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At least 685 records · Page 38Linked to original sources
PubMed1988

Increase of erythrocyte resistance to hemolysis and modification of membrane lipids induced by hemodialysis.

Mechanical fragility, deformability and lipid composition of erythrocyte membranes were studied in 22 uremic dialysed patients before and after dialysis in comparison to controls. While deformability was not affected by a dialysis session, osmotic and saponin resistances to hemolysis were significantly increased after dialysis (p less than 0.001). The lipid composition of erythrocyte membranes was also altered during dialysis, with a notable increase in cholesterol and a different phospholipid distribution, i.e. phosphatidylcholine and sphingomyelin significantly decreased (p less than 0.001). Likewise, the fatty acid distribution showed large variations with an increase in polyunsaturated fatty acid. The acute effect of dialysis on the membrane lipid composition seems to be linked to erythrocyte alterations. Its significance is discussed in relation to the asymmetric transverse distribution of phospholipids previously described in human erythrocyte.

Adult↗
PubMed1988

Modifications of plasma lipids, lipoproteins and apolipoproteins in advanced cancer patients treated with recombinant interleukin-2 and autologous lymphokine-activated killer cells.

Intravenous injection of recombinant interleukin-2 (r-Met-hu-IL-2(Ala-125] and LAK cells induced dramatic changes of lipoproteins in 12 patients with advanced cancer. After r-IL-2 injection (1) total cholesterol was reduced by 47% as a mean, LDL-cholesterol by 62%, HDL-cholesterol by 77%; (2) the triglyceride/cholesterol ratio was greatly increased (352%); (3) apolipoproteins B, A-I and A-II showed a mean reduction of 26%, 55% and 51%, respectively; and (4) very low density lipoproteins relatively increased, and HDL were separated into two definite fractions (I and II). LAK cell administration accentuated all the above effects and in most patients, HDL-fraction I almost completely disappeared. An action on hepatic synthesis of acute phase proteins is pointed out by the increase in C-reactive protein and apolipoprotein S concentrations contrasting with an unexpected reduction of fibrinogen. Surprisingly the drastic changes caused by treatment were quickly and completely reversible.

Acute-Phase Proteins↗
PubMed1987

Modifications of cellular lipids induce insulin resistance in cultured hepatoma cells.

We altered the cellular lipid composition of an insulin sensitive rat hepatoma cell line through supplementation of the culture medium with linoleic acid (18:2) or 25-hydroxycholesterol, and we studied the effects on insulin stimulation of aminoacid transport system A and glycogen synthesis. The basal rate of sodium-dependent aminoisobutyric acid uptake was slightly reduced in hydroxysterol-treated cells and increased in 18:2-enriched cells. Maximal insulin stimulation of transport was decreased by about 40% in both 18:2 and 25-hydroxycholesterol modified cells, as compared to control cells. In addition to reduced responsiveness, the hydroxysterol-treated cells also showed a diminished sensitivity to insulin, as revealed by a right-shift of the dose-response curve leading to a ED50 of 1.2 X 10(-8) M (P less than 0.02), as compared to 2.45 X 10(-9) M in control cells and 2.13 X 10(-9) M in 18:2 enriched cells. Concerning glycogen synthesis, the basal rate was unaffected by 25-hydroxycholesterol supplementation and slightly reduced in cells enriched in 18:2. Maximal insulin stimulation of glycogen synthesis was reduced by about 40% in both types of lipid modified cells. 25-Hydroxycholesterol again provoked a decrease in sensitivity to insulin: the ED50 was enhanced to 4.9 X 10(-9) M (P less than 0.05), as compared to 1.25 X 10(-9) M in control cells and 1.57 X 10(-9) M in 18:2-supplemented cells. Taken together with the previously reported changes of insulin binding to lipid modified hepatoma cells (Bruneau et al. (1987) Biochim. Biophys. Acta 928, 287-296) our results demonstrate an influence of alterations of the cellular lipid composition on both binding and biological actions of insulin, leading to an insulin-resistant state. Divergences between insulin binding and action were obtained and it was suggested that post-binding events may be responsible for the observed changes. Our findings may be relevant to experimental and clinical states of insulin resistance.

