scholarly journals Acquisition of membrane lipids by differentiating glyoxysomes: role of lipid bodies.

1991 ◽  
Vol 115 (4) ◽  
pp. 995-1007 ◽  
Author(s):  
K D Chapman ◽  
R N Trelease

Glyoxysomes in cotyledons of cotton (Gossypium hirsutum, L.) seedlings enlarge dramatically within 48 h after seed imbibition (Kunce, C.M., R.N. Trelease, and D.C. Doman. 1984. Planta (Berl.). 161:156-164) to effect mobilization of stored cotton-seed oil. We discovered that the membranes of enlarging glyoxysomes at all stages examined contained a large percentage (36-62% by weight) of nonpolar lipid, nearly all of which were triacylglycerols (TAGs) and TAG metabolites. Free fatty acids comprised the largest percentage of these nonpolar lipids. Six uncommon (and as yet unidentified) fatty acids constituted the majority (51%) of both the free fatty acids and the fatty acids in TAGs of glyoxysome membranes; the same six uncommon fatty acids were less than 7% of the acyl constituents in TAGs extracted from cotton-seed storage lipid bodies. TAGs of lipid bodies primarily were composed of palmitic, oleic, and linoleic acids (together 70%). Together, these three major storage fatty acids were less than 10% of both the free fatty acids and fatty acids in TAGs of glyoxysome membranes. Phosphatidylcholine (PC) and phosphatidylethanolamine (PE) constituted a major portion of glyoxysome membrane phospholipids (together 61% by weight). Pulse-chase radiolabeling experiments in vivo clearly demonstrated that 14C-PC and 14C-PE were synthesized from 14C-choline and 14C-ethanolamine, respectively, in ER of cotyledons, and then transported to mitochondria; however, these lipids were not transported to enlarging glyoxysomes. The lack of ER involvement in glyoxysome membrane phospholipid synthesis, and the similarities in lipid compositions between lipid bodies and membranes of glyoxysomes, led us to formulate and test a new hypothesis whereby lipid bodies serve as the dynamic source of nonpolar lipids and phospholipids for membrane expansion of enlarging glyoxysomes. In a cell-free system, 3H-triolein (TO) and 3H-PC were indeed transferred from lipid bodies to glyoxysomes. 3H-PC, but not 3H-TO, also was transferred to mitochondria in vitro. The amount of lipid transferred increased linearly with respect to time and amount of acceptor organelle protein, and transfer occurred only when lipid body membrane proteins were associated with the donor lipid bodies. 3H-TO was transferred to and incorporated into glyoxysome membranes, and then hydrolyzed to free fatty acids. 3H-PC was transferred to and incorporated into glyoxysome and mitochondria membranes without subsequent hydrolysis. Our data are inconsistent with the hypothesis that ER contributes membrane lipids to glyoxysomes during postgerminative seedling growth.(ABSTRACT TRUNCATED AT 400 WORDS)

2011 ◽  
Vol 193 (22) ◽  
pp. 6295-6304 ◽  
Author(s):  
Ángel Pech-Canul ◽  
Joaquina Nogales ◽  
Alfonso Miranda-Molina ◽  
Laura Álvarez ◽  
Otto Geiger ◽  
...  

FadD is an acyl coenzyme A (CoA) synthetase responsible for the activation of exogenous long-chain fatty acids (LCFA) into acyl-CoAs. Mutation offadDin the symbiotic nitrogen-fixing bacteriumSinorhizobium melilotipromotes swarming motility and leads to defects in nodulation of alfalfa plants. In this study, we found thatS. melilotifadDmutants accumulated a mixture of free fatty acids during the stationary phase of growth. The composition of the free fatty acid pool and the results obtained after specific labeling of esterified fatty acids with a Δ5-desaturase (Δ5-Des) were in agreement with membrane phospholipids being the origin of the released fatty acids.Escherichia colifadDmutants also accumulated free fatty acids released from membrane lipids in the stationary phase. This phenomenon did not occur in a mutant ofE. coliwith a deficient FadL fatty acid transporter, suggesting that the accumulation of fatty acids infadDmutants occurs inside the cell. Our results indicate that, besides the activation of exogenous LCFA, in bacteria FadD plays a major role in the activation of endogenous fatty acids released from membrane lipids. Furthermore, expression analysis performed withS. melilotirevealed that a functional FadD is required for the upregulation of genes involved in fatty acid degradation and suggested that in the wild-type strain, the fatty acids released from membrane lipids are degraded by β-oxidation in the stationary phase of growth.


