Phospholipid fatty acyl distribution of three fungi indicates positional specificity for n-6vs. n-3 fatty acids

Lipids ◽  
1992 ◽  
Vol 27 (7) ◽  
pp. 505-508 ◽  
Author(s):  
Andrew Kendrick ◽  
Collin Ratledge
Keyword(s):  
Fatty Acids ◽  
Fatty Acyl ◽  
Positional Specificity

Fatty acyl chain structure, orientational order, and the lipid phase transition in Acholeplasma laidlawii B membranes. A review of recent 19F nuclear magnetic resonance studies

1984 ◽  
Vol 62 (11) ◽  
pp. 1134-1150 ◽  
Author(s):  
P. M. Macdonald ◽  
B. D. Sykes ◽  
R. N. McElhaney
Keyword(s):  
Phase Transition ◽  
Fatty Acids ◽  
Nuclear Magnetic Resonance ◽  
Acyl Chain ◽  
Orientational Order ◽  
Membrane Lipid ◽  
Fatty Acyl ◽  
Fatty Acyl Chain ◽  
Lipid Phase ◽  
Lipid Phase Transition

The orientational order parameters of monofluoropalmitic acids biosynthetically incorporated into membranes of Acholeplasma laidlawii B in the presence of a large excess of a variety of structurally diverse fatty acids have been determined via 19F nuclear magnetic resonance (19F NMR) spectroscopy. It is demonstrated that these monofluoropalmitic acids are relatively nonperturbing membrane probes based upon physical (differential scanning calorimetry), biochemical (membrane lipid analysis), and biological (growth studies) criteria. 19F NMR is shown to convey the same qualitative and quantitative picture of membrane lipid order provided by 2H-NMR techniques and to be sensitive to the structural characteristics of the membrane fatty acyl chains, as well as to the lipid phase transition. Representatives of each naturally occurring class of fatty acyl chain structures, including straight-chain saturated, methyl-branched, monounsaturated, and alicyclic-ring-substituted fatty acids, were studied and the 19F-NMR order parameters were correlated with the lipid phase transitions (determined calorimetrically). The lipid phase transition was the prime determinant of overall orientational order regardless of fatty acid structure. Effects upon orientational order attributable to specific structural substituents were discernible, but were secondary to the effects of the lipid phase transition. In the gel state, relative overall order was directly proportional to the temperature of the particular lipid phase transition. Not only the overall order, but also the order profile across the membrane was sensitive to the presence of particular structural substituents. In particular, in the gel state specific fatty acyl structures demonstrated a characteristic disordering effect in the membrane order profile. These various observations can be merged to provide a unified picture of the manner in which fatty acyl chain chemistry modulates the physical state of membrane lipids.

scholarly journals III. Peroxisomal β-oxidation, PPARα, and steatohepatitis

2001 ◽  
Vol 281 (6) ◽  
pp. G1333-G1339 ◽  
Author(s):  
Janardan K. Reddy
Keyword(s):  
Fatty Acids ◽  
Dicarboxylic Acids ◽  
Fatty Acyl ◽  
Branched Chain Fatty Acids ◽  
Oxidation Chain ◽  
Branched Chain ◽  
Cytochrome P 450 ◽  
Oxidation System ◽  
Long Chain ◽  
Chain Fatty Acids

Peroxisomes are involved in the β-oxidation chain shortening of long-chain and very-long-chain fatty acyl-CoAs, long-chain dicarboxylyl-CoAs, the CoA esters of eicosanoids, 2-methyl-branched fatty acyl-CoAs, and the CoA esters of the bile acid intermediates, and in the process, they generate H2O2. There are two complete sets of β-oxidation enzymes present in peroxisomes, with each set consisting of three distinct enzymes. The classic PPARα-regulated and inducible set participates in the β-oxidation of straight-chain fatty acids, whereas the second noninducible set acts on branched-chain fatty acids. Long-chain and very-long-chain fatty acids are also metabolized by the cytochrome P-450 CYP4A ω-oxidation system to dicarboxylic acids that serve as substrates for peroxisomal β-oxidation. Evidence derived from mouse models of PPARα and peroxisomal β-oxidation deficiency highlights the critical importance of the defects in PPARα-inducible β-oxidation in energy metabolism and in the development of steatohepatitis.

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.

