Fatty acids of membrane phospholipids in Drosophila melanogaster lines showing rapid and slow recovery from chill coma

2010 ◽  
Vol 391 (2) ◽  
pp. 1251-1254 ◽  
Author(s):  
Shin G. Goto ◽  
Hiroko Udaka ◽  
Chiaki Ueda ◽  
Chihiro Katagiri
Keyword(s):  
Fatty Acids ◽  
Drosophila Melanogaster ◽  
Membrane Phospholipids ◽  
Slow Recovery ◽  
Chill Coma

scholarly journals Toxoplasma LIPIN is essential in channeling host lipid fluxes through membrane biogenesis and lipid storage

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Sheena Dass ◽  
Serena Shunmugam ◽  
Laurence Berry ◽  
Christophe-Sebastien Arnold ◽  
Nicholas J. Katris ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Phosphatidic Acid ◽  
De Novo ◽  
Lipid Synthesis ◽  
Parasite Development ◽  
Membrane Biogenesis ◽  
Membrane Phospholipids ◽  
Phosphatidic Acid Phosphatase ◽  
Intracellular Parasites ◽  
Parasite Survival

AbstractApicomplexa are obligate intracellular parasites responsible for major human diseases. Their intracellular survival relies on intense lipid synthesis, which fuels membrane biogenesis. Parasite lipids are generated as an essential combination of fatty acids scavenged from the host and de novo synthesized within the parasite apicoplast. The molecular and metabolic mechanisms allowing regulation and channeling of these fatty acid fluxes for intracellular parasite survival are currently unknown. Here, we identify an essential phosphatidic acid phosphatase in Toxoplasma gondii, TgLIPIN, as the central metabolic nexus responsible for controlled lipid synthesis sustaining parasite development. Lipidomics reveal that TgLIPIN controls the synthesis of diacylglycerol and levels of phosphatidic acid that regulates the fine balance of lipids between storage and membrane biogenesis. Using fluxomic approaches, we uncover the first parasite host-scavenged lipidome and show that TgLIPIN prevents parasite death by ‘lipotoxicity’ through effective channeling of host-scavenged fatty acids to storage triacylglycerols and membrane phospholipids.

scholarly journals Adrenaline Stimulation of Phospholipid Metabolism in Adipocyte Ghosts

1987 ◽  
Vol 40 (4) ◽  
pp. 405
Author(s):  
David Mann ◽  
Audrey M Bersten
Keyword(s):  
Fatty Acids ◽  
Arachidonic Acid ◽  
Linoleic Acid ◽  
Adenylate Cyclase ◽  
Phospholipid Metabolism ◽  
Dependent Manner ◽  
Long Chain Fatty Acids ◽  
Membrane Phospholipids ◽  
Dose Dependent ◽  
Stimulation Of

The incorporation of long-chain fatty acids into phospholipids has been detected in adipocyte ghosts that were incubated with [1_14 C] stearic, [1_14 C] linoleic or [l_14C] arachidonic acid. Adrenaline and adenosine activated this incorporation within 15 s of exposure of the ghosts to the hormones and the response was dose dependent. Maximum incorporation of labelled linoleic acid occurred at 10-5 M adrenaline and 10-7 M adenosine. The a-agonist phenylephrine and the ~-agonist isoproterenol were also shown to stimulate the incorporation of fatty acid in a dose dependent manner. Phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine and phosphatidylinositol were each labelled preferentially with linoleic or arachidonic acid. p-Bromophenacylbromide, quinacrine and centrophenoxine inhibited the adrenaline-stimulated incorporation of fatty acids into ghost membrane phospholipids, and p-bromophenacylbromide also reduced the activation of adenylate cyclase by adrenaline. NaF, an activator of adenylate cyclase, like adrenaline, stimulated the incorporation of linoleic acid into ghost membrane phospholipids.

scholarly journals Effect of atorvastatin and rosuvasta tin on the fatty acid spectrum of lymphocyte membranes in patients with unstable angina

2020 ◽  
pp. 92-95
Author(s):  
T.V. Bogdan ◽  
Keyword(s):  
Cardiovascular Disease ◽  
Fatty Acids ◽  
Fatty Acid ◽  
Unstable Angina ◽  
Unsaturated Fatty Acids ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Membrane Phospholipids ◽  
Stabilization Of Membranes ◽  
Dynamic Structures

