[Lipid mobilization activity of the blood in atherosclerosis].
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Adult↗
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Results for “Lipid Mobilization”
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The characteristics of lipid mobilization and peripheral disposition in aged individuals.
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Adult↗
[Activity-mobilizing lipids and blood lipids in patients treated with Mazindol].
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Adolescent↗
Impact of exercise on adipose tissue metabolism in humans.
Mobilization of lipids from adipose tissue during prolonged exercise is of key importance for the supply of energy to the working muscle. During exercise lipid mobilization is mainly stimulated by increased catecholamine production leading to acceleration of the beta-adrenoceptor mediated lipolysis rate in fat cells. This causes breakdown of triglycerides in fat cells to glycerol and free fatty acids, which then are delivered to the blood stream. Decreased insulin production, enhanced adipose tissue blood flow and decreased reesterification of free fatty acids in fat cells contribute to the enhancement of lipid mobilization during strenuous and long-term light exercise. Several additional factors modulate the lipolytic response to exercise as well. Endurance training increases the lipolytic action of catecholamine whereas the opposite occurs during ageing. These alterations are at least in part mediated by changes in the function of the final step in lipolysis activation, the protein kinase-hormone sensitive lipase complex. There are also gender and regional differences in the lipolytic response to exercise. Women mobilize more lipids from the subcutaneous abdominal area than men, whereas a low rate of lipid mobilization from the peripheral subcutaneous areas is observed in either sex. In pathophysiological states, which are associated with catabolism such as fasting and insulin dependent diabetes, there is an enhanced lipolytic response to exercise, because of increased beta-adrenoceptor function.
Adipose Tissue↗
Endotoxin tolerance attenuates LPS-induced TLR4 mobilization to lipid rafts: a condition reversed by PKC activation.
Endotoxin tolerance is characterized by attenuated macrophage activation to subsequent LPS challenge and can be reversed through nonspecific protein kinase C (PKC) activation, and activation by LPS within naïve cells requires the activation of the cell surface receptors CD14 and TLR4 on lipid rafts. The effect of PKC activation and endotoxin tolerance on lipid raft receptor complex assembly is unknown and the focus of this study. Tolerance was induced in THP-1 cells through LPS pre-exposure. Naïve and tolerant cells were stimulated with LPS, with or without PMA pretreatment to activate PKC. TLR4 surface expression and LPS binding were determined by flow cytometry and immunohistochemistry. Cellular and lipid raft protein was analyzed for the presence and activation of the TLR4 complex components. Harvested supernatants were examined for TNF-alpha production. Total TLR4 surface expression and LPS binding were not affected by tolerance induction. LPS stimulation of naïve cells resulted in TLR4 and heat shock protein (HSP)70 lipid raft mobilization, MAPK activation, and TNF-alpha production. LPS stimulation of tolerant cells was associated with attenuation of all of these cellular events. Although PKC activation by PMA had no effect on naïve cells, it did result in reversal in tolerance-induced suppression of TLR4 and HSP70 lipid raft mobilization, MAPK activation, and TNF-alpha production. In addition, the effects associated with PMA were reversed with exposure to a myristoylated PKC-zeta pseudosubstrate. Thus, endotoxin tolerance appears to be induced through attenuated TLR4 formation following LPS stimulation. This complex formation appears to be PKC-dependent, and restoration of PKC activity reverses tolerance.
Cell Line↗
The effect of ATP on the order and the mobility of lipids in the bovine erythrocyte membrane.
The order and the mobility of the lipids in the membrane were measured by the ESR method for the erythrocytes with both normal and modified intracellular concentration of ATP. The lipid order did not depend on the ATP level, but the lipid mobility was affected by the intracellular ATP concentration. The lipid mobility was higher in the cells with a larger concentration of ATP.
Adenosine Triphosphate↗
Effects of thyroxin, cortisol, growth hormone, and prolactin on lipid metabolism of coho salmon, Oncorhynchus kisutch, during smoltification.