Amino Acids↗
PubMedDate not supplied

Modifications in cerebral lipid metabolism by severe glucose deprivation during aging.

Severe glucose deprivation causes extensive derangement of phospholipids, fatty acids and free fatty acids in cerebral cortex of rats of different ages. The hypoglycemia-induced cerebral loss of phospholipids and fatty acids persists after 60 min recovery. Changes in individual classes of lipids are largely affected by aging. In fact, during glucose deprivation and recovery, in adult animals no preferential loss of polyunsaturated fatty acids and ethanolamine phosphoglycerides occurs, suggesting that the loss could be related to oxidative rather than to peroxidative degradation. On the contrary, in senescent rats the quoted events occur, suggesting the hypothesis of a possible peroxidation of cerebral lipids. Pretreatment with some agents is performed to elucidate the aging mode of action. Papaverine (acting on macrocirculation) is uneffective, while raubasine (acting on microcirculation and metabolism) and almitrine (acting on oxygen availability) interfere with the phospholipid and fatty acid metabolism, their action being different according to the rat age.

Aging↗
PubMed2005

Genetic modification of the heart: transgenic modification of cardiac lipid and carbohydrate utilization.

Many recent advances in cardiovascular research have been made possible by the use of transgenic technology. This review will discuss a number of mouse models where transgenic technology has been utilized to alter expression of genes involved in cardiac uptake and metabolism of either lipid or carbohydrate. Particular attention will be paid to the proteins which regulate (1) carbohydrate and lipid transport into cardiomyocytes and (2) the subsequent metabolic process which occur within the cytosol. These steps are important in determining substrate availability for mitochondrial oxidative metabolism. The heart relies predominantly on fatty acids as its major fuel supply, while glucose and lactate provide a small percentage. Under certain conditions, this balance becomes altered such that the heart relies more on glucose, as seen in pathological hypertrophy or may rely almost solely on fatty acids, as observed in cardiac tissue of animal models of diabetes. Initially this switch in metabolic substrate provides adequate energy to maintain normal cardiac function however with time diastolic dysfunction and cardiac failure often occur associated with depletion in high-energy phosphates. The creation of transgenic mice with altered expression of genes involved in carbohydrate and lipid metabolism have provided a unique insight into the fine balance which exits in the mouse heart to maintain energy status and cardiac function. The models discussed in this review define both transport and cytosolic metabolism of lipid and carbohydrate as key cellular processes in the regulation of cardiac function and the pathogenesis of cardiac disease.

Animals↗
PubMedDate not supplied

Glutamate excretion triggering mechanism: a reinvestigation of the surfactant-induced modification of cell lipids.

Lipid alterations induced by surfactants to trigger glutamate excretion were investigated with an industrial strain of Corynebacterium glutamicum. The lipid composition of this strain was determined for cultures in a synthetic medium and in a complex medium. A distribution of complex lipids between the cell wall and the cell membrane is proposed. Depending on growth conditions, 70-85% of the cell fatty acids had saturated chains in cells grown with surfactants. In the synthetic medium up to 80% of the straight-chain fatty acids may have come from the acylated surfactant added to the induce excretion. In industrial fermentation, the maximal excretion rate corresponded to the highest saturated fatty acid content of cells. It was shown by radioactive labelling in the synthetic medium that the addition of the acylated surfactant induced the degradation of more than 50% of the phospholipids. Some phospholipid synthesis occurred at that time using the surfactant (saturated) fatty acids, but the membrane did nor recover its previous phospholipid content. A model is proposed to explain the mechanism of glutamate excretion triggering by surfactants.

Cell Membrane↗
PubMed1993

[Cyclical gestagen (MPA) supplement for continuous transdermal or oral estrogen substitution in postmenopause: modification of serum lipids].

