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At least 289 records · Page 16Linked to original sources
PubMed2002

Control of germination and lipid mobilization by COMATOSE, the Arabidopsis homologue of human ALDP.

Embryo dormancy in flowering plants is an important dispersal mechanism that promotes survival of the seed through time. The subsequent transition to germination is a critical control point regulating initiation of vegetative growth. Here we show that the Arabidopsis COMATOSE (CTS) locus is required for this transition, and acts, at least in part, by profoundly affecting the metabolism of stored lipids. CTS encodes a peroxisomal protein of the ATP binding cassette (ABC) transporter class with significant identity to the human X-linked adrenoleukodystrophy protein (ALDP). Like X-ALD patients, cts mutant embryos and seedlings exhibit pleiotropic phenotypes associated with perturbation in fatty acid metabolism. CTS expression transiently increases shortly after imbibition during germination, but not in imbibed dormant seeds, and genetic analyses show that CTS is negatively regulated by loci that promote embryo dormancy through multiple independent pathways. Our results demonstrate that CTS regulates transport of acyl CoAs into the peroxisome, and indicate that regulation of CTS function is a major control point for the switch between the opposing developmental programmes of dormancy and germination.

ATP Binding Cassette Transporter, Subfamily D, Mem↗
PubMed2002

Arabidopsis seedling growth, storage lipid mobilization, and photosynthetic gene expression are regulated by carbon:nitrogen availability.

The objective of the current work was to establish the degree to which the effects of carbon and nitrogen availability on Arabidopsis seedling growth and development are due to these nutrients acting independently or together. Growth of seedlings on low (0.1 mM) nitrogen results in a significant reduction of seedling and cotyledon size, fresh weight, chlorophyll, and anthocyanin content but a slight increase in endogenous sugars. The addition of 100 mM sucrose (Suc) to the nitrogen-depleted growth media results in a further reduction in cotyledon size and chlorophyll content and an overall increase in anthocyanins and endogenous sugars. Storage lipid breakdown is almost completely blocked in seedlings grown on low nitrogen and 100 mM Suc and is significantly inhibited when seedlings are grown on either low nitrogen or high Suc. Carbohydrate repression of photosynthetic gene expression can only be observed under low nitrogen conditions. Low (0.1 mM) nitrogen in the absence of exogenous carbohydrate results in a significant decrease in chlorophyll a/b-binding protein and ribulose bisphosphate carboxylase small subunit gene transcript levels. Thus, carbon to nitrogen ratio rather than carbohydrate status alone appears to play the predominant role in regulating various aspects of seedling growth including storage reserve mobilization and photosynthetic gene expression.

Anthocyanins↗
PubMed2003

Relation of fatty acid composition in lead-exposed mallards to fat mobilization, lipid peroxidation and alkaline phosphatase activity.

The increase of n-6 polyunsaturated fatty acids (PUFA) in animal tissues has been proposed as a mechanism of lead (Pb) poisoning through lipid peroxidation or altered eicosanoids metabolism. We have studied fatty acid (FA) composition in liver and brain of mallards (Anas platyrhynchos) feeding for 3 weeks on diets containing combinations of low or high levels of vitamin E (20 or 200 UI/kg) and Pb (0 or 2 g/kg). Saturated FA, n-6 PUFA and total concentrations of FA were higher in livers of Pb-exposed mallards, but not in their brains. The percentage of n-6 PUFA in liver and brain was slightly higher in Pb-exposed mallards. The increase of n-6 PUFA in liver was associated with decreased triglycerides and increased cholesterol in plasma, thus could be in part attributed to feed refusal and fat mobilization. The hepatic ratios between adrenic acid (22:4 n-6) and arachidonic acid (20:4 n-6) or between adrenic acid and linoleic acid (18:2 n-6) were higher in Pb exposed birds, supporting the existing hypothesis of increased fatty acid elongation by Pb. Among the possible consequences of increased n-6 PUFA concentration in tissues, we found increased lipid peroxidation in liver without important histopathological changes, and decreased plasma alkaline phosphatase activity that may reflect altered bone metabolism in birds.

