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Dietary fish oil dose-response effects on ileal phospholipid fatty acids and contractility

We have reported that dietary fish oil (FO) leads to the incorporation of long‐chain n−3 PUFA into the gut tissue of small animal models, affecting contractility, particularly of rat ileum. This study examined the FO dose response for the incorporation of n−3 PUFA into ileal tissue and how this corr...

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Bibliographic Details
Published in:Lipids 2005-09, Vol.40 (9), p.925-929
Main Authors: Patten, G.S, Adams, M.J, Abeywardena, M.Y
Format: Article
Language:English
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Summary:We have reported that dietary fish oil (FO) leads to the incorporation of long‐chain n−3 PUFA into the gut tissue of small animal models, affecting contractility, particularly of rat ileum. This study examined the FO dose response for the incorporation of n−3 PUFA into ileal tissue and how this correlated with in vitro contractility. Groups of ten to twelve 13‐wk‐old Wistar‐Kyoto rats were fed 0, 1, 2.5, and 5% FO‐supplemented diets balanced with sunflower seed oil for 4 wk, after which ileal total phospholipid FA were determined and in vitro contractility assessed. For the total phospholipid fraction, increasing the dietary FO levels led to a significant increase first evident at 1% FO, with a stepwise, nonsaturating six‐fold increase in n−3 PUFA as EPA (20∶5n−3), DPA (docosapentaenoic acid, 22∶5n−3), and DHA, but mainly as DHA (22∶6n−3), replacing the n−6 PUFA linoleic acid (18∶2n−6) and arachidonic acid (20∶4n−6) over the dosage range. There was no difference in KCl‐induced depolarization‐driven contractility. However, a significant increase in receptor‐dependent maximal contractility occurred at 1% FO for carbachol and at 2.5% FO for prostaglandin E2, with a concomitant increase in sensitivity for prostaglandin E2 at 2.5 and 5% FO. These results demonstrate that significant increases in ileal membrane n−3 PUFA occurred at relatively low doses of dietary FO, with differential receptor‐dependent increases in contractility observed for muscarinic and prostanoid agonists.
ISSN:0024-4201
1558-9307
DOI:10.1007/s11745-005-1453-6