Effect Of Linoleate Research Articles

Effects of linoleate on cell viability and lipid metabolic homeostasis in goose primary hepatocytes

Studies have shown linoleate could not only promote cell viability but also affect lipid metabolism in mammals. However, to what degree these effects are mediated by steatosis in goose primary hepatocytes is unknown. In this study, the effect of linoleate on the lipid metabolic homeostasis pathway was determined. We measured the mRNA levels of genes involved in triglyceride synthesis, lipid deposition, β-oxidation, and assembly and secretion of VLDL-TGs in goose ( Anser cygnoides) primary hepatocytes. Linoleate significantly increased goose hepatocyte viability, and linoleate at 0.125 mM, 0.25 mM, 0.5 mM and 1.0 mM all showed a significant effect on TG accumulation. However, with increasing linoleate concentrations, the extracellular TG concentration and extracellular VLDL gradually decreased. DGAT1, DGAT2, PPARα, PPARγ, FoxO1, MTP, PLIN and CPT-1 mRNA was detected by real-time PCR. With increasing linoleate concentrations, the changes in DGAT1, DGAT2, PPARα and CPT-1 gene expression, which regulates hepatic TG synthesis and fatty acid oxidation, first increased and then decreased. Additionally, FoxO1 and MTP gene expression was reduced with increasing linoleate concentrations, and the change in PLIN gene expression was increased at all concentrations, similar to the regulation of intracellular TG accumulation. In conclusion, linoleate regulated TG accumulation and increased hepatocyte viability. The data suggest that linoleate does promote goose hepatocyte viability and steatosis, which may up-regulate TG synthesis-relevant gene expression, suppress assembly and secretion of VLDL-TGs, and increase fatty acid oxidation properly to function of goose primary hepatocytes.

Fatty acid-induced differential regulation of the genes encoding peroxisome proliferator-activated receptor-γ coactivator-1α and -1β in human skeletal muscle cells that have been differentiated in vitro

The transcriptional coactivator peroxisome proliferator-activated receptor-gamma coactivator-1alpha (PGC-1alpha) enhances metabolically relevant pathways, such as gluconeogenesis, fatty acid oxidation, thermogenesis, oxidative phosphorylation and mitochondrial biogenesis. Since regulation of the expression of the gene encoding PGC-1alpha (PPARGC1A) by nutrients/metabolites has not been assessed in detail, the aim of this study was to determine whether PPARGC1A (and PPARGC1B) expression is modulated by common plasma fatty acids in human skeletal muscle cells. Human myotubes that had been differentiated in vitro were treated with 0.5 mmol/l myristate (C14:0), palmitate (C16:0), stearate (C18:0), palmitoleate (C16:1omega7), oleate (C18:1omega9) or linoleate (C18:2omega6). PPARGC1A/B mRNA was quantified by RT-PCR. Mitochondrial activity was determined by formazan formation. Untreated cells expressed 28-fold more PPARGC1B mRNA than PPARGC1A mRNA (13.33+/-2.86 vs 0.47+/-0.08 fg/mug total RNA, n=5). PPARGC1A expression was increased two- to three-fold by all unsaturated fatty acids (UFAs) tested (p<0.05 each, n=5). In contrast, saturated fatty acids (SFAs) did not modulate PPARGC1A expression. Furthermore, the effect of linoleate was not blunted by palmitate. PPARGC1B mRNA expression was not increased by either the UFAs or the SFAs. SFAs reduced PPARGC1B expression (p<0.05 for palmitate and stearate, n=5). Notably, linoleate reversed palmitate's repressive effect on PPARGC1B. Myotube mitochondrial activity was increased by all UFAs (p<0.01 each, n=5), but was impaired by the SFA stearate (p<0.001, n=5). We report here that fatty acids differentially regulated expression of the genes encoding the PGC-1 isoforms. Since these effects were accompanied by significant changes in mitochondrial activity, we suggest that the fatty acid-induced regulation of expression of these genes plays an important role in muscle oxidative metabolism.