Numerous studies have demonstrated the superiority of rosuvastatin over other statins in the treatment of cardiovascular disease. It has been proven that rosuvastatin is more effectively lowers low-density lipoprotein cholesterol in patients with cardiovascular disease than other members of this drug group. Despite the known mechanisms of action of statins on blood lipids, their effective use in patients with cardiovascular disease, as well as side effects, the influence of these drugs on the fatty acid spectrum of lymphocyte (LC) membrane phospholipids in patients with ischemic heart disease remains unexplored. The results of the studies cited in the article indicate that, in patients with unstable angina who received the therapy that included rosuvastatin, unlike patients receiving the basic treatment with atorvastatin, the relative phosphate lipid contents of palmitic, stearic, and stearin arachidonic polyunsaturated fatty acids and the amount of unsaturated fatty acids are normalized, which testifies to the stabilization of membranes as dynamic structures.

Slow recovery of the fatty acid composition of sciatic nerve in rats fed a diet initially low in n−3 fatty acids

Lipids ◽  
1987 ◽  
Vol 22 (7) ◽  
pp. 535-538 ◽  
Author(s):  
J. M. Bourre ◽  
A. Youyou ◽  
G. Durand ◽  
G. Pascal
Keyword(s):  
Fatty Acids ◽  
Fatty Acid Composition ◽  
Fatty Acid ◽  
Sciatic Nerve ◽  
Acid Composition ◽  
Slow Recovery

scholarly journals Dietary fat and the diabetic state alter insulin binding and the fatty acyl composition of the adipocyte plasma membrane

1988 ◽  
Vol 253 (2) ◽  
pp. 417-424 ◽  
Author(s):  
C J Field ◽  
E A Ryan ◽  
A B Thomson ◽  
M T Clandinin
Keyword(s):  
Fatty Acids ◽  
Arachidonic Acid ◽  
Plasma Membrane ◽  
Fatty Acid ◽  
Polyunsaturated Fatty Acids ◽  
Insulin Binding ◽  
Fatty Acyl ◽  
Membrane Composition ◽  
Membrane Phospholipids ◽  
Diabetic State

Control and diabetic rats were fed on semi-purified high-fat diets providing a polyunsaturated/saturated fatty acid ratio (P/S) of 1.0 or 0.25, to examine the effect of diet on the fatty acid composition of major phospholipids of the adipocyte plasma membrane. Feeding the high-P/S diet (P/S = 1.0) compared with the low-P/S diet (P/S = 0.25) increased the content of polyunsaturated fatty acids in membrane phospholipids in both control and diabetic animals. The diabetic state decreased the content of polyunsaturated fatty acids, particularly arachidonic acid, in adipocyte membrane phospholipids. The decrease in arachidonic acid in membrane phospholipids of diabetic animals tended to be normalized to within the control values when high-P/S diets were given. For control animals, altered plasma-membrane composition was associated with change in insulin binding, suggesting that change in plasma-membrane composition may have physiological consequences for insulin-stimulated functions in the adipocyte.

scholarly journals Modulation of human type II secretory phospholipase A2 by sphingomyelin and annexin VI

1997 ◽  
Vol 326 (1) ◽  
pp. 227-233 ◽  
Author(s):  
Kamen KOUMANOV ◽  
Claude WOLF ◽  
Gilbert BÉREZIAT
Keyword(s):  
Fatty Acids ◽  
Polyunsaturated Fatty Acids ◽  
Phospholipase A2 ◽  
Cell Membranes ◽  
Red Cell ◽  
Type Ii ◽  
Membrane Phospholipids ◽  
Human Type ◽  
Annexin Vi ◽  
Hydrolysis Of

