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Results for “Lipid Mobilization”

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PubMed2003

Mechanism of magnetization transfer during on-resonance water saturation. A new approach to detect mobile proteins, peptides, and lipids.

The mechanism of magnetization transfer (MT) between water and components of the proton spectrum was studied ex vivo in a perfused cell system and in vivo in the rat brain (n = 5). Water was selectively labeled and spectral buildup consequential to transfer of longitudinal magnetization was followed as a function of time. At short mixing time (T(m)), nitrogen-bound solvent-exchangeable protons were observed, predominantly assigned to amide groups of proteins and peptides. At longer T(m), intramolecular nuclear Overhauser enhancement (NOE) was observed in the aliphatic proton region, leading to a mobile-macromolecule-weighted spectrum that resembles typical protein spectra described in the literature. This effect on the proton spectrum is distinct from that of classical off-resonance MT, which has been shown to be due to the immobile solid-like proton pool. When studying a solution of major brain metabolites under physiological concentrations and conditions (pH), no transfer effects were observed, in line with expectations based on reduced NOE effects in rapidly tumbling molecules and the fast proton exchange rates of amino, amine, SH, and OH groups. The spectral intensities of the amide protons may serve as indicators for pH and cellular levels of mobile proteins and peptides, while the aliphatic components are representative of several types of mobile macromolecules, including proteins, peptides, and lipids.

Animals↗
PubMed1999

Hepatocyte growth factor leads to recovery from alcohol-induced fatty liver in rats.

A fatty liver is characterized by the hyperaccumulation of lipids within hepatocytes and is often caused by excessive alcohol intake. Rats fed ethanol-containing diets for 37 days showed remarkable increase in hepatic lipids and lipid droplet accumulation in the hepatocytes, indicating the onset of alcoholic fatty liver. Administration of hepatocyte growth factor (HGF) for the last seven days of ethanol treatment markedly decreased hepatic lipids to a level lower than that seen before HGF treatment. In contrast, serum levels of lipids and lipoproteins increased with HGF administration. Primary cultured hepatocytes prepared from the fatty liver retained lipid droplets during a 48-hour culture. However, when cultured in the presence of HGF, intracellular lipid concentrations decreased and lipid secretion was enhanced. Consistent with these events, HGF stimulated the rate of protein synthesis of apolipoprotein B (apoB) and enhanced subsequent mobilization of lipids into the medium. These results indicate that HGF administration induced recovery from the fatty liver, at least in part, by enhancing apoB synthesis and the subsequent mobilization of lipids from hepatocytes with fatty change. The possibility that HGF can be therapeutic for subjects with an alcohol-related fatty liver warrants further attention.

Animals↗
PubMed1991

Postparturient metabolic and production responses in cows previously exposed to long-term treatment with somatotropin.

Postparturient metabolic and production responses were studied for 85 multiparous cows consisting of controls and animals that had been previously exposed to long-term treatment with bST. Older cows previously exposed to bST at high doses (51.6 mg/d) had lower milk yields than controls. However, there were no significant differences compared with controls in milk yield for lower dose (17.2 mg/d) older cows or parity 2 cow groups. The bST-treated groups had higher postpartum DMI, lower serum FFA, lower serum beta-hydroxybutyrate levels, and higher serum glucose than controls. Some bST-exposed groups had lower milk fat but higher milk protein levels. All bST-treated groups had significantly lower ratios of C18 to C4 to 10 milk fatty acids. Control cows of both parity groups were in higher body condition and weighed more than bST-treated cows prior to calving. The differences in postpartum metabolism may be attributed to differences in body composition resulting from bST treatment in the prior lactation, because use of body condition score prior to calving as a covariate did not substantially alter responses. The control cows probably had greater reserves of mobilizable lipid. These contentions are supported by changes in milk composition for bST-treated cows, which were consistent with animals of greater appetite, mobilizing less lipid. The bST-treated cows were probably more energetically efficient milk producers because they produced milk from feed rather than from mobilization of tissue stores. These data suggest that bST use in a prior lactation may have potential benefit in reducing risk of metabolic disorders associated with lipid mobilization in the postparturient period.

3-Hydroxybutyric Acid↗
PubMed2004

Implications of lipid raft disintegration: enhanced anti-inflammatory macrophage phenotype.