Effect of Linoleate on Electrochemical Behavior of Stainless Steel in Phosphate Buffer

Abstract Electrochemical behavior of a high-purity, austenitic, low-carbon, stainless steel (SS) surface in the presence of a sodium salt of linoleic acid (C17H31COONa), sodium linoleate (LA), was ...

Mechanisms in the pressor effects of hepatic portal venous fatty acid infusion.

Portal venous infusion of oleate solution has pressor effects. We have examined efferent mechanisms, measured the response to sustained infusion, and determined the effect of linoleate. Eight conscious animals received concurrent infusions of prazosin or vehicle with portal venous infusion of oleate. Oleate alone increased mean arterial pressure from 109.0 +/- 4.1 to 123.0 +/- 5.8 mmHg (P = 0.02), whereas no increase in blood pressure occurred when oleate was infused with prazosin. In 10 rats, concurrent infusion of losartan had no effect on the pressor activity of portal oleate infusion. Twenty-two animals received portal oleate or vehicle as a continuous infusion for 7 days. Mean arterial pressure (126.1 +/- 2.0 vs. 107.8 +/- 2.6 mmHg, P < 0.001) and heart rate (383 +/- 5 vs. 366 +/- 5, P = 0.0257) were increased in oleate-infused animals. No differences in plasma fatty acids, glucose, insulin, pressor hormones, liver enzymes, or in vitro arterial pressor responsiveness were observed. Portal venous infusion of linoleate increased arterial pressure by 12.2 +/- 3.2 mmHg (P = 0.033). These results indicate that alpha-adrenergic activity is necessary for the acute pressor effects of portal oleate, that sustained portal oleate infusion results in persistent blood pressure elevation, and that other long-chain fatty acids besides oleate have pressor effects.

Role of Calcium Ion in Schistosoma mansoni Cercarial Tail Loss Induced by Unsaturated Fatty Acids

Linoleate (C18: 2) and oleate (C18: 1), but not stearate (C18: 0), induced tail removal in cercariae. Linoleate stimulated tail loss more strongly than oleate did. Tail loss induced by linoleate was significantly suppressed by incubating cercariae with ethyleneglycol-bis-(beta-aminoethyl ether) N,N,N',N'-tetraacetic acid (EGTA). Preincubation of cercariae with EGTA for 5 min caused further inhibition of the tail loss. Calcium ionophore A23187 (A23187) increased the cercarial tail-loss rate. When A23187 was combined with linoleate at 0.03 mM, an additive effect on tail loss appeared, whereas the ionophore in combination with linoleate at 0.3 mM had no such effect. EGTA almost completely abolished cercarial tail loss induced by linoleate at both 0.03 and 0.3 mM in the presence and absence of A23187. Linoleate at 3 mM provoked cercarial tail loss even in the presence of EGTA, although the effect of oleate at 3 mM disappeared. Under these conditions, the effect of linoleate was synergistically enhanced by the combination with A23187. A similar, but not significant, synergism took place in cercariae stimulated by oleate. These findings suggest that unsaturated fatty acids enhance calcium influx into cercariae, resulting in triggering tail loss, and, furthermore, that the fatty acids have other potentiating effects on cercarial tail loss. Protein kinases play an insignificant role in fatty acid-induced cercarial tail loss, because a protein kinase C inhibitor, 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H-7), and an inhibitor of various protein kinases, staurosporine, had little or no effect on cercarial tail loss induced by linoleate at 3 mM.