Abstract 458: Obesity-related Alterations in Cardiac Lipid Profile During the Transition to Diastolic Dysfunction

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Vincent G DeMarco ◽  
David A Ford ◽  
Erik Henriksen ◽  
Annayya Aroor ◽  
Javad Habibi ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Diastolic Dysfunction ◽  
Phospholipid Metabolism ◽  
Fatty Acyl ◽  
Acid Oxidation ◽  
Relevant Model ◽  
Insulin Resistant ◽  
Enhanced Production ◽  
Lipid Species ◽  
And Oxidative Stress

Myocardial accumulation of fatty acids and lipid intermediates may contribute to cardiac dysfunction, but the interrelationship between different lipid species to diastolic dysfunction is not clearly understood. Herein, we examined changes in levels and composition of different lipid species during the progression to diastolic dysfunction in a clinically relevant model of obese insulin-resistant db/db mice at 12 and 15 wks of age. Obese db/db mice manifested loss of circadian BP dipping and diastolic dysfunction at 15 wks. Myocardial lipidomic analysis demonstrated elevated ceramides and fatty acids in db/db at 12 wks, but their levels were decreased at 15 wk and this was accompanied by increased fatty acid oxidation and enhanced production of reactive oxygen species. Triacylglyceride and diacylglyceride levels remained elevated at both 12 and 15 wk, but their composition changed to consist of more saturated and less unsaturated fatty acyl at 15 wks of age compared to 12 wk. Dysregulation of phospholipid metabolism persisted at 15 wk in db/db. Changes in triacylglyceride and diacylglyceride composition, phospholipid metabolism, β-oxidation, and oxidative stress that are temporally related to non-dipping of BP and diastolic dysfunction suggest a switch in metabolism of lipid intermediates contributes to the development of diastolic dysfunction in over-nutrition.

scholarly journals Mdm1 maintains endoplasmic reticulum homeostasis by spatially regulating lipid droplet biogenesis

2019 ◽  
Vol 218 (4) ◽  
pp. 1319-1334 ◽  
Author(s):  
Hanaa Hariri ◽  
Natalie Speer ◽  
Jade Bowerman ◽  
Sean Rogers ◽  
Gang Fu ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Endoplasmic Reticulum ◽  
Lipid Droplet ◽  
Lipid Droplets ◽  
Fatty Acyl ◽  
Nutrient Depletion ◽  
Coenzyme A Ligase ◽  
Response To Stress ◽  
Acyl Coenzyme A ◽  
Er Homeostasis

Lipid droplets (LDs) serve as cytoplasmic reservoirs for energy-rich fatty acids (FAs) stored in the form of triacylglycerides (TAGs). During nutrient stress, yeast LDs cluster adjacent to the vacuole/lysosome, but how this LD accumulation is coordinated remains poorly understood. The ER protein Mdm1 is a molecular tether that plays a role in clustering LDs during nutrient depletion, but its mechanism of function remains unknown. Here, we show that Mdm1 associates with LDs through its hydrophobic N-terminal region, which is sufficient to demarcate sites for LD budding. Mdm1 binds FAs via its Phox-associated domain and coenriches with fatty acyl–coenzyme A ligase Faa1 at LD bud sites. Consistent with this, loss of MDM1 perturbs free FA activation and Dga1-dependent synthesis of TAGs, elevating the cellular FA level, which perturbs ER morphology and sensitizes yeast to FA-induced lipotoxicity. We propose that Mdm1 coordinates FA activation adjacent to the vacuole to promote LD production in response to stress, thus maintaining ER homeostasis.

scholarly journals Chlorpromazine and carnitine-dependency of rat liver peroxisomal β-oxidation of long-chain fatty acids

1987 ◽  
Vol 241 (3) ◽  
pp. 783-791 ◽  
Author(s):  
J Vamecq
Keyword(s):  
Fatty Acids ◽  
Cytochrome C ◽  
Cytochrome C Oxidase ◽  
Rat Liver ◽  
Fatty Acyl ◽  
Carnitine Palmitoyltransferase ◽  
Acid Oxidation ◽  
Synthetase Activity ◽  
Mitochondrial Fatty Acid Oxidation ◽  
Mitochondrial Fatty Acid

The enzyme targets for chlorpromazine inhibition of rat liver peroxisomal and mitochondrial oxidations of fatty acids were studied. Effects of chlorpromazine on total fatty acyl-CoA synthetase activity, on both the first and the third steps of peroxisomal beta-oxidation, on the entry of fatty acyl-CoA esters into the peroxisome and on catalase activity, which allows breakdown of the H2O2 generated during the acyl-CoA oxidase step, were analysed. On all these metabolic processes, chlorpromazine was found to have no inhibitory action. Conversely, peroxisomal carnitine octanoyltransferase activity was depressed by 0.2-1 mM-chlorpromazine, which also inhibits mitochondrial carnitine palmitoyltransferase activity in all conditions in which these enzyme reactions are assayed. Different patterns of inhibition by the drug were, however, demonstrated for both these enzyme activities. Inhibitory effects of chlorpromazine on mitochondrial cytochrome c oxidase activity were also described. Inhibitions of both cytochrome c oxidase and carnitine palmitoyltransferase are proposed to explain the decreased mitochondrial fatty acid oxidation with 0.4-1.0 mM-chlorpromazine reported by Leighton, Persico & Necochea [(1984) Biochem. Biophys. Res. Commun. 120, 505-511], whereas depression by the drug of carnitine octanoyltransferase activity is presented as the factor responsible for the decreased peroxisomal beta-oxidizing activity described by the above workers.