Alkaline Phosphatase↗
PubMed1970

Stimulation of lipolysis in adipose tissue in vitro by inhibitors of lipid mobilization.

5-Methylpyrazole-3-carboxylic acid (U-19425) and nicotinic acid, which apparently inhibit lipolysis in vivo as indicated by low plasma FFA and glycerol concentrations, stimulate lipolysis in vitro in adipose tissue removed from fasted rats 30-90 min after treatment. This stimulation is not the result of low initial levels of FFA in adipose tissue. An increased rate of lipolysis is not induced in vitro by preincubating tissue of untreated rats with U-19425. The increase can be blocked in incubated adipose tissue of U-19425-treated animals if U-19425 is added to the incubation medium. The beta-adrenergic blocking agent propranolol, at a concentration which inhibits epinephrine-stimulated lipolysis, does not affect the increase produced by administration of U-19425.

Adipose Tissue↗
PubMed1993

Mechanism of lipid mobilization associated with cancer cachexia: interaction between the polyunsaturated fatty acid, eicosapentaenoic acid, and inhibitory guanine nucleotide-regulatory protein.

During a study of the mechanism of cancer cachexia, a debilitating condition in which catabolism of host muscle and adipose tissue occurs, it has been observed that the process can be effectively reversed in vivo by the polyunsaturated fatty acid, eicosapentaenoic acid (EPA), but not by other PUFA of either the n-3 or n-6 series. In vitro studies showed that EPA blocked the action of a tumour-produced catabolic factor at the level of the adipocyte, and that the effect of EPA also extended to beta-adrenergic stimuli and polypeptide hormones. Again the effect was specific to EPA and appeared to arise from an inhibition of the elevation of cyclic AMP levels in adipocytes in response to varied stimuli. Using isoprenaline stimulated lipolysis as a model system we have shown that EPA has a direct inhibitory effect on isoprenaline-stimulated adenylate cyclase in isolated plasma membrane fractions with half maximal inhibition at a concentration of 165 microM. The inhibitory effect was specific for EPA and was not shown by docosahexaenoic or arachidonic acids. The inhibitory effect of EPA on adenylate cyclase showed properties similar to hormonal inhibition of the enzyme in that it was (i) GTP-dependent, (ii) non-competitive with isoprenaline, (iii) eliminated following treatment of either adipocytes or plasma membrane fractions with pertussis toxin, which is known to ADP-ribosylate the alpha-subunit of an inhibitory guanine nucleotide-regulatory protein (Gi), thus leading to its inactivation. This suggests that inhibition of cyclic AMP formation by EPA was due, at least in part, to a Gi-mediated inhibition of adenylate cyclase activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenocarcinoma↗
PubMed1994

1H MRS of high grade astrocytomas: mobile lipid accumulation in necrotic tissue.

Sixty-four samples from six grade 4 astrocytomas were investigated ex vivo by 1H MRS at 360 MHz and subsequently by histopathology to obtain percentages of viable and necrotic tumour and grey and white matter. MR-visible lipids were detected in 87% of tumour samples. Necrotic foci were < 3 x 3 x 6 mm3. The means of the intensities/unit weight tissue of the lipid resonances at 5.33, 2.80, 1.29 and 0.89 ppm were significantly higher (p < 0.05) for three sets of comparisons: samples with 85-100% vs 50-75%; with 50-75% vs 10-40% and with 10-40% vs 0-5% necrosis. For the lipid resonance at 2.04 ppm the difference in the means was significant only for samples with 50-75% compared to those with 85-100% necrosis, because for samples with < 50% necrosis resonances from glutamine and possibly small amounts of glutamate, gamma-aminobutyrate and N-acetylaspartate anions contribute significantly to the spectral area at 2.0 ppm. We conclude that necrotic foci below MRI resolution yield the resonances at 1.3 and 0.9 ppm, and contribute to the intense resonance at 2.0 ppm observed in in vivo 1H spectra of some high grade astrocytomas.

Astrocytoma↗
PubMed1992

Effects of flavonoids on cyclic AMP phosphodiesterase and lipid mobilization in rat adipocytes.