Effects of Linoleate and Arachidonate Deficiencies on Reproduction and Spermatogenesis in the Cat

The inability of the cat to convert significant quantities of linoleate [18:2(9,12)] to arachidonate [20:4(5,8,11,14)] in the liver makes the cat a useful model for studying the specific physiological roles of these two fatty acids. In these studies, cats were fed purified diets that were either deficient in essential fatty acids (EFAs) or that provided linoleate with or without arachidonate. Male cats that were fed the EFA-deficient diet for approximately 2 years exhibited extensive degeneration of the testes, and the fatty acid composition of testes changed in a manner consistent with EFA deficiency. Linoleate prevented testis degeneration. Levels of arachidonate, 22:4n6, and 22:5n6 were higher in testis phospholipids of cats supplied with linoleate than in the deficient cats, indicating that the testis of the cat has the capacity to desaturate and elongate linoleate. In contrast, female cats that were fed diets lacking arachidonate were unable to bear live kittens, whether linoleate was provided in the diet or not. Arachidonate, supplied by oral supplements of ethyl arachidonate or by animal fat in the diet, significantly improved reproduction. Thus, linoleate appears to meet the requirements for spermatogenesis in males, but dietary arachidonate is essential for adequate reproduction in female cats.

Comparative Studies on the Effects of Linoleate and Methyl Linoleate and Their Hydroperoxides on the Respiration and Reactivities of Rat Heart Mitochondria1

Linoleate hydroperoxide and linoleate at concentrations of 100-140 nmol-mg protein activated state 4 respiration of rat heart mitochondria 4.2-fold, increased the apparent enthalpy change of the respiration per gram atom of oxygen consumed from -148 to -226 kJ/O and completely inhibited oxidative phosphorylation. Methyl linoleate hydroperoxide or methyl linoleate did not show the same effects. Further addition of linoleate hydroperoxide or linoleate induced oligomycin-insensitive Mg-ATPase to a level 5 or 2 times, respectively, that obtained with 120 muM dinitrophenol, accompanied by clearing of the mitochondrial suspension and release of malate dehydrogenase from the matrix. Methyl linoleate hydroperoxide had the same effects except that the induced Mg-ATPase activity retained oligomycin sensitivity. Methyl linoleate did not show either effect.

Lipoxygenase-like enzyme in bat testis microsomes

Microsomes, separated from rat testes, were found capable of oxidizing linoleate and arachidonate. The enzyme activity was solubilized with 1% Triton X-100 in acetate buffer (pH 5.0) and purified by affinity chromatography. The overall purification from the starting preparation was approx. 40-fold. The affinity-purified enzyme was almost homogeneous as determined by electrophoresis in polyacrylamide gel. The enzyme was characterized as lipoxygenase-like from its spectrum, specificity, effect of linoleate on its fluorescence and linoleate oxidation products. Three types of compounds separated by thinlayer chromatography were generally present in the lipoxygenase-like enzyme reaction on linoleic acid: substrate fatty acid, polar by-products and hydroperoxides. The hydroperoxides were analyzed by infrared spectra and mass spectrometry and showed the presence of both 9- and 13-hydroxy isomers.

The Effects of Linoleate and Acetate on the Growth and Lipid Composition of Mycelium of Agaricus bisporus

The Effects of Linoleate and Acetate on the Growth and Lipid Composition of Mycelium of Agaricus bisporus

Influence of fatty-acid composition of infant formulas on the development of arteriosclerosis and on the lipid composition of blood and tissues. II. Further lipid studies.

Six liquid diets, widely varying in linoleate content, were fed to 50 infant rhesus monkeys. Some were transferred to monkey chow, and some of these to a high hydrogenated fat plus 2% corn oil diet. Our results confirm the previously reported hypercholesterolemic effect of bovine butterfat and the protective effect of linoleate against such hypercholesterolemia. Animals given large amounts of linoleate in their diets reflected this in the pattern of their blood and tissue fatty acids. However, judging by the erythrocyte and tissue levels of arachidonic acid, they tended to convert a smaller percentage of the total linoleate to arachidonate than animals reveiving considerably smaller amounts of linoleate. This was true whether the animals were infants, adolescents, or approaching sexual maturity.

Effects of Linoleate and Dietary Fat Level on Plasma and Liver Cholesterol and Vascular Lesions of the Cholesterol-fed Rat

Effects of Linoleate and Dietary Fat Level on Plasma and Liver Cholesterol and Vascular Lesions of the Cholesterol-fed Rat