Vitamin A deficiency reduces liver and colon docosahexaenoic acid levels in rats fed high linoleic and low alpha-linolenic acid diet

Zhou, Dequan; Zaiger, G.; Ghebremeskel, Kebreab; Crawford, Michael; Reifen, Ram

doi:10.1016/j.plefa.2004.07.005

Cited by 13 publications

(10 citation statements)

References 38 publications

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“…In Zellweger’s, ALD, and Acox ko, 22:6n-3 drops while 22:5n-6 rises; however, in vitamin A deficient mice, the opposite is found: 22:6n-3 rises and 22:5n-6 drops. The latter paper (Zhou et al, 2004) specifically suggests, as we have (Infante et al, 2002), that common enzyme pathways for 22:6n-3 and 22:5n-6 cannot explain these results. Plausible hypotheses are that isoforms based on FADS AT exist that operate with high selectivity on specific PUFA and are differently regulated, and/or that the unknown function(s) of FADS3 are PUFA-specific.…”

Section: Resultsmentioning

confidence: 61%

“…However, alternative hypotheses involving n-3 or n-6 specific desaturases have been proposed from time to time which suggest that the competition may, at least in part, be “apparent”. A compelling example is the reciprocal changes in concentration of 22:6n-3 and 22:5n-6 that are found associated with specific metabolic conditions, for instance in tissues of Zellweger’s syndrome (Martinez, 1992) or adrenoleukodystrophy (ALD) patients(Martinez, 1990), acyl CoA knockout (Acox ko) mice (Infante et al, 2002), and in vitamin A deficient mice (Zhou et al, 2004). In Zellweger’s, ALD, and Acox ko, 22:6n-3 drops while 22:5n-6 rises; however, in vitamin A deficient mice, the opposite is found: 22:6n-3 rises and 22:5n-6 drops.…”

Section: Resultsmentioning

confidence: 99%

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Novel fatty acid desaturase 3 (FADS3) transcripts generated by alternative splicing

Park

Kothapalli

Reardon

et al. 2009

Gene

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Fatty acid desaturase 1 and 2 (FADS1 and FADS2) code for the key desaturase enzymes involved in the biosynthesis of long chain polyunsaturated fatty acids in mammals. FADS3 shares close sequence homology to FADS1 and FADS2 but the function of its gene product remains unknown. Alternative transcripts (AT) generated by alternative splicing (AS) are increasingly recognized as an important mechanism enabling a single gene to code for multiple gene products. We report the first AT of a FADS gene, FADS3, generated by AS. Aided by ORF Finder, we identified putative coding regions of eight AT for FADS3 with 1.34 kb (classical splicing), 1.14 (AT1), 0.77 (AT2), 1.25 (AT3), 0.51 (AT4), 0.74 (AT6), and 1.11 (AT7). In addition we identified a 0.51 kb length transcript (AT5) that has a termination codon within intron 8-9. The expression of each AT was analyzed in baboon neonate tissues and in differentiated and undifferentiated human SK-N-SH neuroblastoma cells. FADS3 AT are expressed in 12 neonate baboon tissues and showed reciprocal increases and decreases in expression changes in response to human neuronal cell differentiation. FADS3 AT, conserved in primates and under metabolic control in human cells, are a putative mediator of LCPUFA biosynthesis and/or regulation.

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Section: Resultsmentioning

confidence: 61%

Section: Resultsmentioning

confidence: 99%

Novel fatty acid desaturase 3 (FADS3) transcripts generated by alternative splicing

Park

Kothapalli

Reardon

et al. 2009

Gene

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“…The rats were randomly assigned to 8 groups (n=8); 2 groups (DSS and TNBS colitic groups) were fed the CO, FO, SO and SO&A diets each. Three weeks after the beginning of the experiment, the rats colitis was induced as described previously [23], by replacing their normal drinking water with water containing 5% DSS (wt/v, prepared daily, mol wt 36,000-50,000, MP Biomedicals, USA) for 7 days or by A C C E P T E D M A N U S C R I P T…”

Section: Accepted Manuscriptmentioning

confidence: 99%

α-Linolenic acid (ALA) is an anti-inflammatory agent in inflammatory bowel disease

Reifen

Karlinsky

Stark

et al. 2015

The Journal of Nutritional Biochemistry

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“…Previously (16), we showed that vitamin A deficiency enhances OA and reduces DHA levels in liver and colon choline (CPG) and ethanolamine (EPG) phosphoglycerides in rats fed a diet deficient in n-3 and sufficient in n-6 FA. The finding was rather intriguing since vitamin A deficiency would have been expected to reduce the levels of both DHA and OA owing to a reduction of activation of RXR and consequently impaired peroxisomal proliferation.…”

mentioning

confidence: 99%

Vitamin A deficiency enhances docosahexaenoic and Osbond acids in liver of rats fed an α‐linoleic acid‐adequate diet

Zhou

Ghebremeskel

Crawford

et al. 2006

Lipids

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The synthesis of docosahexaenoic (DHA, 22:6n-3) and Osbond acid (OA, 22:5n-6) is regulated by the heterodimer of peroxisome proliferator-activated receptor and retinoid X receptor (RXR). 9-Cis retinoic acid, a metabolite of vitamin A, is the most potent ligand of RXR. We tested whether vitamin A deficiency impairs DHA and OA synthesis in rats fed a vitamin A- and alpha-linolenic acid (ALA)-sufficient (VASALAS), vitamin A-sufficient and ALA-deficient (VASALAD), vitamin A-deficient and ALA-sufficient (VADALAS), or vitamin A- and ALA-deficient (VADALAD) diet. After 7 wk of feeding, liver and colon choline (CPG) and ethanolamine (EPG) phosphoglyceride FA were analyzed. The VADALAS compared with the VASALAS rats had elevated levels of both DHA (P< 0.05) and OA (P < 0.005) in liver CPG and EPG. In contrast, the VADALAD group had a lower DHA (P < 0.01) and higher OA (P < 0.005) level in CPG and EPG of both tissues than their VASALAD counterparts. ALA deficiency reduced DHA and enhariced OA levels in liver and colon CPG and EPG in both the vitamin A-sufficient (VASALAS vs. VASALAD) and -deficient (VADALAS vs. VADALAD) rats (P < 0.005). The study demonstrates that ALA deficiency reduced DHA and enhanced OA levels in tissue membranes, and dietary vitamin A deficiency has a profound effect on membrane DHA and OA in rat tissues. Both vitamin A and DHA are involved in a myriad of vital physiological functions pertaining to growth and development and health. Hence, there is a need for a further study to unravel the mechanism by which vitamin A influences membrane DHA and OA.

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Vitamin A deficiency reduces liver and colon docosahexaenoic acid levels in rats fed high linoleic and low alpha-linolenic acid diet

Cited by 13 publications

References 38 publications

Novel fatty acid desaturase 3 (FADS3) transcripts generated by alternative splicing

Novel fatty acid desaturase 3 (FADS3) transcripts generated by alternative splicing

α-Linolenic acid (ALA) is an anti-inflammatory agent in inflammatory bowel disease

Vitamin A deficiency enhances docosahexaenoic and Osbond acids in liver of rats fed an α‐linoleic acid‐adequate diet

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