A Combination of (ω–3) Polyunsaturated Fatty Acids, Polyphenols and L-Carnitine Reduces the Plasma Lipid Levels and Increases the Expression of Genes Involved in Fatty Acid Oxidation in Human Peripheral Blood Mononuclear Cells and HepG2 Cells

2011 ◽  
Vol 58 (2) ◽  
pp. 133-140 ◽  
Author(s):  
Ulla Radler ◽  
Herbert Stangl ◽  
Sigrid Lechner ◽  
Gerhard Lienbacher ◽  
Rainer Krepp ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Mononuclear Cells ◽  
Human Peripheral Blood ◽  
Plasma Lipid ◽  
Acid Oxidation ◽  
Lipid Levels ◽  
Peripheral Blood Mononuclear ◽  
Expression Of Genes ◽  
Blood Mononuclear Cells

scholarly journals Evaluation of Metabolic Defects in Fatty Acid Oxidation Using Peripheral Blood Mononuclear Cells Loaded with Deuterium-Labeled Fatty Acids

2019 ◽  
Vol 2019 ◽  
pp. 1-11
Author(s):  
Miori Yuasa ◽  
Ikue Hata ◽  
Keiichi Sugihara ◽  
Yuko Isozaki ◽  
Yusei Ohshima ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Mononuclear Cells ◽  
Acid Oxidation ◽  
Peripheral Blood Mononuclear ◽  
Metabolic Defects ◽  
Diagnostic Indices ◽  
Blood Mononuclear Cells ◽  
Cycle Disorders

Because tandem mass spectrometry- (MS/MS-) based newborn screening identifies many suspicious cases of fatty acid oxidation and carnitine cycle disorders, a simple, noninvasive test is required to confirm the diagnosis. We have developed a novel method to evaluate the metabolic defects in peripheral blood mononuclear cells loaded with deuterium-labeled fatty acids directly using the ratios of acylcarnitines determined by flow injection MS/MS. We have identified diagnostic indices for the disorders as follows: decreased ratios of d27-C14-acylcarnitine/d31-C16-acylcarnitine and d23-C12-acylcarnitine/d31-C16-acylcarnitine for carnitine palmitoyltransferase-II (CPT-II) deficiency, decreased ratios of d23-C12-acylcarnitine/d27-C14-acylcarnitine for very long-chain acyl-CoA dehydrogenase (VLCAD) deficiency, and increased ratios of d29-C16-OH-acylcarnitine/d31-C16-acylcarnitine for trifunctional protein (TFP) deficiency, together with increased ratios of d7-C4-acylcarnitine/d31-C16-acylcarnitine for carnitine palmitoyltransferase-I deficiency. The decreased ratios of d1-acetylcarnitine/d31-C16-acylcarnitine could be indicative of β-oxidation ability in patients with CPT-II, VLCAD, and TFP deficiencies. Overall, our data showed that the present method was valuable for establishing a rapid diagnosis of fatty acid oxidation disorders and carnitine cycle disorders and for complementing gene analysis because our diagnostic indices may overcome the weaknesses of conventional enzyme activity measurements using fibroblasts or mononuclear cells with assumedly uncertain viability.

scholarly journals The effects of fish oil and high or low linoleic acid intake on fatty acid composition of human peripheral blood mononuclear cells

2007 ◽  
Vol 99 (1) ◽  
pp. 147-154 ◽  
Author(s):  
Camilla T. Damsgaard ◽  
Hanne Frøkiær ◽  
Lotte Lauritzen
Keyword(s):  
Fatty Acid Composition ◽  
Fatty Acid ◽  
Acid Composition ◽  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Human Peripheral Blood ◽  
Peripheral Blood Mononuclear ◽  
Chain Pufa ◽  
Blood Mononuclear Cells

Dietary intake of 18: 2n-6 and 18: 3n-3 may affect endogenous production and incorporation of n-3 long-chain PUFA (LCPUFA) from fish oils (FO). This double-blinded controlled 2 × 2-factorial 8-week intervention investigates the effects of high and low 18: 2n-6 intake in combination with FO-supplementation on tissue fatty acid composition. Healthy young men (n 64) were randomized to capsules with FO or olive oil (control) (4·4 (2·0–5·6) ml/d) and to either sunflower oil and margarine (S/B) or rapeseed oil and a butter spread (R/K) to provide a high or a low 18: 2n-6 intake. Diet was measured by 4-d weighed dietary records at baseline, during and 8 weeks after the intervention and tissue incorporation as fatty acid composition of peripheral blood mononuclear cells (PBMC). The fat intervention gave a mean difference in the 18: 2n-6 intake of 7·3 g/d (95 % CI 4·6, 10·0) and a similar 18: 3n-3 intake in the groups. The R/K groups had a 0·2 % fatty acid (FA%) (95 % CI 0·0, 0·4, P = 0·02) higher content of 22: 5n-3 in the PBMC, a tendency of slightly higher 20: 5n-3 (P = 0·06), but no more 22: 6n-3 (P = 0·83) than the S/B groups. FO effectively raised the PBMC content of all n-3 LCPUFA (P < 0·001). The fat intervention did not markedly influence the effect of FO; the mean PBMC content of n-3 LCPUFA was 10·3 (sem 0·3) FA% in the FO+S/B group and 10·6 (sem 0·2) FA% in the FO+R/K group. In conclusion, increasing the 18: 2n-6 intake did not have any pronounced effect on incorporation of n-3 LCPUFA in PBMC, either alone or with simultaneous FO supplementation.

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