofluorescein (ODAF), we have investigated lipid topology and dynamics in the plasma membrane of ejaculated bull spermatozoa. Contrary to reports in the literature, we have found that DiIC(16) stains only dead or damaged spermatozoa whereas ODAF intercalates into the plasma membrane of both live and dead cells, each type showing a distinctive staining pattern. FRAP analysis with ODAF revealed that diffusion coefficients on live spermatozoa are significantly faster on the acrosome and postacrosome (29.3x10(-9) cm2/second) than on the midpiece and principal piece (11.8x10(-9) cm2/second). Recovery (R) is >90% in all domains. ODAF diffusion also shows regionalized temperature-sensitivity with a 4-fold increase over the sperm head and a 1.8-fold increase on the tail between 20 degrees C and 37 degrees C. Remarkably, dead or permeabilized spermatozoa rapidly develop a large immobile phase (R<25%) over the whole plasma membrane. This rigidification is temperature insensitive and irreversible suggesting major changes in the physical state of membrane lipids. It is concluded that lipid diffusion in the plasma membrane of live bull spermatozoa is rapid and varies significantly between surface domains. Following permeabilization or cell death, however, a large immobile phase develops indicating substantial changes in membrane lipid disposition.
Animals↗
Flexible charged macromolecules on mixed fluid lipid membranes: theory and Monte Carlo simulations.
Fluid membranes containing charged lipids enhance binding of oppositely charged proteins by mobilizing these lipids into the interaction zone, overcoming the concomitant entropic losses due to lipid segregation and lower conformational freedom upon macromolecule adsorption. We study this energetic-entropic interplay using Monte Carlo simulations and theory. Our model system consists of a flexible cationic polyelectrolyte, interacting, via Debye-Hückel and short-ranged repulsive potentials, with membranes containing neutral lipids, 1% tetravalent, and 10% (or 1%) monovalent anionic lipids. Adsorption onto a fluid membrane is invariably stronger than to an equally charged frozen or uniform membrane. Although monovalent lipids may suffice for binding rigid macromolecules, polyvalent counter-lipids (e.g., phosphatidylinositol 4,5 bisphosphate), whose entropy loss upon localization is negligible, are crucial for binding flexible macromolecules, which lose conformational entropy upon adsorption. Extending Rosenbluth's Monte Carlo scheme we directly simulate polymer adsorption on fluid membranes. Yet, we argue that similar information could be derived from a biased superposition of quenched membrane simulations. Using a simple cell model we account for surface concentration effects, and show that the average adsorption probabilities on annealed and quenched membranes coincide at vanishing surface concentrations. We discuss the relevance of our model to the electrostatic-switch mechanism of, e.g., the myristoylated alanine-rich C kinase substrate protein.
Adsorption↗
3,5 DIIODOTHYROACETIC ACID MOBILIZATION OF RAT LIVER LIPID AND RELATIVE TOXICITY OF ORAL TRIAC AND TRIPROP.
Explore the source record for details and available documents.
Acetates↗
Mobility of proteins and lipids in membranes.
Explore the source record for details and available documents.
Adenylyl Cyclases↗
On the hypolipemic properties of bendaline.
Bendaline, like tiadenol, clofibrate and clofibric acid generally inhibits: a) some hyperlipemias and lipoidoses induced by either an increased exogenous supply of lipids or the stimulation of cholesterol synthesis or mobilization of lipids; b) platelet aggregation in vitro.
Animals↗
Lipid peroxidation as a mechanism of alcoholic liver injury: role of iron mobilization and microsomal induction.
Lipid peroxidation has been invoked as a mechanism of alcoholic liver injury but its role has been controversial and the mechanism by which it occurs is unclear. Catalytic iron is known to play an important role in cellular injury and is produced during mobilization of ferritin iron. In vivo administration of a large acute dose of ethanol (5 g/kg) which produces hepatic lipid peroxidation in chow-fed rats resulted in mobilization of non-heme iron. The generation of NADH from alcohol metabolism via ADH or superoxide from acetaldehyde-xanthine oxidase mobilized iron from horse spleen ferritin in vitro. Chronic feeding of alcohol as 36% of energy for 6 weeks does not itself produce peroxidation in the rat but potentiates acute effects of ethanol. It produced microsomal induction which enhanced iron-stimulated lipid peroxidation and increased hepatic non-heme iron. Carbon monoxide increased rather than decreased accumulation of microsomal peroxidation products in vitro suggesting that cytochrome P-450 reductase mediates peroxidation but cytochrome P-450 may metabolize products. Incubation at lowered oxygen tensions equivalent to those observed in the perivenular zone (pO2 = 24 mmHg) enhanced in vitro iron mobilization but decreased peroxidation. Lipid peroxidation and its stimulation by iron mobilization and microsomal induction may be an important contributory mechanism of alcohol-induced liver injury.