Thirty-one flavonoids were tested for their effects on low Km phosphodiesterase with cyclic AMP as the substrate. Quercetin, luteolin, scutellarein, phloretin and genistein showed inhibitory potencies comparable to or greater than 3-isobutyl-2-methylxanthine (EC50 30-50 microM). Only four compounds namely, catechin, epicatechin, taxifolin and fustin stimulated the enzyme activity (stimulatory EC50 130-240 microM). The most potent phosphodiesterase (PDE) inhibitors were aglycones that had a C2.3 double bond, a keto group at C4 and hydroxyls at C3' and/or C4'. However, when the C-ring is opened then the requirement for the C2.3 double bond is eliminated. The same series of flavonoids were also tested for their lipolytic activity. The structural features required for effective synergistic lipolysis (with epinephrine) were generally similar to that required for potent PDE inhibition except that, for lipolytic activity, an intact C-ring was necessary. Fisetin and quercetin having the above-mentioned structure showed a dose- and time-dependent increase in lipolysis which was synergistic with epinephrine. Only butein and hesperetin showed inhibition of epinephrine-induced lipolysis, and their effect was dose-dependent. A time-course study indicated that hesperetin was able to delay the lipolytic action of epinephrine. It is most likely that the lipolytic effects of these compounds were not a result of PDE inhibition, as the orders of potency for the two activities had poor correlation. Apparently, the effective lipolytic flavonoids were also potent PDE inhibitors but not all the PDE inhibitors were able to induce lipolysis.

1-Methyl-3-isobutylxanthine↗
PubMed1990

Processing of the lipid-mobilizing peptide beta-lipotropin in rabbit adipose tissue.

beta-Lipotropin, a pituitary peptide, is a strong stimulator of lipolysis in rabbit adipose tissue. This polypeptide is shown to be degraded by intact fat pads, homogenized adipose tissue and adipocytes of the rabbit dependent on the amount of adipose tissue, time and the pH of the incubation medium. In subcellular fractions of rabbit adipocytes the proteolytic activity could be localized into the cytosol and the microsomal fraction. To obtain information about the processing of beta-lipotropin in its target cell lipolysis and degradation of this polypeptide were investigated in the presence of inhibitors of distinct cellular mechanisms and in different physiological states such as obesity and starvation. Thus, the stronger lipolytic response in adipocytes from obese rabbits respectively animals fed ad libitum was accompanied by a significantly increased degradation in comparison to lean respectively starved rabbits. The six lysosomotropic agents (chloroquine, NH4Cl, propranolol, quinacrine, acridine orange and tetracaine), the proteinase inhibitors alpha 2-macroglobulin and monodansylcadaverine, cellular ATP depletion by 2-deoxy-D-glucose and 2,4-dinitrophenol and the omission of Ca2+ ions from the incubation medium inhibited dose-dependently the lipolytic activity as well as the degradation of beta-lipotropin in intact and homogenized adipose tissue. Inhibitors of the cytoskeleton such as colchicine, cytochalasin B, vinblastine and concanavalin A also reduced lipolysis but only the degradation in intact adipose tissue. It can be concluded that after receptor-mediated uptake the cytoskeleton and lysosomal proteases are involved in the processing of beta-lipotropin.

Adipose Tissue↗
PubMed1997

Absence of response to oestrus induction and synchronization treatment is related to lipid mobilization in suckled beef cows.