Juvenile coho salmon, Oncorhynchus kisutch, were either immersed in thyroxin-containing water (T4; 20 micrograms/ml) or implanted with cortisol (5 mg), bovine growth hormone (GH; 1.5 microgram/g body wt), or ovine prolactin (PRL; 1.5 microgram/g body wt), both early and late in smoltification. T4 and cortisol treatment stimulated lipid mobilization in parr. T4-stimulated lipid mobilization was indicated by decreased total lipids, primarily as triacylglycerols, and increased lipolytic enzyme (triacylglycerol lipase) activity in the liver and dark muscle. T4-stimulated lipid mobilization from mesenteric fat was indicated by decreased total tissue mass and by increased lipase activity. Cortisol caused significant reductions in total lipid concentration and triacylglycerol content of the liver and dark muscle; these effects were accompanied by increased lipase activity. Cortisol treatment did not affect mesenteric fat total lipid concentration, total tissue mass, or triacylglycerol content. However, cortisol implantation did enhance mesenteric fat lipase activity. Thyroxin and cortisol treatment failed to elicit alterations in the pattern of tissue lipid mobilization of smolts. GH stimulated lipid mobilization from coho salmon parr. Depletion of liver total lipids was accompanied by increased lipolytic enzyme (triacylglycerol lipase) activity. GH had limited effects on dark muscle and mesenteric fat. In smolts, GH had virtually no effect on lipid mobilization. PRL strongly stimulated lipid mobilization in parr; this effect was evident in all depots studied (liver, dark muscle, mesenteric fat). Decreases in total lipid concentration, or in total tissue mass (mesenteric fat), were accompanied by increased lipase activity and generally resulted in reduced tissue triacylglycerol content. Smolts appeared refractory to PRL treatment. Smolts (characteristically possessing elevated liver lipase activity) that were hypophysectomized exhibited low levels of liver lipase activity. Cortisol replacement restored enzyme activity to approximately the same levels as those observed in sham-operated controls. GH replacement restored lipase activity, but not to the levels observed in sham-operated controls. These results indicate that T4, cortisol, GH, and PRL all stimulate lipid mobilization in developing salmon by enhancement of lipolysis and suggest that T4, cortisol, GH, and PRL are among the factors which contribute to smoltification-associated lipid depletion.
Adaptation, Physiological↗
Age-dependence of the lateral mobility of lipids in hepatocyte plasma membrane of male rats and the effect of life-long dietary restriction.
The lateral diffusion constant of lipids (D(1)) in hepatocyte plasma membranes was measured in liver smears by means of the fluorescence recovery after photobleaching (FRAP) method, applying the label, N-4-nitrobenzo-2-oxa-1,3-diazolyl phosphatidylethanolamine (NBD-PE). Nineteen ad libitum fed, male Fischer-344 rats in four age groups (2.1-29.8 months of age) were studied. A highly significant negative linear age-correlation of D(1) (cc = 0.958) was found. D(1) values were 1.39 x 10(-9) cm2/s in the young rats, and only 6.77 x 10(-10) cm2/s in the oldest rats. Lipid lateral mobility is changing in parallel with that of proteins, having been measured previously also with the FRAP method by the authors. Fractional recovery values (FR%) of the lipids were lower than those of proteins even in the young ages, but also decreased linearly with age, therefore, the parameter, D, x FR decreased even steeper with age than D(1) itself. D(1) was also measured in a group of six male Fischer 344 rats having been kept on dietary restriction (DR) since their age of 1 month until 30 months of age (applying the every-other-day (EOD) feeding). DR caused an increase of D(1), compared with the age-matched ad libitum fed animals: the mean was 9.24 x 10(-10) cm(2)/s. FR% and D(I), x FR again increased considerably under DR. The results are interpreted in terms of the increased protein and lipid turnover under DR.
Journal Article↗
Intermediary metabolism of adipose tissue.
