Mechanisms and physiological roles of fatty acid chain elongation in microsomes and mitochondria

Seubert, W.; Podack, Eckhard R.

doi:10.1007/bf01659936

Cited by 104 publications

(34 citation statements)

References 55 publications

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“…Thus, palmitoleic acid (C16:1n-7), oleic acid (C18:1n-9) and cisvaccenic acid (C18:1n-11) are the main products of this reaction. Chain elongation by another enzymatic system, the fatty acid elongase system, will produce eicosanoic acid (C20:1n-9), erucic acid (C22:1n-13) and nervonic acid (C24:1n-9) by elongation of oleic acid (Seubert & Podack, 1973). Linoleic acid (C18:2n-6) was the most predominant PUFA in the tissues (Table 6c).…”

Section: Discussionmentioning

confidence: 99%

Effects of various dietary n-3 / n-6 fatty acid ratios on the performance and body composition of broilers

Coetzee¹,

Hoffman²

2002

SA J. An. Sci.

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Different combinations of saturated and unsaturated fatty acids were fed to broilers to establish their effect on the fatty acid composition of the broiler carcass and the abdominal fat pad. Six combinations of Canola acid oil (CAO, high levels of C18:3n-3 and monounsaturated fatty acids) and Famarol acid oil (FAO, high levels of C18:2n-6 and saturated fatty acids) were included in the broiler diets from one day of age to six weeks of age, viz. 100% FAO, 80% FAO-20% CAO, 60% FAO-40% CAO, 40% FAO-60% CAO, 20% FAO-80% CAO, 100% CAO. There were no statistically significant differences between dietary groups in weight gain (1.71 ± 0.059 kg) or feed conversion ratios (1.97 ± 0.051 g feed/g gain). No significant differences between treatments were found in the moisture (66.20 ± 0.112%), protein (17.63 ± 0.484%), lipid (15.92 ± 1.507%) and ash (0.95 ± 0.115%) concentration of the carcasses, nor in the moisture (28.77 ± 0.112%), protein (3.03 ± 0.484%), lipid (63.32 ± 9.789%) and ash (0.45 ± 0.135%) concentrations of the abdominal fat pads. With the increase in dietary CAO levels, the mean percentages of C18:2n-6 and C20:4n-6 in the carcasses decreased respectively with 1.78% units from 20.88% and 0.35% units from 1.05%, whilst C18:3n-3 and longer chain n-3 fatty acids such as C20:5n-3 and C22:6n-3 increased respectively with 2.25% units from 1%, 0.1% units from 0.1% and 0.67% units from 0.2%. The same tendency was seen in the abdominal fat pads where C18:2n-6 and C20:4n-6 decreased respectively with 1.55% units from 20.75% and 0.98% units from 1.2% with an increase in dietary CAO, whilst C18:3n-3, C20:5n-3 and C22:6n-3 increased respectively with 2.13% units from 1.15%, 0.45% units from 0.03% and 0.95% units from 0.05%. The n-3/n-6 ratio in the carcasses and abdominal fat pads increased respectively with 0.16% units from 0.06% and 0.19% units from 0.06% with an increase in dietary CAO. These results clearly indicate that dietary CAO enriched with α-linolenic acid lowered the saturated fatty acid concentrations in broiler carcasses and abdominal fat pads with 4.88% units and 10.63% units respectively, and increased the monounsaturated fatty acid concentrations with 3.87% units and 7.25% units, respectively and polyunsaturated fatty acid concentrations with 1.02% units and 2.38% units, respectively. The results of this experiment showed that substitution of Famarol oil with Canola oil in broiler diets can increase the ratio of n-6 to n-3 fatty acids in broiler carcasses and abdominal fat pads to 5:1, a ratio more suitable for human health. Increasing the level of n-3 fatty acids in the diets was also effective in reducing the level of saturated fatty acids in the carcasses and abdominal fat pads of broiler chickens resulting in "healthier" chickens.