BACKGROUND: Lipid rafts are membrane microdomains characterized by an enriched cholesterol environment and appear to serve as a platform for signaling. Their role within the macrophage during endotoxin exposure is unknown. METHODS: THP-1 cells were subjected to lipopolysaccharide stimulation with or without methyl-beta-cyclodextrin (MbetaCD) pretreatment, a cholesterol depleting agent. Cell surface expression of toll-like receptor-4 (TLR4) and platelet-activating factor receptor (PAFr) was determined by flow cytometry. Membrane receptor components and activation of the mitogen-activated protein kinases (MAPK) was determined from lipid raft and cellular protein by immunoblot. Inflammatory mediator production was determined from harvested supernatants by enzyme-linked immunosorbent assay. RESULTS: Surface expression of TLR4 and PAFr was not affected by MbetaCD. Lipopolysaccharide stimulation led to TLR4 mobilization to lipid rafts, MAPK activation, and inflammatory mediator production. Pretreatment with MbetaCD did not affect TLR4 mobilization to lipid rafts, but did result in lost lipid raft expression of the PAFr coupled G-protein, Galpha1. MbetaCD treatment led to selective attenuation of MAPK activation through ERK 1/2. This dysregulated signaling was associated with attenuated production of tumor necrosis factor-alpha, but increased production of interleukin-10. CONCLUSION: Lipid raft disintegration results in lost expression of Galpha1, dysregulated MAPK signaling, and selective anti-inflammatory mediator production. Therefore, modulation of lipid raft cholesterol content may represent a potential mechanism for regulation of macrophage phenotypic differentiation.

Cell Line↗
PubMed2004

Changes in lipid class and fatty acid composition during development in white seabream (Diplodus sargus) eggs and larvae.

To establish the changes which occur during embryogenesis and early larvae development, eggs, yolk-sac larvae (one day old larvae) and absorbed yolk-sac larvae (three day old larvae) of white sea bream were examined for lipid class and fatty acid composition. The development was characterized by a decrease in all lipid classes with the exception of phosphatidylserine (PS) and fatty free acids (FFA) which increased, and sphingomyelin (SM) which remained unchanged. The changes observed in lipid class content and the decrease in fatty acids in total lipid (TL) reflect the utilization and mobilization of lipids during both embryogenesis and early larvae development. Fluctuations in the relative composition of fatty acids in phosphatidylcholine (PC) during development suggest a selective bulk uptake and catabolism of fatty acids in this lipid class. Unlike PC, catabolism of triacylglycerol (TG) fatty acid appears to be non-selective. During development, the decrease in levels of polyunsaturated fatty acids (PUFA) eicosapentaenoic (20:5n-3, EPA) and docosahexaenoic (22:6n-3, DHA) in total lipid denotes their utilization as energy substrate by Diplodus sargus larvae.

Age Factors↗
PubMed2005

Lipid rafts are involved in C95 (4,8) agrin fragment-induced acetylcholine receptor clustering.

During development of the neuromuscular junction, high densities of acetylcholine receptors accumulate beneath the overlying nerve terminal. A defining feature of mature synapses is the sharp demarcation of acetylcholine receptor density, which is approximately 1000-fold higher in the postsynaptic as compared with the contiguous extrasynaptic muscle membrane. These high densities of receptors accumulate by at least four mechanisms, re-distribution of existing surface receptors, local synthesis of new receptors, decreased turnover of synaptic receptors, and limitation of diffusion of sub-neural, aggregated receptors. The limitation of receptor diffusion within the membrane is likely in part due to the anchoring of acetylcholine receptor complexes to components of the cytoskeleton. Here we have tested the idea that lipid rafts--mobile, cholesterol enriched microdomains within the lipid bilayer--are another mechanism by which acetylcholine receptors are clustered in the postsynaptic apparatus. Using mouse C2C12 cells, a muscle cell line, we show that a carboxy terminal 95 amino acid fragment [C95 (4,8)] of the extracellular matrix molecule agrin that is essential for nerve-induced postsynaptic differentiation, promotes the redistribution of acetylcholine receptors into lipid rafts. Disruption of lipid rafts before agrin treatment largely inhibits de novo agrin-induced acetylcholine receptor clustering. Moreover, mature acetylcholine receptor clusters are destabilized if lipid rafts are disrupted. These results show that lipid rafts are important in both the initial clustering and later stabilization of agrin-induced acetylcholine receptor clusters and also suggest that lipid rafts may contribute to the postsynaptic localization of acetylcholine receptors in vivo.

Agrin↗
PubMed2003

Arrays of mobile tethered vesicles on supported lipid bilayers.