Conjectural results have been reported on the capacity of inflammatory secreted phospholipase A2 (sPLA2) to hydrolyse mammalian membrane phospholipids. Development of an assay based on the release of non-esterified fatty acids by the enzyme acting on the organized phospholipid mixture constituting the membrane matrix has led to the identification of two prominent effectors, sphingomyelin (SPH) and annexin. Recombinant human type II sPLA2 hydrolyses red-cell membrane phospholipids with a marked preference for the inner leaflet. This preference is apparently related to the high content of SPH in the outer leaflet, which inhibits sPLA2. This inhibition by SPH is specific for sPLA2. Cholesterol counteracts the inhibition of sPLA2 by SPH, suggesting that the SPH-to-cholesterol ratio accounts in vivo for the variable susceptibility of cell membranes to sPLA2. Different effects were observed of the presence of the non-hydrolysable D-α-dipalmitoyl phosphatidylcholine (D-DPPC), which renders the membranes rigid but does not inhibit sPLA2. Annexin VI was shown, along with other annexins, to inhibit sPLA2 activity by sequestering the phospholipid substrate. The present study has provided the first evidence that annexin VI, in concentrations that inhibit hydrolysis of purified phospholipid substrates, stimulated the hydrolysis of membrane phospholipids by sPLA2. The activation requires the presence of membrane proteins. The effect is specific for type II sPLA2 and is not reproducible with type I PLA2. The activation by annexin VI of sPLA2 acting on red cell membranes results in the preferential release of polyunsaturated fatty acids. It suggests that type II sPLA2, in conjunction with annexin VI, might be involved in the final step of endocytosis and/or exocytosis providing the free polyunsaturated fatty acids acting synergistically to cause membrane fusion.

scholarly journals The Efficacy of Polyunsaturated Fatty Acids as Protectors against Calcium Oxalate Renal Stone Formation: A Review

Nutrients ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 1069
Author(s):  
Allen L. Rodgers ◽  
Roswitha Siener
Keyword(s):  
Fatty Acids ◽  
Polyunsaturated Fatty Acids ◽  
Fish Oil ◽  
Calcium Oxalate ◽  
Renal Stone ◽  
Stone Formation ◽  
Membrane Phospholipids ◽  
Dietary Pufa ◽  
Evening Primrose ◽  
Different Types

In the pathogenesis of hypercalciuria and hyperoxaluria, n-6 polyunsaturated fatty acids (PUFAs) have been implicated by virtue of their metabolic links with arachidonic acid (AA) and prostaglandin PGE2. Studies have also shown that n-3 PUFAs, particularly those in fish oil—eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA)—can serve as competitive substrates for AA in the n-6 series and can be incorporated into cell membrane phospholipids in the latter’s place, thereby reducing urinary excretions of calcium and oxalate. The present review interrogates several different types of study which address the question of the potential roles played by dietary PUFAs in modulating stone formation. Included among these are human trials that have investigated the effects of dietary PUFA interventions. We identified 16 such trials. Besides fish oil (EPA+DHA), other supplements such as evening primrose oil containing n-6 FAs linoleic acid (LA) and γ-linolenic acid (GLA) were tested. Urinary excretion of calcium or oxalate or both decreased in most trials. However, these decreases were most prominent in the fish oil trials. We recommend the administration of fish oil containing EPA and DHA in the management of calcium oxalate urolithiasis.

scholarly journals The Anti-Inflammatory and Antioxidant Properties of n-3 PUFAs: Their Role in Cardiovascular Protection

Biomedicines ◽  
2020 ◽  
Vol 8 (9) ◽  
pp. 306 ◽  
Author(s):  
Francesca Oppedisano ◽  
Roberta Macrì ◽  
Micaela Gliozzi ◽  
Vincenzo Musolino ◽  
Cristina Carresi ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Polyunsaturated Fatty Acids ◽  
Vascular Reactivity ◽  
Molecular Mechanisms ◽  
Antioxidant Properties ◽  
Cardiac Cells ◽  
Membrane Phospholipids ◽  
Mitochondrial Functions ◽  
Anti Inflammatory ◽  
Inflammatory Effect

Polyunsaturated fatty acids (n-3 PUFAs) are long-chain polyunsaturated fatty acids with 18, 20 or 22 carbon atoms, which have been found able to counteract cardiovascular diseases. Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), in particular, have been found to produce both vaso- and cardio-protective response via modulation of membrane phospholipids thereby improving cardiac mitochondrial functions and energy production. However, antioxidant properties of n-3 PUFAs, along with their anti-inflammatory effect in both blood vessels and cardiac cells, seem to exert beneficial effects in cardiovascular impairment. In fact, dietary supplementation with n-3 PUFAs has been demonstrated to reduce oxidative stress-related mitochondrial dysfunction and endothelial cell apoptosis, an effect occurring via an increased activity of endogenous antioxidant enzymes. On the other hand, n-3 PUFAs have been shown to counteract the release of pro-inflammatory cytokines in both vascular tissues and in the myocardium, thereby restoring vascular reactivity and myocardial performance. Here we summarize the molecular mechanisms underlying the anti-oxidant and anti-inflammatory effect of n-3 PUFAs in vascular and cardiac tissues and their implication in the prevention and treatment of cardiovascular disease.

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