1989 ◽  
Vol 256 (4) ◽  
pp. F688-F696 ◽  
Author(s):  
H. D. Humes ◽  
V. D. Nguyen ◽  
D. A. Cieslinski ◽  
J. M. Messana

Phospholipase activation with resulting phospholipid breakdown and lipid byproduct accumulation may play a critical role in hypoxic cell injury. To explore this role, mildly hypoxic rabbit renal proximal tubules (PT) in suspension were treated in vitro with exogenous phospholipase A2 (PLA2). This treatment produced severe tubule cell injury measured by alterations in tubule cation homeostasis, respiratory rates, and adenosine nucleotide metabolism. This injury was associated with loss of the major membrane phospholipids, phosphatidylcholine (PC) and phosphatidylethanolamine (PE), with accumulation of lipid byproducts, lysophosphatidylcholine (LPC), lysophosphatidylethanolamine (LPE), and free fatty acids (FFA). Addition of fatty acid-free bovine serum albumin (BSA) to PTs reduced markedly FFA levels and improved significantly derangements in metabolic parameters of hypoxic PTs treated with exogenous PLA2, suggesting that FFA accumulation was a critical factor in this injury process. Effects of increasing durations of hypoxia (30, 45, and 60 min) with or without reoxygenation recovery demonstrated increased FFA levels, especially polyunsaturated FFA, which correlated better with the degree of hypoxic injury than alterations in membrane phospholipid and lysophospholipid levels. PTs undergoing hypoxia and reoxygenation recovery exposed to BSA were not protected. Although 60 min of hypoxia with 60 min reoxygenation produced accumulation of FFA to levels nearly identical to those seen in hypoxic PTs treated with exogenous PLA2 and BSA, with a similar distribution of various FFA species, hypoxia/reoxygenation produced a more severe degree of cell injury than that observed with hypoxia plus exogenous PLA and BSA.(ABSTRACT TRUNCATED AT 250 WORDS)


2006 ◽  
Vol 291 (5) ◽  
pp. E885-E890 ◽  
Author(s):  
Dominik G. Haider ◽  
Friedrich Mittermayer ◽  
Georg Schaller ◽  
Michaela Artwohl ◽  
Sabina M. Baumgartner-Parzer ◽  
...  

The detrimental effect of elevated free fatty acids (FFAs) on insulin sensitivity can be improved by thiazolidinediones (TZDs) in patients with type 2 diabetes mellitus. It is unknown whether this salutary action of TZD is associated with altered release of the insulin-mimetic adipocytokine visfatin. In this study, we investigated whether visfatin concentrations are altered by FFA and TZD treatment. In a randomized, double-blind, placebo-controlled, parallel-group study 16 healthy volunteers received an infusion of triglycerides/heparin to increase plasma FFA after 3 wk of treatment with rosiglitazone (8 mg/day, n = 8) or placebo ( n = 8), and circulating plasma visfatin was measured. As a corollary, human adipocytes were incubated with synthetic fatty acids and rosiglitazone to assess visfatin release in vitro. The results were that rosiglitazone treatment increased systemic plasma visfatin concentrations from 0.6 ± 0.1 to 1.7 ± 0.2 ng/ml ( P < 0.01). Lipid infusion caused a marked elevation of plasma FFA but had no effect on circulating visfatin in controls. In contrast, elevated visfatin concentrations in subjects receiving rosiglitazone were normalized by lipid infusion. In isolated adipocytes, visfatin was released into supernatant medium by acute addition and long-term treatment of rosiglitazone. This secretion was blocked by synthetic fatty acids and by inhibition of phosphatidylinositol 3-kinase or Akt. In conclusion, release of the insulin-mimetic visfatin may represent a major mechanism of metabolic TZD action. The presence of FFA antagonizes this action, which may have implications for visfatin bioactivity.


1998 ◽  
Vol 79 (5) ◽  
pp. 382-387
Author(s):  
V. A. Trofimov ◽  
A. P. Vlasov ◽  
М. М. Minnebaev

The considerable increase of the free fatty acids part, phospholipid lysophorms and the decrease of the main membrane lipids level are found in tissue lipids spectrum in peritonitis. The changes in organ li pids composition in many cases are correlated with those in blood plasma. Hence, the complex estimation of blood li pids is an adequate method of determining the biochemical lipid disorders intensity on the organ level.


1958 ◽  
Vol s3-99 (47) ◽  
pp. 315-332
Author(s):  
VISHWA NATH ◽  
BRIJ L. GUPTA ◽  
BACHAN LAL

1. Three kinds of lipid bodies have been described in the oogenesis of the cockroach, Periplaneta americana (i) L1 bodies, present in the earliest oocyte, which persist till the oocyte measures approximately mm and contain phoapholipids only, possibly having more lecithint than cephalins; (ii) L2bodies, which first arise in the oocyte measuring 0.4 mm and have a complete or incomplete sheath of phoapholipida surrounding a medulla of triglycerides (rather highly saturated); (iii) L3 bodies, which are the only type of lipids present in the oocytea measuring more than 0.65 mm and consist of triglycerides only (rather highly saturated). 2. Some of the larger L3 bodies give a ‘ringed’ or ‘crescentic’ appearance in Sudan black when used at room temperatures (12° C to 40° C) but appear mostly solid when this colouring agent is used at 6o° C. 3. Mitochondria, which remain as fine granules throughout the course of oogenesis, contain proteins and phospholipids. They seem to have some lipids which are masked normally but are unmasked after acetone extraction, with a resulting increase in sudanophilia. 4. Yolk globules appear in the oocytes meaauring approximately 0.5 mm. They contain a protein-carbohydrate complex. 5.The bacterioid objects described by earlier workers have been shown to contain phospholipids and free fatty acids. They possibly play an active role in the lipid synthesis of the cell.