We report a new system of laterally mobile, arrayed vesicles that are encoded with DNA to control tethering to fluid-supported phospholipid bilayers. The motion of individual fluorescently labeled vesicles, specifically bound, are easily visualized by fluorescence video microscopy and observed to collide reversibly on the surface. This system is an ideal model for studying interactions involving membranes, in particular integral membrane proteins.

Fluorescent Dyes↗
PubMed1988

Lateral mobility of proteins and lipids in the red cell membrane and the activation of adenylate cyclase by beta-adrenergic receptors.

Models of beta-adrenergic signal transduction in red blood cell membranes frequently assume that at least one of the membrane-bound components is laterally mobile and distributes the hormonal signal in the membrane plane. However, direct measurements reveal that protein lateral mobility in the red cell membrane is severely restricted. Furthermore, the spectrin-actin compartmentalizes the cytoplasmic face of the red cell membrane into a regular array of small elementary areas. These considerations support models in which the beta-adrenergic signal is spread in the membrane plane by a molecule which has binding sites on the membrane but diffuses in the aqueous compartment.

Adenylyl Cyclases↗
PubMed2006

Peroxisomal carnitine acetyl transferase is required for elaboration of penetration hyphae during plant infection by Magnaporthe grisea.

Magnaporthe grisea, the causal agent of rice blast disease, invades plant tissue due to the action of specialized infection structures called appressoria, which are used to breach the leaf cuticle and allow development of intracellular, infectious hyphae. In this report we demonstrate that peroxisomal carnitine acetyl transferase (CAT) activity is necessary for appressorium function, and in particular, for the elaboration of primary penetration hyphae. The major CAT activity in M. grisea is encoded by the PTH2 gene, which shows elevated expression in response to acetate and lipid, and is regulated by the cyclic AMP response pathway. Furthermore, a Pth2-GFP fusion protein colocalizes with a peroxisomal marker protein. Targeted deletion of PTH2, generated mutants that were completely non-pathogenic, lacked CAT activity and were unable to utilize a range of lipid substrates. The impairment of appressorium function in Deltapth2 was associated with a delay in lipid reserve mobilization from germ tubes into developing infection cells, and abnormal chitin distribution in infection structures. Addition of glucose to Deltapth2 mutants partially restored the ability to cause rice blast disease and lipid reserve mobilization. Taken together, our findings provide evidence that Pth2 plays a role in the generation of acetyl CoA pools necessary for appressorium function and rapid elaboration of penetration hyphae during host infection.

Carnitine O-Acetyltransferase↗
PubMed1978

Effects of altered free fatty acid mobilization on the metabolic response to exercise.

This study was designed to evaluate the metabolic response to limitation of fat mobilization during severe exercise in man. To this end, we assessed the relationship between fat mobilization, lipid-ketone physiology, and exercise-induced elevations in the counter-regulatory hormones. Ten well trained athletes ran a 10-mile premeasured course in as short a time as possible during both a placebo and an experimental study. In the experimental study, fat mobilization was inhibited by the oral administration of 2 g of nicotinic acid. Blood samples for multiple substrate and hormonal assay were obtained 2 h before exercise, immediately before exercise, and immediately after exercise. In the experimental study, nicotinic acid effectively blocked the expected rise in plasma free fatty acid concentration observed in the placebo study. Although blunted, the exercise-induced rise in plasma ketone concentration persisted in spite of the reduced free fatty acid levels. The significance of the concommitant exagerated rise in glucagon and GH in stimulating ketogenesis is discussed. The inhibition of fat mobilization did not reduce the mean time required to run 10 miles. Since muscle uptake of free fatty acid is directly proportional to the plasma concentration of this substrate, our study suggests that the inability to mobilize fat does not prevent severe exercise for 70 min.

Amino Acids↗
PubMed1980

Reduced lateral mobility of a fluorescent lipid probe in cholesterol-depleted erythrocyte membrane.

The effect of cholesterol depletion of the human erythrocyte membrane on the lateral diffusion rate of a fluorescent lipid probe is reported. At low temperature (-5 to 5 degrees C), the diffusion of the probe is 50% slower in the cholesterol-depleted membrane than in non-depleted membrane. At high temperatures (30 to 40 degrees C), probe mobility is not affected by cholesterol depletion. These results suggest that cholesterol suppresses aspects of phospholipid phase changes in animal cells in a manner consistent with its behavior in artificial bilayers and multilayers. Whole erythrocytes were depleted of 30--50% of their cholesterol by incubation with a sonicated dispersion of dipalmitoyl phosphatidylcholine. Cells were then labeled with 3,3'-dioctadecylindocarbocyanine (diI), a phospholipid-like fluorescent dye, and hemolyzed into spherical ghosts. The rate of lateral motion of diI was measured by observing the fluorescence recovery after local photobleaching with a focused laser spot. The diffusion rate of the lipid probe in both control and cholesterol-depleted erythrocyte membrane is substantially smaller than in any cell or model membrane previously measured.