Since postmenopause unopposed oestrogen replacement therapy (ERT) increases the incidence of endometrial carcinoma, the addition of a progestin in non-hysterectomised women is mandatory for hormonal substitution. On the other hand, progestins have a negative influence on serum lipids and may thus put in question the benefits of the ERT with regard to the cardiovascular risk. Progestins lower HDL and increase LDL in a dose-dependent way according to their chemical structure. In the present non-randomised study, the influence of a cyclic combined oestrogen progestin substitution on the serum lipids has been measured. From a total of 90 apparently healthy postmenopausal patients, 59 received a transdermal ERT with 17 beta-Estradiol (Estraderm TTS 50), whereas 31 women obtained a daily dose of 0.625 mg conjugated equine oestrogens (CE) perorally. Additionally all patients were given 10 mg medroxyprogesterone-acetate (MPA) daily during the first 10 days of each month. After 6 months of therapy, the following changes of serum lipids, expressed as percentage of initial values, were measured: total cholesterol in the transdermal group -2.3% (n.s.), in the peroral group -11.8% (p < 0.00001); triglycerides -3.7% (n.s.) resp. +8.6% (n.s.); HDL cholesterol + 0.2% (n.s.) resp. -1.8% (n.s.); LDL cholesterol +1.3% (n.s.) resp. -14.8% (p < 0.00001). The calculated atherogenic indices showed a decrease in the peroral substituted group of -6.5% (n.s.) for the HDL/total cholesterol ratio and -14.8% (p < 0.002) for the LDL/HDL ratio.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Cutaneous↗
PubMed1999

Modification of serum lipids and cardiovascular risk by estrogenic active compounds.

Cardiovascular disease is an important cause of death among women. After the menopause there is a steep elevation of low-density lipoprotein (LDL) cholesterol and lipoprotein(a) concomitantly with other risk factors, followed by a striking increase in arteriosclerotic vascular disease, compatible with a lack of estrogens as a causative factor. The benefit of hormone replacement therapy has been documented in several large studies, although rigorous randomized trials are still under way. However, cardiovascular events have been reduced by approximately 50%. In order to optimize beneficial effects and minimize side-effects, the characteristics of selective estrogenic active compounds are a major target of research. The anti-estrogens are the prototype of partial and selective estrogen functions. The components of conjugated estrogens are under investigation for their specific effects. For example, both 17 alpha-dihydroequilin sulfate and 17 alpha-dihydroequilenin sulfate seem to exert antioxidant activity without significant proliferative effects on uterine or breast tissues. This suggests a selective estrogenic activity dependent on the predominant type of estrogen receptor in the particular tissue. Equilin sulfate exerts a significantly stronger antioxidant activity than 17 beta-estradiol in vitro, and delta 8-estrone sulfate increases the lag time for low-density lipoprotein oxidation in vivo. These actions on lipoproteins may add to the quantitative changes of lipoproteins, while other effects are independent of lipoproteins. The 17 alpha-dihydroequilin sulfate and equilin sulfate improved the action of insulin in vivo. Data from rhesus monkeys treated with 17 alpha-dihydroequilenin sulfate indicate that additional mechanisms are probably responsible for the observed cardiovascular protection. Further studies need to be conducted in order to identify selective estrogen receptor modulators and assess their potential, especially in lowering cardiovascular risk.

Aged↗
PubMed2003

Modification of plant lipids for human health: development of functional land-based omega-3 fatty acids.

We have remodeled canola seeds to accumulate the omega-3 fatty acid, stearidonic acid (SDA). In doing so, we have demonstrated the feasibility of developing a land-based source of functional omega-3 fatty acids on a large scale. Land-based omega-3 fatty acids represent a sustainable source of omega-3 fatty acids that can be produced on large acreages and delivered to consumers in a wide variety of functional foods. And unlike alpha-linolenic acid, SDA can provide eicosapentaenoic acid equivalence at moderate intakes. Widely applied, SDA-enriched foods could become a valuable tool for delivering recommended levels of omega-3 fatty acids to large portions of the population. By obviating the need for dietary changes, SDA-enriched foods may facilitate increased compliance with recommendations for daily omega-3 intakes.

Biotechnology↗
PubMed1983

Modification of the lipid moiety of the enterobacterial common antigen by the "Pseudomonas factor".

