Journal
JOURNAL OF NUTRITION
Volume 141, Issue 4, Pages 548-553Publisher
AMER SOC NUTRITION-ASN
DOI: 10.3945/jn.110.127118
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Funding
- USDA Coperative State Research, Education, and Extension Service-National Research Initiative [2005-00827]
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Because dietary arachicdonate (ARA) and its ecosanod derivatives are major regulators of intestinal homeostasis and repair following injury, we evaluated the effects of dietary ARA on desaturation and elongation of C-13-18:2(n-6) and mRNA abundance of Delta 6-desaturase (Gamma ADS2), elongase (ELOVL5), and Delta-5-desaturase (FADS1) in liver and intestine. Day-old pigs (n = 96) were fed milk based formula contain ng 0, 0.5, 2.5, or 5% ABA or 5% eicosapentaenoic acid of total fatty acids for 4, 8, and 16 d. In river, the desaturation rate [nmol/(g tissue.h)]o.C-13-18:2(n-6) to C-13-18:3(n-6) decreased 56% between 4 and 16 d but was not affected by diet. Whereas accumulation in C-13-20:3(n-6) also decreased with age by 67%, at increased linearly with increasing dietary ARA (P < 0.06). In comparison, artestinal flux was similar to 50% less than liver flux and was unaffected by age, but desaturation to C-13-18:3(n-6) increased linearly (by 57%) in pigs fed ABA diets (P < 0.001), equaling the rate observed in sow-fed controls. In both river are intestine, alternate elongation to C-13-20:2(n-6) (via Delta-8-desaturase) was markedly elevated in pigs fed the 0% ARA diet compared with all other dietary treatments (P < 0.01). transcript abundance of FADS2, ELOVL5, and FADS1 was rot affected in liver by diet (P > 0.05) but decreased precipitously between birth and d 4 (similar to 70%; P < 0.05). In contrast intestinal abundance of FADS2 and FADS1 increased 60% from d 4 to 16. In conclusion, dietary ARA regulated the desaturase-elongase pathway in a tissue-specific manner. In liver, ARA had modest effects on (n-6) fatty ace box, and intestinal FADS2 activity and mRNA increased. Additionally, hepatic flux decreased with postnatal age, whereas intestinal flux did not change. J. Nutr. 141. 548-553, 2011.
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