Energy status, follicular growth, oestradiol and LH secretion were investigated in 17 suckled Charolais cows synchronised 59.0 +/- 3.6 days after calving with a 10 day ear implant containing 3 mg of Norgestomet. The cows received 3 mg of Norgestomet and 5 mg of oestradiol valerate by IM injection at implant insertion (day 0) and 600 IU PMSG at implant removal (day 10). They were artificially inseminated (AI) 48 and 72 h after implant removal. Energy status was assessed by measuring weekly plasma concentrations of non-esterified fatty acids (NEFA), beta hydroxy-butyrate (BHB), glucose and insulin 7 weeks before AI. Progesterone plasma concentrations were measured during the same period to assess the presence of a functional corpus luteum. Follicular growth was followed daily by ultrasonography from day -3 to day 13. Oestradiol secretion was measured on day -3, day 6 and day 10 from five hourly samples. Oestradiol and LH plasma concentrations were measured hourly from 29 to 48 h after implant removal for seven cows. Cows were checked for pregnancy by ultrasonography 45 days after AI. Pregnant cows (P) were compared with non-pregnant cows (NP) for energy status, follicular growth, and oestradiol secretion by split-plot ANOVA. Two cows (11.8%) were cyclic before treatment, seven ovulated after treatment (41.2%) and five were found pregnant 45 days after AI (29.4%). There was no difference in body condition score and body weight between P and NP cows on day 0 (2.5 +/- 0.2 and 685 +/- 24 kg vs 2.5 +/- 0.1 and 670 +/- 13 kg; P > 0.05). Mean plasma NEFA concentrations before treatment were significantly lower in P than in NP cows (218 +/- 29 mu eq/L vs 279 +/- 18 mu eq/L; P < 0.05). No significant differences between P and NP cows were found for BHB, glucose and insulin concentrations. P cows presented more medium sized follicles (5 mm < or = diameter < 10 mm) than NP females during the period of observation (2.65 +/- 0.19 vs 2.50 +/- 0.12; P = 0.05). Plasma oestradiol concentrations were not different between P and NP cows on day -3 (8.4 +/- 0.7 pg/mL vs 7.7 +/- 0.4 pg/mL, P > 0.05), day 6 (10.4 +/- 0.6 pg/mL vs 9.8 +/- 0.4 pg/mL, P > 0.05) but were higher in P than in NP cows on day 10 (10.9 +/- 0.6 pg/mL vs 7.8 +/- 0.4 pg/mL; P < 0.05). After implant removal, oestradiol secretion only increased in P cows and a LH peak occurred whereas no increases in oestradiol (11.0 +/- 0.4 pg/mL vs 6.3 +/- 0.3 pg/mL, P < 0.05) and LH (6.0 +/- 0.5 ng/mL vs 1.2 +/- 0.5 ng/mL, P < 0.05) secretion were observed in NP cows. The conclusion was that follicular growth, oestradiol secretion, ovulation and pregnancy rate after oestrus synchronisation treatment are related to mobilization of energy stores before treatment in suckled beef cows in the same body condition score.

Animals↗
PubMedDate not supplied

Differentiation of the P-gp and MRP1 multidrug resistance systems by mobile lipid 1H-NMR spectroscopy and phosphatidylserine externalization.

We have previously demonstrated that proton NMR spectra of fatty acid chains in erythroleukemia K562 wild-type cells and their MDR1 counterparts show variations related to the phenotype over-expressing the P-glycoprotein (P-gp). Human lung cancer cells whose multidrug resistance (MDR) counterparts over-express the multidrug resistance-associated protein MRP1 have not yet been studied by NMR. Both P-gp and MRP1 belong to the same ATP-binding cassette transporter superfamily. A comparison of NMR spectra from both these multidrug-resistance phenotypes showed that the results previously obtained on the MDR1 family are not valid for MRP1. Furthermore, flow cytofluorimetry studies with external phosphatidylserine labelling showed that P-gp and MRP1 overexpressions have strong but differentiated effects on cell lipid pools.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2001

Oxidative burst and 1H-NMR-detectable mobile lipids in neutrophils.

Neutrophils exposed to pro-inflammatory substances have an increased capability to respond to a membrane receptor-binding stimulus triggering an oxidative burst. One other considered sign of neutrophil activation is the appearance of a high-resolution 'H-NMR spectrum probably resulting from a rearrangement of neutral lipids in the membrane. The relationship between these two events is here studied. Neutrophils were recovered from a subcutaneous fungal infection using two murine lineages that respond differently to infection. It was concluded that rearrangement of lipids in the membrane, observable by NMR, appears also in neutrophils that do not exhibit the classical sign of activation, that is the increased expression of membrane receptors.

Animals↗