Analysis of the Acyl-CoAs That Accumulate during the Peroxisomal β-Oxidation of Arachidonic Acid and 6,9,12-Octadecatrienoic Acid

Chen, Qi; Luthria, Devanand L.; Sprecher, Howard

doi:10.1006/abbi.1997.0461

Cited by 14 publications

(6 citation statements)

References 38 publications

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“…The small fraction of radioactivity in the brain aqueous extract, approximately 10% of the total, is consistent with these reports and with results from the dietary injection of AA (Wijendran et al 2002) and cell culture experiments (Spector et al 1999). Within brain, AA can be b-oxidized in peroxisomes (Chen et al 1998), retro-converted to other fatty acids in peroxisomes and microsomes (Luthria et al 1997), elongated to adrenic acid (22 : 4n)6) in microsomes (Horrocks 1989), or b-oxidized to two-carbon fragments for the later synthesis of glucose, amino acids and saturated fatty acids (Rapoport et al 1997). That all fatty acid radioactivity in the brain lipid extract represented [1-14 C]AA (Fig.…”

Section: Discussionsupporting

confidence: 88%

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In vivoimaging detects a transient increase in brain arachidonic acid metabolism: a potential marker of neuroinflammation

Lee

Villacreses

Rapoport

et al. 2004

Journal of Neurochemistry

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In a rat model of neuroinflammation produced by an intracerebral ventricular infusion of bacterial lipopolysaccaride (LPS), we measured the coefficients of incorporation (k*) of arachidonic acid (AA, 20 : 4n)6) from plasma into each of 80 brain regions, using quantitative autoradiography and intravenously injected [1-14 C]AA. Compared with control rats infused with artificial cerebrospinal fluid (aCSF), k* was increased significantly in 25 brain areas, many of them close to the CSF compartments, following 6-days of LPS infusion. The increases, ranging from 31 to 76%, occurred in frontal, motor, somatosensory, and olfactory cortex, thalamus, hypothalamus, and septal nuclei, and basal ganglia. Following 28 days of LPS infusion, k* was increased significantly in only two brain regions. Direct analyses of microwaved brain showed that 93 ± 3 (SD) and 94 ± 4% of brain radioactivity was in the organic extract as radiolabeled AA in the 6-day control and LPS-infused animals, respectively, compared with 91 ± 3 and 87 ± 6% in the 28-day control and LPS-infused animals. These results confirm that brain AA metabolism is disturbed after 6 days of LPS exposure, show this increase is transient, and that these changes can be detected and localized using in vivo imaging with radiolabeled AA.

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Section: Discussionsupporting

confidence: 88%

“…1999). Within brain, AA can be β‐oxidized in peroxisomes (Chen et al . 1998), retro‐converted to other fatty acids in peroxisomes and microsomes (Luthria et al .…”

Section: Discussionmentioning

confidence: 99%

In vivoimaging detects a transient increase in brain arachidonic acid metabolism: a potential marker of neuroinflammation

Lee

Villacreses

Rapoport

et al. 2004

Journal of Neurochemistry

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“…Ech1 was significantly up regulated with FISH alone (1.1, 1.6*, 1.4), consistent with the need to isomerize numerous double bonds during β-oxidation. It is not clear why FUNG did not also up regulate transcripts, as LC-PUFA are generally reported to up regulate this isomerase [51]. The present data generally suggest LC-PUFA increased FA oxidation by down regulating Acly; and up regulating Cpt-1 and -2, Ech1 and Acadm.…”

Section: Resultscontrasting

confidence: 43%

Untitled

et al. 2002

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BackgroundThe functions, actions, and regulation of tissue metabolism affected by the consumption of long chain polyunsaturated fatty acids (LC-PUFA) from fish oil and other sources remain poorly understood; particularly how LC-PUFAs affect transcription of genes involved in regulating metabolism. In the present work, mice were fed diets containing fish oil rich in eicosapentaenoic acid and docosahexaenoic acid, fungal oil rich in arachidonic acid, or the combination of both. Liver and hippocampus tissue were then analyzed through a combined gene expression- and lipid- profiling strategy in order to annotate the molecular functions and targets of dietary LC-PUFA.ResultsUsing microarray technology, 329 and 356 dietary regulated transcripts were identified in the liver and hippocampus, respectively. All genes selected as differentially expressed were grouped by expression patterns through a combined k-means/hierarchical clustering approach, and annotated using gene ontology classifications. In the liver, groups of genes were linked to the transcription factors PPARα, HNFα, and SREBP-1; transcription factors known to control lipid metabolism. The pattern of differentially regulated genes, further supported with quantitative lipid profiling, suggested that the experimental diets increased hepatic β-oxidation and gluconeogenesis while decreasing fatty acid synthesis. Lastly, novel hippocampal gene changes were identified.ConclusionsExamining the broad transcriptional effects of LC-PUFAs confirmed previously identified PUFA-mediated gene expression changes and identified novel gene targets. Gene expression profiling displayed a complex and diverse gene pattern underlying the biological response to dietary LC-PUFAs. The results of the studied dietary changes highlighted broad-spectrum effects on the major eukaryotic lipid metabolism transcription factors. Further focused studies, stemming from such transcriptomic data, will need to dissect the transcription factor signaling pathways to fully explain how fish oils and arachidonic acid achieve their specific effects on health.

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“…As soon as [1-14C]labeled 4,7,10,13,16-22;5 and 4,7,10,13,16, t 9-22:6 are produced, their continued degradation requires both NADPH-dependent 2,4-dienoyl-CoA reductase and A3,A2-enoyl-CoA isomerase which is a component part of the peroxisomal trifunctional enzyme (20). In all of our studies, when an acid with its first double bond at position 4 is incubated with peroxisomes, or when an acid is produced with its first double bond at position 4, metabolites with their first two double bonds at the 2-trans-4-cis-positions always accumulate (8,9,21,22). These results suggest that the reaction catalyzed by the reductase is a control step in the peroxisomal degradation of unsaturated fatty acids.…”

Section: Peroxisomal Fatty Acid Metabolismmentioning

confidence: 50%

Regulation of the biosynthesis of 22:5n‐6 and 22:6n‐3: A complex intracellular process

Sprecher

Chen

Yin

1999

Lipids

Self Cite

121

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Both 22:4n-6 and 22:5n-3 are synthesized from n-6 and n-3 fatty acid precursors in the endoplasmic reticulum. The synthesis of both 22:5n-6 and 22:6n-3 requires that 22:4n-6 and 22:5n-3 are metabolized, respectively, to 24:5n-6 and 24:6n-3 in the endoplasmic reticulum. These two 24-carbon acids must then move to peroxisomes for partial degradation followed by the movement of 22:5n-6 and 22:6n-3 back to the endoplasmic reticulum for use as substrates in membrane lipid biosynthesis. Clearly an understanding of the control of intracellular fatty acid movement as well as of the reactions carried out by microsomes, peroxisomes, and mitochondria are all required in order to understand not only what regulates the biosynthesis of 22:5n-6 and 22:6n-3 but also why most tissue lipids selectively accumulate 22:6n-3.

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Analysis of the Acyl-CoAs That Accumulate during the Peroxisomal β-Oxidation of Arachidonic Acid and 6,9,12-Octadecatrienoic Acid

Cited by 14 publications

References 38 publications

In vivoimaging detects a transient increase in brain arachidonic acid metabolism: a potential marker of neuroinflammation

In vivoimaging detects a transient increase in brain arachidonic acid metabolism: a potential marker of neuroinflammation

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Regulation of the biosynthesis of 22:5n‐6 and 22:6n‐3: A complex intracellular process

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