Metabolism of ruminant adipocytes involves the synthesis and mobilization of lipids. Rates of lipid synthesis from the uptake of preformed fatty acids (via lipoprotein lipase) and de novo synthesis of fatty acids are related to the energy balance. Acetate is the major carbon source for fatty acid synthesis with NADPH originating from the pentose cycle and the isocitrate cycle. Ruminant adipose tissue lacks the ability to utilize for lipogenesis those substrates that generate mitochondrial acetyl CoA because of an absence of ATP citrate-lyase and NADP-malate dehydrogenase. Lipid mobilization in ruminant adipocytes is apparently regulated via cAMP levels and a summary of the compounds investigated for lipolytic responses is presented. The control of lipid synthesis and mobilization is interrelated in ruminant adipose tissue. The coordinated manner in which these two functions are regulated is examined with regard to adipocyte responses to insulin and epinephrine. In both lipid synthesis and lipid mobilization, ruminant adipocytes are uniquely different from nonruminant adipose tissue. The physiological significance and possible basis for these species differences in adipose metabolism are discussed.
Adipose Tissue↗
Regional differences in the lateral mobility of plasma membrane lipids in a molluscan embryo.
Regional and temporal differences in plasma membrane lipid mobility have been analyzed during the first three cleavage cycles of the embryo of the polar-lobe-forming mollusc Nassarius reticulatus by the fluorescence photobleaching recovery (FPR) method, using 1,1'-ditetradecyl 3,3,3',3'-tetramethylindocarbocyanine iodide (C14diI) as a fluorescent lipid probe. During this period of development the lateral diffusion coefficient of membrane lipids is consistently greater in the vegetal polar lobe area as compared to the animal plasma membrane area (on average 30%), demonstrating the existence of an animal-vegetal polarity in plasma membrane properties. At third cleavage, the differences between animal and vegetal plasma membrane region become even more pronounced; in the four animal micromeres the diffusion coefficient (D) and mobile fraction (MF) are 2.9 +/- 0.2 X 10(-9) cm2/sec and 51 +/- 2%, respectively, while in the four vegetal macromeres D = 5.0 +/- 0.3 X 10(-9) cm2/sec and MF = 78 +/- 2%. Superimposed upon the observed animal-vegetal polarity, the lateral diffusion in the polar lobe membrane area shows a cell-cycle-dependent modulation. The highest mean values for D are reached during the S phase (ranging from 7.0 to 7.8 X 10(-9) cm2/sec in the three cycles measured), while at the end of G2 phase and during early mitosis mean values for D have decreased significantly (ranging from 5.0 to 5.9 X 10(-9) cm2/sec). Diffusion rates in the animal membranes of the embryo are constant during the three successive cell cycles (D = 4.3-5.0 X 10(-9) cm2/sec), except for a peak at the S phase of the first cell cycle (D = 6.0 X 10(-9) cm2/sec). These results are discussed in relation with previously observed ultrastructural heterogeneities in the Nassarius egg plasma membrane. It is speculated that the observed animal-vegetal polarity in the organization of the egg membrane might play an important role in the process of cell diversification during early development.
Animals↗
Do specific linoleate 13-lipoxygenases initiate beta-oxidation?
The germination process of oilseed plants is characterized by a mobilization of the storage lipids which constitute the major carbon source for the growing seedling. Despite the physiological importance of the lipid mobilization, the mechanism of this process is not well understood. Recently, it was found that a specific linoleate 13-lipoxygenase is induced during the stage of lipid mobilization in various oilseed plants and that this enzyme is translocated to the membranes of the lipid storage organelles, the so called lipid bodies. Lipoxygenase expression was paralleled by the occurrence of enantiospecific hydro(pero)xy polyenoic fatty acid derivatives in the storage lipids suggesting the in vivo action of the enzyme. Furthermore, it was reported that oxygenated polyenoic fatty acids, in particular as 13(S)-hydro(pero)xy-9(Z),11(E)-octadecanoic acid [13(S)-H(P)ODE], are cleaved preferentially from the storage lipids when compared with their non-oxygenated linoleate residues. These findings may suggest that 13(S)-H(P)ODE may constitute the endogenous substrate for beta-oxidation during lipid mobilization of oilseed plants.