Animals↗
Defective calcium influx in rat myelomonocytic leukemia cells which are resistant to differentiation-inducing effects of lipid A.
We compared the calcium mobilization in parent lipid A-sensitive leukemia cells (P2) and lipid A-resistant cells (LR) after treating them with lipid A in order to clarify the signal transduction involved in the differentiation induced by lipid A. Lipid A induced differentiation in P2 cells; however, LR cells were completely resistant to it. A dramatic elevation of intracellular free calcium ion concentration ([Ca2+]i) occurred in P2 cells, but only a slight elevation of [Ca2+]i in LR cells. Calcium ionophore in combination with lipid A induced differentiation in LR cells. An elevation of [Ca2+]i observed in P2 cells was abrogated by an addition of EGTA, which partially inhibited the differentiation of P2 cells stimulated by lipid A. Altogether, these data indicate that calcium influx is essential for the differentiation of P2 cells stimulated by lipid A and that defective calcium influx is responsible for the resistance to lipid A in LR cells.
Animals↗
Cholesterol-mediated changes of neutral cholesterol esterase activity in macrophages. Mechanism for mobilization of cholesteryl esters in lipid droplets by HDL.
Cholesteryl esters (CE) in lipid droplets undergo a continual cycle of hydrolysis and reesterification by neutral cholesterol esterase (N-CEase) and acyl CoA:cholesterol acyltransferase (ACAT), respectively. The mechanism by which HDL mobilizes CE from lipid droplets in J774 A.1 cells was investigated, focusing on N-CEase activity. We asked whether HDL enhances the activity and, if so, what signals induce the change of the activity. An incubation of cells with HDL enhanced the decline of cholesteryl-[l-14C]-oleate in foam cells and increased N-CEase activity in the supernatant of cell homogenate in a concentration-dependent manner, whereas incubation with LDL decreased the activity. In addition, N-CEase activity was fivefold higher when cells were cultured in 10% lipoprotein-deficient serum (LPDS) medium (2 micrograms cholesterol/mL) than when cultured in 10% fetal calf serum medium (31 micrograms cholesterol/mL), suggesting that changes in N-CEase activity are mediated by cholesterol. An addition of cholesterol (0 to 30 micrograms/mL) in LPDS medium markedly inhibited N-CEase activity with a concomitant increase in cellular cholesterol concentration. This inhibitory effect of cholesterol was also observed in mouse peritoneal macrophages. In vitro addition of cholesterol did not affect N-CEase activity. Treatment of cells with HMG-CoA reductase inhibitors enhanced N-CEase activity, whereas ACAT inhibitor decreased the activity. Northern blot analysis of N-CEase mRNA showed that the expression was not altered by the presence of cholesterol in LPDS medium. These results suggest that cholesterol downregulates N-CEase activity, probably through cholesterol-dependent appearance of some factors.
Animals↗
[Role of isoprenoid chain of lateral mobility of alpha-tocopherol in lipid bilayer].
Using the quenching effect of the fluorescence by nitroxyl radicals the lateral mobility of chromanols in the lipid bilayer was studied. The lateral mobility of the chromanols was shown to increase when the length of phytol chain was diminished. The result is consistent with the idea that antioxidant affect of the chromanols depends on their lateral mobility.
Chromans↗
Apocytochrome c binding to negatively charged lipid dispersions studied by spin-label electron spin resonance.