Carbocyanines↗
PubMed1984

Effect of alpha-tocopherol on lipid peroxidation and acyl chain mobility of liver microsomes from vitamin E-difficient rat.

Effects of alpha-tocopherol on lipid peroxidation and membrane fluidity were studied in liver microsomes from vitamin E (alpha-tocopherol)-deficient rats using NADPH as a substrate. Microsomes containing various contents of alpha-tocopherol were prepared by incubation with various concentrations of alpha-tocopherol in ethanol solution. NADPH-dependent lipid peroxidation decreased the content of polyunsaturated fatty acids, arachidonic acid and 4, 7, 10, 13, 16, 19-docosahexaenoic acid. The treatment with alpha-tocopherol before peroxidation reduced the production of lipid peroxides and the change in fatty acid composition even at the lowest content of alpha-tocopherol dealt with in this experiment, 0.2 molar fraction, while addition of alpha-tocopherol after peroxidation resulted in a slight inhibition of peroxide production and small alteration in fatty acid composition. By an ESR measurement using stearate spin probe, the alpha-tocopherol incorporated into microsomes did not alter the acyl chain mobility up to 0.2 molar fraction but reduced the mobility above 0.2 molar fraction. The acyl chain mobility was markedly decreased by lipid peroxidation. The decrease of membrane fluidity was repressed in microsomes treated with alpha-tocopherol before peroxidation, but was not repressed in microsomes treated after peroxidation. The experiment using artificial membranes of egg yolk phosphatidylcholine and rat liver phosphatidylcholine revealed that the effect of alpha-tocopherol on membrane fluidity depends on the fatty acid composition of phospholipid, especially the content of arachidonic acid. On the other hand, the mobility of the fatty acyl chain was not affected by spermine at concentrations which could inhibit lipid peroxidation. These results suggest that the inhibitory effect of alpha-tocopherol on lipid peroxidation is due to antioxidant activity rather than the indirect effect of membrane stabilization.

Acylation↗
PubMed1989

Reduced lateral mobility of a fluorescent lipid analog in cell membranes of rat fibroblasts transformed by simian virus 40.

In order to study the difference between normal and transformed cells, lateral motion of fluorescent molecules embedded into cell membranes of rat clonal fibroblasts and its SV40-transformed derivative cells was measured by the FPR technique. The lateral diffusion coefficient of a fluorescent fatty acid analog, F18, was smaller in transformed cells than normal cells. This indicates that the lipid phase of membranes from transformed cells is less fluid than that from normal cells. On the other hand, the lateral diffusion coefficient of S-F-concanavalin A was identical in both cells. These results suggest that the mobility of different molecules on the membranes is controlled by different mechanisms.

Animals↗
PubMed2006

Surface-supported bilayers with transmembrane proteins: role of the polymer cushion revisited.

Protein lateral mobility in surface-supported bilayers is often much lower than the mobility of the lipids. In the present study we explore whether the incorporation of a PEG cushion between the bilayer and the substrate increases the lateral mobility of transmembrane proteins in bilayers produced via directed assembly, a method based on Langmuir-Blodgett deposition techniques. In our experiments, the PEG cushions were incorporated by adding PEG lipids to the protein/lipid monolayer at the air/water interface, at the first step of bilayer assembly. The protein and lipid mobilities in 160 different bilayers, with various PEG molecular weights and PEG lipid concentrations, were measured and compared. We found that the measured diffusion coefficients do not depend on the PEG molecular weight or the PEG lipid concentration and are very similar to the values measured in the absence of PEG. Therefore, contrary to our expectations, we found that a PEG cushion does not necessarily increase protein mobility, suggesting that the low protein mobility is not a consequence of protein-substrate interactions. Furthermore, we showed that the low protein mobility is not due to protein aggregation. The major determinant of protein mobility in surface-supported bilayer systems appears to be the method of bilayer assembly. While proteins were always mobile if the bilayers were prepared using the directed assembly method, in the presence and absence of a PEG cushion, other bilayer assembly protocols resulted in complete lack of protein mobility.

Adsorption↗