RAPID MODULATION OF LUNG AND LIVER MACROPHAGE PHOSPHOLIPID FATTY-ACIDS IN ENDOTOXEMIC RATS BY CONTINUOUS ENTERAL FEEDING WITH N-3 AND GAMMA-LINOLENIC FATTY-ACIDS

Dienoic eicosanoids derived from phospholipid arachidonic acid (AA) in lung and liver macrophages promote leukosequestration, thrombosis, an d tissue injury. Current enteral diets (diet A) are enriched with lino leic acid (LA), a precursor of AA. Novel diets low in LA and containin g eicosapentaenoic acid (EPA) and gamma-linolenic acid (GLA) foster fo rmation of less inflammatory eicosanoids. The study objective was to a ssess the rapidity and extent of LA and AA displacement in vivo from a lveolar macrophage (AM phi), lung, and liver Kupffer and endothelial ( KE) cell phospholipids in rats fed enterally with diets enriched with 5.3% (by wt) EPA and either 1.2% or 4.6% GLA (diets B and C, respectiv ely). After surgical placement of catheters, the rats were fed enteral ly and co-infused intravenously with either endotoxin or vehicle conti nuously for 3 or 6 d. Rats given either diet B or C had significantly lower (P < 0.01) relative percentages of AA and LA within the AM phi, lung, and KE cell phospholipids, and concomitantly higher percentages of EPA compared with rats infused with diet A after 3 d of enteral fee ding irrespective of endotoxin co-infusion. Incorporation of dihomo-ga mma-linolenic acid (DHGLA), the metabolite of GLA, into lung and KE ph ospholipids was significant in rats given diet C. Most of the changes in fatty acid composition occurred by day 3. The polyunsaturated fatty acid composition of AM phi, lung, and KE cell phospholipids can be ra pidly modified by continuous short-term enteral feeding with EPA- and GLA-enriched diets irrespective of concurrent endotoxemia.