Cucumis sativus↗
Lateral mobility of plasma membrane lipids in normal and transformed keratinocytes.
In this study we have examined possible differentiation-dependent modulations in plasma membrane lipid properties in normal keratinocytes, SV-40 transformed keratinocytes (SVK14) and a number of squamous carcinoma (SCC) cells. In normal keratinocytes the lateral diffusion coefficient of plasma membrane lipids (D) differs significantly for cells cultured permanently under low and normal Ca2+-conditions (5.16 x 10(-9) and 3.27 x 10(-9) cm2/s, respectively). When differentiation is induced by exposing low Ca2+-cultured cells to normal Ca2+ concentrations D increases to 7.07 x 10(-9) cm2/s during the initial hours of differentiation followed by a gradual sustained decrease to values also observed in cells cultured permanently under normal Ca2+-conditions. In SCC and SVK14 cells a similar initial transient increase in lateral lipid mobility is observed upon initiation of differentiation, but, in contrast to normal keratinocytes, no sustained decrease in D is seen upon prolonged culturing under normal Ca2+ conditions. The results indicate that the deficiency of the transformed cells to respond to Ca2+-induced differentiation might involve transformation-dependent alterations in membrane structure and function.
Calcium↗
Distinguishing individual lipid headgroup mobility and phase transitions in raft-forming lipid mixtures with 31P MAS NMR.
A model membrane system composed of egg sphingomyelin (SM), 1,2-dioleoyl-sn-glycero-3-phosphocholine (DOPC), and cholesterol was studied with static and magic angle spinning (31)P NMR spectroscopy. This model membrane system is of significant biological relevance since it is known to form lipid rafts. (31)P NMR under magic angle spinning conditions resolves the SM and DOPC headgroup resonances allowing for extraction of the (31)P NMR parameters for the individual lipid components. The isotropic chemical shift, chemical shift anisotropy, and asymmetry parameter can be extracted from the spinning side band manifold of the individual components that form liquid-ordered and liquid-disordered domains. The magnitude of the (31)P chemical shift anisotropy and the line width is used to determine headgroup mobility and monitor the gel-to-gel and gel-to-liquid crystalline phase transitions of SM as a function of temperature in these mixtures. Spin-spin relaxation measurements are in agreement with the line width results, reflecting mobility differences and some heterogeneities. It will be shown that the presence of DOPC and/or cholesterol greatly impacts the headgroup mobility of SM both above and below the liquid crystalline phase transition temperature, whereas DOPC displays only minor variations in these lipid mixtures.
Cholesterol↗
Adipose tissue mobilization is unaffected by obesifying hypothalamic knife cuts.
Unilateral electrolytic lesions of the medial hypothalamus have previously been reported to spare starvation-induced lipid mobilization from the ipsilateral retroperitoneal fat pad. This suggests that deficient lipid mobilization contributes to the enhanced lipid deposition which results when such lesions are bilateral. In contrast, unilateral parasagittal hypothalamic knife cuts, which also obesify when bilateral, failed to prevent starvation-induced ipsilateral lipid mobilization. This finding indicates that impairment of neurally mediated lipid mobilization is probably neither a necessary nor a sufficient feature of hypothalamic obesity.
Adipose Tissue↗
Correlation between the occurrence of 1H-MRS lipid signal, necrosis and lipid droplets during C6 rat glioma development.