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Section: Discussionmentioning

confidence: 99%

Effects of various dietary n-3 / n-6 fatty acid ratios on the performance and body composition of broilers

Coetzee¹,

Hoffman²

2002

SA J. An. Sci.

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“…Chain elongation and other biotransformation of fatty acids have been shown to occur primarily in the ER (1,2). The mitochondrial chain elongation system is a reversal of the fatty acid ␤-oxidation system; thus, acetyl-CoA, instead of malonylCoA, is used for the condensation reaction, and the resulting ␤-keto acyl-CoA undergoes the same series of reactions as described above (3). The physiological function of the mitochondrial chain elongation system is not clear (4).…”

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confidence: 99%

Molecular Cloning and Expression of Mammalian Peroxisomaltrans-2-Enoyl-coenzyme A Reductase cDNAs

Das

Uhler

Hajra

2000

Journal of Biological Chemistry

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Chain elongation of fatty acids is an important cellular process and is believed to occur in the endoplasmic reticulum of all eukaroytic cells. Herein we describe the cloning and characterization of a peroxisomal NADPHspecific trans-2-enoyl-CoA reductase, the key enzyme for a proposed peroxisomal chain elongation pathway. The reductase was solubilized and partially purified from guinea pig liver peroxisomes by affinity chromatography. On SDS-polyacrylamide gel electrophoresis, a 40-kDa band was identified as the enzyme, and its partial amino acid sequence (27 amino acids) was determined. A full-length cDNA for the reductase was cloned from a guinea pig liver cDNA library. The open reading frame of this nucleotide sequence encodes a 302-amino acid polypeptide with a calculated molecular mass of 32.5 kDa. Full-length mouse and human cDNA clones encoding homologous proteins have also been isolated. All of these translated polypeptides have the type I peroxisomal targeting signal, AKL, at the carboxyl terminus. The identity of the cloned enoyl-CoA reductase cDNAs was confirmed by expressing the guinea pig and human cDNAs in Escherichia coli. The His-tagged recombinant enzymes were found to have very high NADPH-specific 2-enoyl-CoA reductase activity with similar properties and specificity as the liver peroxisomal reductase. Both the natural and the recombinant enzyme catalyze the reduction of trans-2-enoyl-CoAs of varying chain lengths from 6:1 to 16:1, having maximum activity with 10:1 CoA. Northern blot analysis demonstrated that a single transcript of 1.3 kilobases is present in most mouse tissues, with particularly high concentrations in liver and kidney.In mammalian cells, the fatty acid chain elongation system has been shown to be present in both endoplasmic reticulum (ER) 1 and mitochondria (1). The ER pathway is similar to the fatty acid synthesis system. In this multistep process, malonylCoA first condenses with acyl-CoA to form a ␤-keto acyl-CoA with two additional carbons with the release of CO 2 . The ␤-keto acyl-CoA then undergoes reduction of the ketone group followed by dehydration to form a 2-enoyl-CoA, which is then reduced by NADH or NADPH to form the longer (ϩ2C) acylCoA. Chain elongation and other biotransformation of fatty acids have been shown to occur primarily in the ER (1, 2). The mitochondrial chain elongation system is a reversal of the fatty acid ␤-oxidation system; thus, acetyl-CoA, instead of malonylCoA, is used for the condensation reaction, and the resulting ␤-keto acyl-CoA undergoes the same series of reactions as described above (3). The physiological function of the mitochondrial chain elongation system is not clear (4). Contradictory findings have been reported regarding the presence of another cellular fatty acid chain elongation system in mammalian peroxisomes. Nagi et al. (5) initially reported the absence of an elongation system in rat liver peroxisomes. However, Horie et al. (6) later provided good evidence for the presence of an active peroxisomal chain elongation system in ...