scholarly journals Fatty Acyl Esters of Hydroxy Fatty Acid (FAHFA) Lipid Families

Metabolites ◽  
2020 ◽  
Vol 10 (12) ◽  
pp. 512
Author(s):  
Paul L. Wood
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Hydroxy Fatty Acid ◽  
Fatty Acyl ◽  
Hydroxy Fatty Acids ◽  
Wax Esters ◽  
Hydroxyl Group ◽  
Cellular Functions ◽  
Health And Disease ◽  
Branched Chain

Fatty Acyl esters of Hydroxy Fatty Acids (FAHFA) encompass three different lipid families which have incorrectly been classified as wax esters. These families include (i) Branched-chain FAHFAs, involved in the regulation of glucose metabolism and inflammation, with acylation of an internal branched-chain hydroxy-palmitic or -stearic acid; (ii) ω-FAHFAs, which function as biosurfactants in a number of biofluids, are formed via acylation of the ω-hydroxyl group of very-long-chain fatty acids (these lipids have also been designated as o-acyl hydroxy fatty acids; OAHFA); and (iii) Ornithine-FAHFAs are bacterial lipids formed by the acylation of short-chain 3-hydroxy fatty acids and the addition of ornithine to the free carboxy group of the hydroxy fatty acid. The differences in biosynthetic pathways and cellular functions of these lipid families will be reviewed and compared to wax esters, which are formed by the acylation of a fatty alcohol, not a hydroxy fatty acid. In summary, FAHFA lipid families are both unique and complex in their biosynthesis and their biological actions. We have only evaluated the tip of the iceberg and much more exciting research is required to understand these lipids in health and disease.

scholarly journals A Futile Metabolic Cycle of Fatty Acyl-CoA Hydrolysis and Resynthesis in Corynebacterium glutamicum and Its Disruption Leading to Fatty Acid Production

2020 ◽  
Author(s):  
Masato Ikeda ◽  
Keisuke Takahashi ◽  
Tatsunori Ohtake ◽  
Ryosuke Imoto ◽  
Haruka Kawakami ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Free Fatty Acids ◽  
Corynebacterium Glutamicum ◽  
Candidate Genes ◽  
Outer Layer ◽  
Acid Production ◽  
Fatty Acyl ◽  
Fatty Acid Production ◽  
Mycolic Acids

Fatty acyl-CoA thioesterase (Tes) and acyl-CoA synthetase (FadD) catalyze opposing reactions between acyl-CoAs and free fatty acids. Within the genome of Corynebacterium glutamicum, several candidate genes for each enzyme are present, although their functions remain unknown. Modified expressions of the candidate genes in the fatty acid producer WTΔfasR led to identification of one tes gene (tesA) and two fadD genes (fadD5 and fadD15), which functioned positively and negatively in fatty acid production, respectively. Genetic analysis showed that fadD5 and fadD15 are responsible for utilization of exogenous fatty acids and that tesA plays a role in supplying fatty acids for synthesis of the outer layer components mycolic acids. Enzyme assays and expression analysis revealed that tesA, fadD5, and fadD15 were co-expressed to create a cyclic route between acyl-CoAs and fatty acids. When fadD5 or fadD15 was disrupted in wild-type C. glutamicum, both disruptants excreted fatty acids during growth. Double disruptions of them resulted in a synergistic increase in production. Additional disruption of tesA revealed a canceling effect on production. These results indicate that the FadDs normally shunt the surplus of TesA-generated fatty acids back to acyl-CoAs for lipid biosynthesis and that interception of this shunt provokes cells to overproduce fatty acids. When this strategy was applied to a fatty acid high-producer, the resulting fadDs-disrupted and tesA-amplified strain exhibited a 72% yield increase relative to its parent and produced fatty acids, which consisted mainly of oleic acid, palmitic acid, and stearic acid, on the gram scale per liter from 1% glucose. IMPORTANCE The industrial amino acid producer Corynebacterium glutamicum has currently evolved into a potential workhorse for fatty acid production. In this organism, we obtained evidence showing the presence of a unique mechanism of lipid homeostasis, namely, a formation of a futile cycle of acyl-CoA hydrolysis and resynthesis mediated by acyl-CoA thioesterase (Tes) and acyl-CoA synthetase (FadD), respectively. The biological role of the coupling of Tes and FadD would be to supply free fatty acids for synthesis of the outer layer components mycolic acids and to recycle their surplusage to acyl-CoAs for membrane lipid synthesis. We further demonstrated that engineering of the cycle in a fatty acid high-producer led to dramatically improved production, which provides a useful engineering strategy for fatty acid production in this industrially important microorganism.

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