No abstract

The results of early enteral feeding with FOSL-HN after surgery in this follow-up study provide further support to claims of safety, tolerance, and improved physiologic function. There was an associated reduction in eicosanoid production from PBMCs, which is presumed to be the principal mechanism for these effects.

Background: Sesamin, a nonfat constituent of sesame oil, inhibits ⌬ 5 -desaturase activity, resulting in accumulation of dihomo-␥-linolenic acid (DGLA), which displaces arachidonic acid (AA) and consequently decreases the formation of proinflammatory 2-series prostaglandins. Objective: We sought to determine whether dietary supplementation with sesamin augments the antiinflammatory effects of dietary linseed oil in rats. Design: We investigated the effects of continuous tube feedings of emulsions containing safflower oil or linseed oil with sesamin (SO+ and LO+) or without sesamin (SO and LO) on liver fatty acid composition and on endotoxin-induced production of prostaglandin E 2 , 6-keto-prostaglandin F 1␣ , and tumor necrosis factor ␣ (TNF-␣) by whole blood from rats (n = 6 per diet group). Results: We found a significant accumulation of DGLA only in the liver phospholipids of animals fed SO+ and LO+ (1.8 ± 0.2 and 1.4 ± 0.3 mol%, respectively), which suggests that sesamin inhibited ⌬ 5 -desaturation of nϪ6 fatty acids. These changes were associated with significant reductions in plasma prostaglandin E 2 concentrations in animals fed SO+ compared with those fed SO (P < 0.05). Despite a significant reduction in tissue AA content in the LO group, the prostaglandin E 2 concentrations did not differ significantly from those of the SO group. Plasma concentrations of TNF-␣ were significantly lower (P < 0.05) in the animals fed LO+ than in those fed SO (199 ± 48 and 488 ± 121 ng/L, respectively). Conclusion: These data indicate that in rats, tube feedings of diets containing sesamin exerted antiinflammatory effects that were augmented by concurrent consumption of linseed oil. Am J Clin Nutr 2000;72:804-8.

Sesamin, present in sesame seed oil (SSO), can inhibit Δ-5-desaturase activity and cause accumulation of dihomo-γ-linolenic acid (DGLA), which displaces arachidonic acid, and subsequently decrease production of dienoic eicosanoids. The effects of diets containing both SSO and Quil A, a saponin that emulsifies fats and potentiates the immune responses, were also studied. A mixture of oils having a fatty-acid composition similar to that of SSO served as a control diet. The levels of docosapentaenoic acid in mice fed Quil-A-supplemented diets and of DGLA in those fed SSO diets were markedly higher in the liver. These changes were associated with a significant reduction in the plasma prostaglandin-E₁₊₂ and thromboxane-B₂ levels in response to an intraperitoneal injection of a lethal dose of lipopolysaccharide (LPS) endotoxin (LD₅₀ 20 mg/kg). The levels of interleukin (IL-)6 were elevated and those of IL-1β were decreased in mice consuming Quil-A-supplemented diets. The 1L-10 levels that were elevated in all mice after LPS exposure, remained higher (even at 9 h) only in those fed Quil-A-supplemented diets, but declined rapidly in others. During a 48-hour observation period following LPS injection, all control animals died, and survival was 40% in the SSO group, and 27 and 50%, respectively, in those fed Quil-A-supplemented control and SSO diets. These data suggest that SSO and Quil A when present in the diet exerted cumulative effects that resulted in a decrease in the levels of dienoic eicosanoids with a reduction in IL-1β and a concomitant elevation in the levels of IL-10 that were associated with a marked increase in survival in mice.