Dietary Arachidonate Differentially Alters Desaturase-Elongase Pathway Flux and Gene Expression in Liver and Intestine of Suckling Pigs1,21,2

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Abstract

Because dietary arachidonate (ARA) and its eicosanoid derivatives are major regulators of intestinal homeostasis and repair following injury, we evaluated the effects of dietary ARA on desaturation and elongation of 13 C-18:2(n–6) and mRNA abundance of Δ-6-desaturase ( FADS2 ), elongase ( ELOVL5 ), and Δ-5-desaturase ( FADS1 ) in liver and intestine. Day-old pigs ( n = 96) were fed milk-based formula containing 0, 0.5, 2.5, or 5% ARA or 5% eicosapentaenoic acid of total fatty acids for 4, 8, and 16 d. In liver, the desaturation rate [nmol/(g tissue·h)] of 13 C-18:2(n–6) to 13 C-18:3(n–6) decreased 56% between 4 and 16 d but was not affected by diet. Whereas accumulation in 13 C-20:3(n–6) also decreased with age by 67%, it increased linearly with increasing dietary ARA ( P < 0.06). In comparison, intestinal flux was ~50% less than liver flux and was unaffected by age, but desaturation to 13 C-18:3(n–6) increased linearly (by 57%) in pigs fed ARA diets ( P < 0.001), equaling the rate observed in sow-fed controls. In both liver and intestine, alternate elongation to 13 C-20:2(n–6) (via Δ-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 not affected in liver by diet ( P > 0.05) but decreased precipitously between birth and d 4 (~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 acid flux, and intestinal FADS2 activity and mRNA increased. Additionally, hepatic flux decreased with postnatal age, whereas intestinal flux did not change.

Abbreviations used:

ARA
arachidonate
EPA
eicosapentaenoic acid
EFA
essential fatty acid
RER
relative expression ratio
SRC
sow-reared control

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1

Supported by USDA Cooperative State Research, Education, and Extension Service-National Research Initiative grant 2005–00827.

2

Author disclosures: S. K. Jacobi, X. Lin, B. A. Corl, H. A. Hess, R. J. Harrell, and J. Odle, no conflicts of interest.

3

Present address: Virginia Polytechnic Institute, Department of Dairy Science, 2020 Litton-Reaves Hall, Blacksburg, VA 24061-0315; E-mail:[email protected]