Metabolism of dietary α‐linolenic acid vs. eicosapentaenoic acid in rat immune cell phospholipids during endotoxemia

Abstract

Short-term (i.e., 3 d) continuous enteral feeding of diets containing eicosapentaenoic (EPA) and gamma-linolenic (GLA) polyunsaturated fatty acids (PUFA) to endotoxemic rats reduces the levels of arachidonic acid (AA) and linoleic acid (LA) in alveolar macrophage (AM) and liver Kupffer and endothelial (K&E) cell phospholipids with attendant decreases in prostaglandin formation by these cells in vitro. Diets that contain alpha-linolenic acid (LNA) as a substrate for endogenous formation of EPA may not be as effective in facilitating these immune cell modifications given the limited activity of delta6 desaturase. In the present study we compared the effectiveness of an LNA-enriched diet vs. an (EPA + GLA)-enriched diet to displace phospholipid AA from AM and liver K&E cells in vivo in endotoxemic rats fed enterally for 3 or 6 d. We determined the fatty acid composition of AM and K&E cell phospholipids by gas chromatography. We found that AM and K&E cells from rats that had received the EPA + GLA diet for 3 d had significantly (P < 0.001) higher mole percentage of EPA and the GLA metabolite, dihomoGLA, than corresponding cells from rats given the LNA diet or a control diet enriched with LA. Rats given the LNA diet had relatively low levels of stearidonic acid, EPA and other n-3 PUFA, while rats given the LA diet had low levels of GLA and dihomoGLA. We conclude that diets enriched with LNA or LA may not be as effective as those enriched with EPA + GLA for purposes of fostering incorporation of EPA or dihomoGLA into and displacement of AA from macrophage phospholipids under pathophysiologic conditions commonly found in acutely septic patients.

Comparison of growth and fatty acid metabolism in rats fed diets containing equal levels of γ‐linolenic acid from high γ‐linolenic acid canola oil or borage oil

“…Descriptive and inferential statistics were computed on all continuous data for each parameter. The sample size was based primarily on the historical adequacy in similar studies using this model (12,13). Group differences were determined by t test and repeated measures of analysis of variance (ANOVA) across time points.…”

Dietary 18:3ω3 influences immune function and the tissue fatty acid response to antigens and adjuvant

“…Therefore, 18:33 may in fact have different immunomodulatory properties then 20:53 and 22:63. A few reports that have directly compared 18:33 to fish oils (rich in 20:53 and 22:63) have found that they share some but not all immunomodulatory properties [9][10][11][12]. Interestingly, studies showing that 18:33 does not modulate immune function have been carried out in healthy (immunocompetent) subjects [10,12].…”

The Acute Respiratory Distress Syndrome: Role of Nutritional Modulation of Inflammation Through Dietary Lipids

“…It is important that immune formulas be initiated in a timely fashion because the physiologic effects of fish-oil supplementation on the inflammatory cell membrane may take several days to become apparent. 28 The clinician should not wait until ARDS is fully manifest before starting immunonutrition. These formulas should be started at the first signs of ALI, with aggressive advancement of infusion rate to target caloric goal.…”

“…Data shown as mean Ϯ SD; n ϭ 6 to 8/group. * p Ͻ .05 relative to LA and ALA (data from Palombo et al28 ). ALA, ␣-linolenic acid; EPA ϩ GLA, eicosapentaenoic acid plus ␥-linolenic acid; LA, linoleic acid; DGLA, dihomo-g-linolenic acid; AA, arachidonic acid.…”

“…33 GLA can also be formed from LA, although as mentioned above, this pathway is inhibited during critical illness. 28 GLA is elongated in the liver to DGLA that in turn is metabolized by 1 of 3 pathways: (1) by COX to prostaglandin E 1 (PGE 1 ); (2) by 15-LO to 15-hydroxyeicosatrienoic acid (15-HETrE); and (3) by ⌬-5 desaturase to AA 34 (Fig. 6).…”