The interaction of apocytochrome c with aqueous dispersions of phosphatidylserine from bovine spinal cord and with other negatively charged phospholipids has been studied as a function of pH and salt concentration by using spin-label electron spin resonance (ESR) spectroscopy and chemical binding assays. The ESR spectra of phospholipids spin-labeled at different positions on the sn-2 chain indicate a generalized decrease in mobility of the lipids, while the characteristic flexibility gradient toward the terminal methyl end of the chain is maintained, on binding of apocytochrome c to phosphatidylserine dispersions. This perturbation of the bulk lipid mobility or ordering is considerably greater than that observed on binding of cytochrome c. In addition, a second, more motionally restricted, lipid component is observed with lipids labeled close to the terminal methyl ends of the chains. This second component is not observed on binding of cytochrome c and can be taken as direct evidence for penetration of apocytochrome c into the lipid bilayer. It is less strongly motionally restricted than similar spectral components observed with integral membrane proteins and displays a steep flexibility gradient. The proportion of this second component increases with increasing protein-to-lipid ratio, but the stoichiometry per protein bound decreases from 4.5 lipids per 12 000-dalton protein at low protein contents to 2 lipids per protein at saturating amounts of protein. Apocytochrome c binding to phosphatidylserine dispersions decreases with increasing salt concentration from a saturation value corresponding to approximately 5 lipids per protein in the absence of salt to practically zero at 0.4 M NaCl.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
EPR study of lipid phase in renal cortical membrane organelles from intact and cadmium-intoxicated rats.
Numerous studies have demonstrated various structure/function correlations at the level of transport proteins in the kidney cell membranes and various intracellular organelles. However, characterization of the lipid phase of these membranes is rare. Here, we report the differences in lipid organization and dynamics of the brush-border membranes (BBM), basolateral membranes (BLM) and endocytotic vesicles (EV), isolated from the kidney cortex of intact rats, studied with the EPR spectroscopy of the spin-labeled membrane lipids. The EPR spectra were analyzed by comparing experimentally observed line shapes with the line shapes calculated according to the theoretical model developed for liquid crystals. In the fitting procedure, three different lipid domains were assumed, which revealed clear differences in the lipid ordering and rotational correlation times, as well as in the lipid partition of these domains in each of the three types of membranes. A similar approach, used to compare the spectroscopic characteristics of BBM from control and cadmium-intoxicated rats, showed significantly changed ordering and increased molecular mobility in the lipid phase of BBM from Cd-treated animals. As tested by an established fluorescence assay, the Cd-induced changes in the lipid mobility co localized with approximately 5-fold higher conductance of BBM for potassium, with unchanged conductance for protons.
Animals↗
The Prader-Willi syndrome. Regulation of fat transport.
Studies of fat mobilization and transport are reported in six patients with the Prader-Willi syndrome. Two patients had carbohydrate intolerance. One of these had a low and the other an augmented insulin response to glucose challenge. Following challenge with glucose, three of the four nondiabetics had normal insulin responses or increased responses consistent with their obesity; the other nondiabetic had insulinopenia. Measurements of the effects of norepinephrine, insulin, glucose, and 5-methylpyrazole-3-carboxylic acid on plasma levels of FFA, glycerol, and ketones provide no evidence for abnormal regulation of mobilization of fat from adipose tissue. Measurements of plasma lipids and postheparin lipolytic activity are consistent with normal uptake of fat into adipose tissue, and normal fatty acid composition of adipose tissue gives no evidence for abnormal lipogenesis.
Adipose Tissue↗
Lipid hapten containing membrane targets can trigger specific immunoglobulin E-dependent degranulation of rat basophil leukemia cells.
We have studied the binding of liposomes containing dinitrophenylated lipid to rat basophil leukemia cells armed with monoclonal anti-dinitrophenyl IgE. The liposomes were either "fluid" at 37 degrees C (dimyristoylphosphatidylcholine or an equimolar binary mixture dipalmitoylphosphatidylcholine and cholesterol) or "solid" (dipalmitoylphosphatidylcholine, distearoylphosphatidylcholine, or dibehanoylphosphatidylcholine). We have also studied the immune mediated degranulation of these cells induced by the above lipid membrane targets. In some cases both studies were carried out with liposomes containing various surface densities of lipid haptens. From these studies we conclude that freely mobile nonaggregated lipid haptens in bilayer membrane targets can trigger efficient serotonin release from rat basophil leukemia cells in the presence of specific antihapten IgE. Solid target membranes are also effective as stimulators of serotonin release. The release of serotonin depends strongly on the surface density of lipid haptens over a narrow range of surface densities. These studies with lipid membrane targets having well defined physical properties indicate the need for generalized molecular models of receptor-mediated cell triggering.
Animals↗