Pseudomonas aeruginosa produces a factor (PF) which affects the enterobacterial common antigen (ECA); resulting in failure of the antigen to modify erythrocytes for hemagglutination by ECA antibodies. In the present study the nature of PF was determined. Pronase treatment abolished its activity, indicating the protein nature of PF. PF-treated ECA no longer coated erythrocytes but still reacted with ECA antibodies in immunoelectrophoresis tests with monospecific antiserum to ECA, although differences were noted between the precipitation patterns of PF-treated and untreated ECA. Therefore, PF does not significantly affect the antigenic determinant of ECA but rather affects its lipid carrier, an L-glycerophosphatide. Accordingly, differences in the sugar chain could not be detected by high-voltage paper electrophoretic examinations of partial hydrolysates of PF-treated and untreated ECA. PF liberates all fatty acids from ECA, similarly to commercial lipases, as evidenced by the liberation of unsubstituted glycerol upon HF degradation at 0 degrees C of PF-treated ECA. The lipase activity of PF is indicated also by the observation that a strain of P. aeruginosa with reduced lipase production and an exolipase-negative strain affect ECA either less or not at all. We conclude that PF is a lipase acting on the lipid moiety of ECA, which is responsible for the coating of erythrocytes, but not significantly on the serological determinant, the amino sugar chain.

Antigens, Bacterial↗
PubMed2005

Polyunsaturated fatty acids interfere with formation of the immunological synapse.

Polyunsaturated fatty acids (PUFAs) exert inhibitory effects on T cell-mediated immune responses. Activation of T cells in vivo depends on formation of an immunological synapse (IS) at the T cell/antigen-presenting cell (APC) interface. Here, we analyzed effects of PUFA treatment on the formation of the IS and APC-induced human T cell activation. In T cells treated with the PUFA eicosapentaenoic (EPA; 20:5,n-3) and arachidonic acid (20:4,n-6), stimulated by superantigen-presenting cells or APCs, relocalization to the IS of distinct molecules [F-actin, talin, leukocyte functional antigen-1alpha, clusters of differentiation (CD)3epsilon] was inhibited markedly compared with cells treated with saturated fatty acid, whereas relocalization of protein kinase Ctheta to the IS remained unaffected. CD3-induced, sustained phosphorylation of nucleotide exchange factor Vav, which controls cytoskeletal rearrangements underlying IS formation, was significantly reduced in EPA-treated Jurkat and peripheral blood T cells. In addition, T cell raft disruption by methyl-beta-cyclodextrin treatment and experiments with a chimeric linker for activation of T cell proteins, which is resistant to PUFA effects on lipid rafts, revealed modifications of lipid rafts as a crucial factor for PUFA-mediated inhibition of APC-stimulated cytoskeletal rearrangements. Furthermore, the efficiency of T cell/APC conjugate formation was significantly reduced with EPA-treated T cells, as was stimulation of CD69 expression, which is not altered following antibody-mediated T cell activation. In conclusion, PUFA treatment of T cells qualitatively and quantitatively alters IS formation, thereby extending T cell signaling defects to pathways that are not intrinsically altered in PUFA-treated T cells when stimulated by antibodies.

Antigen-Presenting Cells↗
PubMed1988

Interaction between oxygen and cell membranes: modification of membrane lipids to enhance pulmonary artery endothelial cell tolerance to hypoxia.

Because high partial pressures of oxygen (O2) can cause peroxidative cleavage of membrane lipids, it is plausible to hypothesize that hyperoxia alters the physical state and composition of lipids in the membranes of pulmonary endothelial cells and that manipulation of the lipid profile may modify endothelial cell tolerance to hyperoxic injury. To test this, porcine pulmonary artery endothelial cells were exposed to 95% O2 at 1 atmosphere absolute (ATA) in the presence or absence of cis vaccenic acid (CVA), a monounsaturated fatty acid (C18:1#11). Plasma membrane fluidity was assessed by fluorescence spectroscopy, plasma membrane lipid composition was quantitated using thin layer and gas chromatography, and cytotoxicity was monitored by measuring release of lactate dehydrogenase (LDH). Hyperoxia caused peroxidation of membrane lipids and decreased fluidity in three distinct lipid domains within the plasma membrane. Incubation with CVA was associated with a reduction in the degree of unsaturation of the constituent fatty acids within all plasma membrane lipid subclasses except monoglycerides. CVA-treated cells were also more resistant to hyperoxic injury as judged by LDH release. These results support the hypothesis that cells with membranes in which the fatty acyl chains are more resistant to the disordering effects of high O2 tensions may be more resistant to O2 toxicity.

Animals↗