Analysis of polyunsaturated fatty acids in blood serum after fish oil administration

Liebich, H.M.; Wirth, Christoph; Jakober, B.

doi:10.1016/0378-4347(91)80468-r

Cited by 37 publications

(17 citation statements)

References 8 publications

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“…In an earlier study, when 9 g/day of fish oil (containing 1.6 g of EPA) was orally administered to German patients with hyperlipoproteinemia, the EPA levels as total lipids in plasma increased from 119 70 to 619 172 µmol/l (mean SD), and the EPA levels as free fatty acids in plasma increased from 7 3 to 40 10 µmol/l (mean SD) (45). Thus, the concentrations of EPA (30-300 µmol/l) used in this study seemed to be within clinical and physiological ranges.…”

Section: Discussionmentioning

confidence: 94%

Eicosapentaenoic Acid Suppresses Basal and Insulin-Stimulated Endothelin-1 Production in Human Endothelial Cells

et al. 2003

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Section: Discussionmentioning

confidence: 94%

Eicosapentaenoic Acid Suppresses Basal and Insulin-Stimulated Endothelin-1 Production in Human Endothelial Cells

et al. 2003

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“…The concentrations of free fatty acids used in our incubations, may be obtained in plasma by dietary supplementation. 38 We also complexed PUFA to albumin and thus our studies were performed in a physiologically relevant way. It is even possible that PUFA may affect proliferation of leukemia cells in vivo as demonstrated in mice bearing the myeloid leukemia T27A.…”

Section: Discussionmentioning

confidence: 99%

Multiplication and death-type of leukemia cell lines exposed to very long-chain polyunsaturated fatty acids

et al. 1998

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Polyunsaturated fatty acids (PUFA) may reduce cell multiplication in cultures of normal, as well as transformed, white blood cells. We assessed the sensitivity of 14 different leukemia cell lines to PUFA by measuring cell number after 3 days of incubation. Ten of the examined cell lines were sensitive to 30, 60 and/or 120 M of arachidonic, eicosapentaenoic and docosahexaenoic acid, whereas four cell lines were resistant. The sensitivity to PUFA was not associated with any particular cell lineage, clinical origin or specific mRNA pattern of bcl-2 and c-myc. Effects on cell viability were assessed by studying cell membrane integrity, DNA fragmentation and cell morphology. The sensitive cell lines Raji and Ramos died by necrosis and apoptosis, respectively, during incubation with eicosapentaenoic acid, whereas the viability of the resistant U-698 cell line was unaffected. The effects of EPA on Raji cells, was counteracted by vitamin E, indicating that lipid peroxidation was involved. However, apoptosis induced by eicosapentaenoic acid in Ramos cells, was unaffected by vitamin E, as well as eicosanoid synthesis inhibitors. In conclusion, our results indicate that a majority of leukemia cell lines are sensitive to PUFA. This sensitivity may be caused by induction of apoptosis or necrosis by very long-chain polyunsaturated fatty acids.

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“…2). Nevertheless, feeding humans or rats fish oil, a rich source of n3-PUFA, is reported to increase 20:5n-3, 22:5n-3, and 22:6n-3 in blood (32) and liver (23), respectively. Because PPAR␣ is required for n3-PUFA effects on hepatic CYP4A and acyl CoA oxidase induction (16), we predict that future studies will describe the enrichment of the NEFA pool and L-FABP with 20-and 22-carbon PUFA following fish oil feeding.…”

Section: -Carbon N3-pufa Regulation Of Ppar␣-becausementioning

confidence: 99%

Unsaturated Fatty Acid Regulation of Peroxisome Proliferator-activated Receptor α Activity in Rat Primary Hepatoctes

Pawar

Jump

2003

Journal of Biological Chemistry

183

151

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Peroxisome proliferator-activated receptors (PPARs ␣, ␤, ␥1, and ␥2) are widely regarded as monitors of intracellular nonesterified fatty acid (NEFA) levels. As such, fatty acid binding to PPAR leads to changes in the transcription of many genes involved in lipid metabolism and storage. Although the composition of the intracellular NEFA pool is likely an important factor controlling PPAR activity, little information is available on factors affecting its composition. Accordingly, we have examined the effects of exogenous fatty acids on PPAR␣ activity and NEFA pool composition in rat primary hepatocytes. Prior to the addition of fatty acids to primary hepatocytes, nonesterified unsaturated fatty acid levels are very low, representing <0.5% of the total fatty acid in the cell. The relative abundance of putative PPAR␣ ligands in the NEFA pool is 20:4n-6 ‫؍‬ 18:2n-6 ‫؍‬ 18:1n-9 > 22:6n-3 > 18:3n-3/6 ‫؍‬ 20:5n-3. Of these fatty acids, only 20:5n-3 and 22:6n-3 consistently induced PPAR␣ activity. Metabolic labeling of primary hepatocytes indicated that both 14 C-18:1n-9 and 14 C-20:5n-3 are rapidly assimilated into neutral and polar lipids. Although the addition of 18:1n-9 had no effect on NEFA pool composition, 20:5n-3 mass increased >15-fold within 90 min. Changes in NEFA pool 20:5n-3 mass correlated with dynamic changes in the PPAR␣-regulated transcript mRNA CYP4A . Metabolic labeling also indicated that a significant fraction of 14 C-20:5n-3 was elongated to 22:5n-3. Cells treated with 22:5n-3 or 22:6n-3 led to a significant accumulation of 20:5n-3 in the NEFA pool through a process that requires peroxisomal ␤-oxidation and fatty acyl CoA thioesterase activity. Further analyses suggest that 20:5n-3 and 22:6n-3, but not 22:5n-3, are active ligands for PPAR␣. These studies suggest that basal fatty acid levels in the NEFA pool coupled with rates of fatty acid esterification, elongation, desaturation, peroxisomal ␤-oxidation, and fatty acyl thioestease activity are important determinants controlling NEFA pool composition and PPAR␣ activity.

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Analysis of polyunsaturated fatty acids in blood serum after fish oil administration

Cited by 37 publications

References 8 publications

Eicosapentaenoic Acid Suppresses Basal and Insulin-Stimulated Endothelin-1 Production in Human Endothelial Cells

Eicosapentaenoic Acid Suppresses Basal and Insulin-Stimulated Endothelin-1 Production in Human Endothelial Cells

Multiplication and death-type of leukemia cell lines exposed to very long-chain polyunsaturated fatty acids

Unsaturated Fatty Acid Regulation of Peroxisome Proliferator-activated Receptor α Activity in Rat Primary Hepatoctes

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