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Zhou, Dequan (2007) The effect of dietary Vitamin A on rat liver and colon membrane Omega 6 and Omega 3 polyunsaturated fatty acids which has implications for colonic inflammation. Doctoral thesis, London Metropolitian University.
Vitamin A regulates activation of enzymes for in vivo metabolism of linoleic and alpha-linolenic (ALA) acids. This nutrient also influences the release of precursor fatty acids of eicosanoids from membranes. Current evidence indicates that inflammation enhances eicosanoid production. The aim of this thesis study is to elucidate the effects of dietary vitamin A on ro6 and ro3 PUFA composition in rat liver and colon membrane phospholipids which has an implication for colonic inflammation. Our studies observed that vitamin A deficiency enhanced docosapentaenoic (DPAro6) and reduced docosahexaenoic (DHA) in colon and liver phosphatidylcholine (PC) and phosphatidylethanolamine (PE) of the ALA deficient rats (P<0.0005). However, it increased both fatty acids in the liver PC and PE of the ALA sufficient rats (P<0.05). Supplementation of vitamin A reduced di-homo gamma linolenic (DHGLA) and eicosapentaenoic (EPA) in both liver phospholipids of the ALA sufficient rats (P<0.05). Colonic inflammation increased arachidonic acid (AA) and DHA in the PC and reduced EPA in the PE in colon of the vitamin A sufficient rats. However, it did not alter AA, DHGLA, EPA and DHA levels in both phospholipids in deficient rats (P>0.05). In conclusion, vitamin A deficiency consistently increases rat liver membrane DPAro6. However, it enhances liver DHA when ALA is adequate but reduces liver DHA when ALA is limited. This suggests that the two fatty acids are synthesised by different pathways. In contrast, supplementation of vitamin A did not enhance the proportions of DHA and DPAro6 in rat liver and colon membrane phospholipids . The finding implies that its metabolite (9-cis retinoic acid) might not involve the activation of fatty acid peroxisomal p-oxidation for DHA synthesis. The enhanced AA and DHA and reduced EPA in the outer leaflet of the target tissue suggests that the target tissue may modulate inflammatory reactions by regulating the level of precursor fatty acids of anti-inflammatory eicosanoids and incorporate main structural fatty acids dor its membrane repair.
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