Interaction of Free Fatty Acids with Fish Muscle in Vitro

1974 ◽  
Vol 31 (1) ◽  
pp. 111-113 ◽  
Author(s):  
E. A. Childs

When fresh fish muscle (Ophiodon elongatus) was exposed to free fatty acids (safflower oil hydrolysate), the whole myofibril lost its suspensibility more readily than its component proteins lost their solubility. SDS-acrylamide gel electrophoresis indicated that tropomyosin was the most readily insolubilized protein. In the presence of 0.04% formaldehyde, effects of the free fatty acids were increased approximately threefold.

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.


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.


1973 ◽  
Vol 134 (4) ◽  
pp. 1067-1081 ◽  
Author(s):  
Anthony McAllister ◽  
S. P. Allison ◽  
Philip J. Randle

1. The extractions of glucose, lactate, pyruvate and free fatty acids by dog heart in vivo were calculated from measurements of their arterial and coronary sinus blood concentration. Elevation of plasma free fatty acid concentrations by infusion of intralipid and heparin resulted in increased extraction of free fatty acids and diminished extractions of glucose, lactate and pyruvate by the heart. It is suggested that metabolism of free fatty acids by the heart in vivo, as in vitro, may impair utilization of these substrates. These effects of elevated plasma free fatty acid concentrations on extractions by the heart in vivo were reversed by injection of dichloroacetate, which also improved extraction of lactate and pyruvate by the heart in vivo in alloxan diabetes. 2. Sodium dichloroacetate increased glucose oxidation and pyruvate oxidation in hearts from fed normal or alloxan-diabetic rats perfused with glucose and insulin. Dichloroacetate inhibited oxidation of acetate and 3-hydroxybutyrate and partially reversed inhibitory effects of these substrates on the oxidation of glucose. In rat diaphragm muscle dichloroacetate inhibited oxidation of acetate, 3-hydroxybutyrate and palmitate and increased glucose oxidation and pyruvate oxidation in diaphragms from alloxan-diabetic rats. Dichloroacetate increased the rate of glycolysis in hearts perfused with glucose, insulin and acetate and evidence is given that this results from a lowering of the citrate concentration within the cell, with a consequent activation of phosphofructokinase. 3. In hearts from normal rats perfused with glucose and insulin, dichloroacetate increased cell concentrations of acetyl-CoA, acetylcarnitine and glutamate and lowered those of aspartate and malate. In perfusions with glucose, insulin and acetate, dichloroacetate lowered the cell citrate concentration without lowering the acetyl-CoA or acetylcarnitine concentrations. Measurements of specific radioactivities of acetyl-CoA, acetylcarnitine and citrate in perfusions with [1-14C]acetate indicated that dichloroacetate lowered the specific radio-activity of these substrates in the perfused heart. Evidence is given that dichloroacetate may not be metabolized by the heart to dichloroacetyl-CoA or dichloroacetylcarnitine or citrate or CO2. 4. We suggest that dichloroacetate may activate pyruvate dehydrogenase, thus increasing the oxidation of pyruvate to acetyl-CoA and acetylcarnitine and the conversion of acetyl-CoA into glutamate, with consumption of aspartate and malate. Possible mechanisms for the changes in cell citrate concentration and for inhibitory effects of dichloroacetate on the oxidation of acetate, 3-hydroxybutyrate and palmitate are discussed.


2015 ◽  
Vol 37 (5) ◽  
pp. 1767-1778 ◽  
Author(s):  
Mohamed Asrih ◽  
Christophe Montessuit ◽  
Jacques Philippe ◽  
François R. Jornayvaz

Background/Aims: Fibroblast growth factor 21 (FGF21) is a key mediator of glucose and lipid metabolism. However, the beneficial effects of exogenous FGF21 administration are attenuated in obese animals and humans with elevated levels of circulating free fatty acids (FFA). Methods: We investigated in vitro how FFA impact FGF21 effects on hepatic lipid metabolism. Results: In the absence of FFA, FGF21 reduced lipogenesis and increased lipid oxidation in HepG2 cells. Inhibition of lipogenesis was associated with a down regulation of SREBP-1c, FAS and SCD1. The lipid-lowering effect was associated with AMPK and ACC phosphorylation, and up regulation of CPT-1α expression. Further, FGF21 treatment reduced TNFα gene expression, suggesting a beneficial action of FGF21 on inflammation. In contrast, the addition of FFA abolished the positive effects of FGF21 on lipid metabolism. Conclusion: In the absence of FFA, FGF21 improves lipid metabolism in HepG2 cells and reduces the inflammatory cytokine TNFα. However, under high levels of FFA, FGF21 action on lipid metabolism and TNFα gene expression is impaired. Therefore, FFA impair FGF21 action in HepG2 cells potentially through TNFα.


1969 ◽  
Vol 24 (2) ◽  
pp. 130-136 ◽  
Author(s):  
Richard J. Cenedella ◽  
John J. Jarrell ◽  
L.H. Saxe

1969 ◽  
Vol 25 (2) ◽  
pp. 128-128 ◽  
Author(s):  
A. Kershbaum ◽  
H. Osada ◽  
D. J. Pappajohn ◽  
S. Bellet

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