The aim of this study was to investigate the possible correlation between the 1H MRS mobile lipid signal, necrosis and lipid droplets in C6 rat glioma. First, the occurrence of necrosis and lipid droplets was determined during tumor development, by a histological analysis performed on 34 rats. Neither necrosis nor lipid droplets were observed before 18 days post-implantation. At later stages of development, both necrosis and lipid droplets were apparent, the lipid droplets being mainly located within the necrotic areas. Using a second group of eight rats, a temporal correlation was evidenced between mobile lipid signal detected by in vivo single-voxel one- (136 ms echo time) and two-dimensional J-resolved 1H MR spectroscopy, and the presence of necrosis and lipid droplets on the histological sections obtained from the brains of the same rats. Finally, spatial distribution of the mobile lipid signal was analyzed by chemical-shift imaging performed on a third group of eight animals, at the end of the tumor growth. The spectroscopic image corresponding to the resonance of mobile lipids had its maximum intensity in the center of the tumor where necrotic regions were observed on the histological sections. These necrotic areas contained large amounts of lipid droplets. All these results suggest that mobile lipids detected in vivo by 1H MRS (136 ms echo time) in C6 rat brain glioma arise mainly from lipid droplets located in necrosis.
Animals↗
Interactions between major nutrients in the diet and the lactational performance of rats.
The effect on lactational performance of replacing feed carbohydrate with fat at two different protein levels was studied. Lactating Sprague-Dawley rats with a standardized litter size of thirteen pups were allocated one of eight feeds containing either 300 or 150 g protein/kg organic matter (OM) and ranging in fat content from 100 to 550 g/kg OM from day 2 until day 14 of lactation. Daily food intake, live-weight gains, and changes in body composition of both dams and litters were measured. Feeds of low protein content resulted in a significant decline (P < 0.001) in lactational performance despite a significant increase (P < 0.001) in maternal protein mobilization. Maternal lipid mobilization was not significantly affected by feed composition. Litter lipid gain was significantly increased (P < 0.05) as fat replaced carbohydrate in the high-protein feeds, due to an increase in maternal energy intake. In contrast, lactational performance was severely depressed (P < 0.001) as fat replaced carbohydrate in the low-protein feeds. This interaction between feed components on lactational performance was in accordance with the hypothesis that the heat production of lactating rats is maximal and, hence, constraining intake.
Animals↗
Lipid lateral mobility in the plasma membrane of whole plant cells.
Fluorescence photobleaching recovery was used to measure the apparent lateral diffusion coefficient and mobile fraction of a fluorescent lipid probe in the plasma membranes of whole plant cells, i.e., in the presence of cell walls. Interfering fluorescence from the cell wall was reduced by extensive washing and then subtracted from the recovery recordings. Mobility characteristics of plasma membrane lipids in whole cells were found to be very similar to those in protoplasts.
Cell Membrane↗
Some hormonal influences on glucose and ketone body metabolism in normal human subjects.
Control of glucose and ketone body metabolism is integrated by a variety of hormones. Insulin is the major anabolic hormone, and its actions are antagonized by rapidly acting catabolic hormones, such as glucagon and the catecholamines, and by others such as cortisol, growth hormone and the thyroid hormones, which generally have more delayed effects. In the normal human subject, the effects of catabolic hormones to raise blood glucose are limited by a compensatory increase in insulin secretion, and these effects are enhanced in insulin deficiency. Hyperketonaemic actions of the catabolic hormones may result from increased supply of non-esterified fatty acids from lipolysis, although glucagon has a major direct action to increase ketogenesis at the liver. As expected, these actions are also restricted in normal humans by the compensatory rise in insulin secretion. Hyperketonaemia does, however, occur with adrenaline (epinephrine) and noradrenaline (norepinephrine), even in the presence of mildly elevated insulin concentrations. These catecholamines may assume particular importance in mobilization of lipid fuels in milder forms of stress, when insulin secretion is normal or mildly increased. In severe stress, when there is catecholamine-induced suppression in insulin secretion, lipolytic and hyperketonaemic effects of all the catabolic hormones may be manifest. Starvation in humans also results in diminished insulin secretion and increased catabolic hormone secretion. The relative importance of individual hormones in lipid mobilization during starvation is uncertain, although glucagon, growth hormone, noradrenaline and, possibly, dopamine may all play a part.
3-Hydroxybutyric Acid↗