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“…However, the last reaction is catalyzed by the NADdependent enoyl-CoA reductase instead of the Co-Q dependent acetyl-Co-A dehydrogenase. In this way, the reaction is thermodynamically favored in the direction of chain elongation -which corresponds to fat synthesis [43]. Since fatty chain elongation consumes 2 moles of NADH in each cycle, this pathway provides a suitable mechanism to maintain the mitochondrial redox balance [23,24] (Figure 13).…”

Section: Figure 10mentioning

confidence: 99%

“…lipid synthesis) during anoxia/ischemia has been demonstrated in various organisms starting with invertebrate models and finding its way towards biomedicine [43,44]. But most important for cardiovascular diseases FA chain elongation has been observed in ischemic arterial tissue [35] and ischemic mammalian heart [45].…”

Section: Figure 10mentioning

confidence: 99%

The Discovery of Two Novel Biomarkers in a High-Fat Diet C56bl6 Obese Mouse Model for Non-Adipose Tissue: A Comprehensive LCMS Study at Hind Limb, Heart, Carcass Muscle, Liver, Brain, Blood Plasma and Food Composition Following a Lipidomics LCMS-Based Approach

Ginneken¹,

Verheij²,

Vries³

et al. 2016

Cell Mol Med

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Citation: Ginneken V, Verheij E, de Vries E, et al. The discovery of two novel biomarkers in a high-fat diet C56bl6 obese model for non-adipose tissue: A comprehensive lcms study at hind limb, heart, carcass muscle, liver, brain, blood plasma and food composition following a lipidomics lcms-based approach. Cell Mol Med 2016, 2:3. AbstractAim/Objective: This study was designed to find via a highfat (HF) diet induced insulin resistant (IR) and/or type-2 diabetes (T2DM) C57Bl/6 mouse model potential novel biomarkers. Major aiming is to find following this lipidomics based approach novel safe biomarkers applicable for humans with IR/T2DM that can be used in the assessment of diagnosis, intensive treatment, clinical use and new drug development. In addition, the biomarker has to be found in blood-plasma simultaneously while is not a component of the HF-diet. Methods:Reversed phase liquid chromatography coupled to mass spectrometry (LC-MS) were used to quantify and qualify the rearrangement and repartitioning of fat stores in the heart-, hind limb-, carcass-muscle, liver, brain, and blood plasma of this mice model following a systems biology lipidomics based approach.Results: Two potential biomarkers were found for this HFdiet mouse model. The first biomarker was a 20:3 cholesteryl-ester (20:3-ChE) which significantly increased (P ≤ 0.016) in the fatty heart with 1317% while it rose very significantly (P ≤ 0.00001) in blood plasma with 1013% in the HF diet group in comparison to the control-group. (Co).The second biomarker was a 36:1 phosphatidylcholine (36:1-PC), which rose significantly (P ≤ 0.025) mainly in heart muscle with 400% while concentrations increased significantly strongly (P ≤ 0.002) in blood plasma with 1493% in the high-fat diet vs. Co. As an earlier defined prerequisite, both compounds were not found in the food. Conclusion:The 20:3-ChE biomarker (dihomo-γ-linolenic; 20:3 n-6) has been classified as a potential type 2 diabetes biomarker (T2DM) biomarker in a human cohort of the uppsala longitudinal study of adult men (ULSAM). In addition, we give a biochemical explanation for the 36:1-PC as hypoxic biomarker for cardiovascular diseases (CVD) diagnosis and therapy. Both biomarkers are interesting candidates for further validation in human cohorts.

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Mechanisms and physiological roles of fatty acid chain elongation in microsomes and mitochondria

Cited by 104 publications

References 55 publications

Effects of various dietary n-3 / n-6 fatty acid ratios on the performance and body composition of broilers

Effects of various dietary n-3 / n-6 fatty acid ratios on the performance and body composition of broilers

Molecular Cloning and Expression of Mammalian Peroxisomaltrans-2-Enoyl-coenzyme A Reductase cDNAs

The Discovery of Two Novel Biomarkers in a High-Fat Diet C56bl6 Obese Mouse Model for Non-Adipose Tissue: A Comprehensive LCMS Study at Hind Limb, Heart, Carcass Muscle, Liver, Brain, Blood Plasma and Food Composition Following a Lipidomics LCMS-Based Approach

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