1981 ◽  
Vol 36 (1-2) ◽  
pp. 62-70 ◽  
Author(s):  
Margrit Bertrams ◽  
Käthe Wrage ◽  
Ernst Heinz

Abstract De novo-synthesis of glycerolipids in chloroplasts is initiated by a stroma enzyme which catalyzes the formation of lyso-phosphatidic acid from glycerophosphate and acyl-CoA. When these substrates are added to isolated, intact chloroplasts, only glycerophosphate can readily pass through the chloroplast envelope which represents a permeation barrier for acyl-CoA, although higher thioester concentrations destroy this membrane system. At low concentrations of acyl-CoA, which do not impair the envelope, intact chloroplasts metabolize exogenous acyl-CoA in two ways to give free fatty acids and labelled phosphatidyl choline. This indicates that the envelope thioesterase can use exogenous substrates. Isolated, intact chloroplasts fixing radioactive CO2 label free fatty acids and acylglycerols but not galactolipids, since they cannot convert 3-phosphoglycerate into UDP-galactose which in vivo is supplied by the cytoplasm. This cooperation was simulated in vitro by adding all enzymes and cofactors necessary for conversion of 3-phosphoglycerate into UDP-galactose to intact chloro­plasts which then formed labelled monogalactosyl diacylglycerol from labelled CO2. The time required to transfer envelope-made galactolipids from the envelope into thylakoids was studied by incubating intact chloroplasts with radioactive UDP-galactose, subsequent osmotic disruption of organelles with concomitant enzymatic degradation of UDP-galactose followed by separation of envelopes and thylakoids. Only after short times (< 1min) appreciable proportions 920-30%) of radioactive galactolipid export from envelopes into thylakoids.


BioTechniques ◽  
2015 ◽  
Vol 58 (5) ◽  
Author(s):  
Ana F Oliveira ◽  
Daniel A Cunha ◽  
Laurence Ladriere ◽  
Mariana Igoillo-Esteve ◽  
Marco Bugliani ◽  
...  
Keyword(s):  

1974 ◽  
Vol 31 (1) ◽  
pp. 99-108 ◽  
Author(s):  
R. C. Noble ◽  
J. H. Moore ◽  
C. G. Harfoot

1. Studies have been made of the effects of different concentrations of either free or esterified linoleic acid on the biohydrogenation of linoleic acid by rumen micro-organisms in vitro. A comparison has been made with the changes which occurred in the fatty acid compositions of rumen free fatty acids and plasma triglycerides of sheep given intraruminal infusions of linoleic acid or maize oil.2. In the in vitro experiments, with increasing concentrations of 18:2 added as the free fatty acid, a decreasing proportion of this 18:2 was hydrogenated to 18:0 andtrans-11-octadecenoic acid accumulated. The accumulation of large amounts oftrans-11-octadecenoic acid was accompanied in all instances by the accumulation of a conjugated diene identified ascis-9,trans-11-octadecadienoic acid. There appeared to be a product–precursor relationship between the conjugated diene and thetrans-11 monoene.3. When linoleic acid was presented in vitro as the triglyceride, the extent to which hydrogenation occurred was, in all instances, greater than when equivalent amounts of 18:2 were presented as the free acid. Only small amounts of thecis-9,trans-11 diene were detected, and there was no apparent product–precursor relationship between this conjugated diene and the C18monoenoic acids. The C18monoenoic acids that accumulated consisted of bothcisandtransisomers; thecisisomers consisted largely ofcis-9- andcis-11-octadecenoic acids, which together comprised about 30% of the C18monoenoic acids present.4. The infusion of free linoleic acid into the rumen of sheep resulted in an increase in the proportion of total 18:1 and a decrease in the proportions of 16:0 and 18:0 in the total rumen free fatty acids. This increase which occurred in the concentration of 18:1 consisted predominantly of thetrans-11 isomer. A concomitant increase in the concentration of the C18trans-11 acid was observed to occur in the fatty acids of the plasma triglycerides. Infusion of maize oil into the rumen of sheep resulted in little change in the fatty acid compositions of either the free fatty acids in the rumen or the triglycerides of the plasma.5. The findings in vitro and in vivo are discussed with reference to each other and with reference to the possibility that biohydrogenation of 18:2 derived from the triglyceride proceeds by a different pathway from that of 18:2 presented as the free acid.


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