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These enzymes are activated by calcium and inhibited by cyclic AMP [58]. PGEI, a potent stimulator of adenylate cyclase. inhibits phospholipase activity in human platelets [59]. Impairment of PGE production may allow increased phospholipase activity and increased synthesis of proinflammatory PGs and Us. Analogous situations exist in cystic fibrosis (60] and Crohn disease [61], in which increased omega nutrition PG production accompanies decreased EFA levels. In fact, administering LA to patients with cystic fibrosis results in a decrease in the formation of PGF2. [60]. Thus impaired EFA metabolism in allergic individuals omega nutrition would produce a distortion of PG/ LT synthesis rather than omega nutrition a global decrease. Moreover, an increase in membrane viscosity might operate to activate phospholipase or impair adenylate cyclase. This concept is represented in Figure 2b. The enzymes that metabolize LA also desaturate and elongate LNA [36]. While the enzymes of PUFA synthesis generally show a higher affinity for n3 EFAs, the n3 EFAs form a tiny fraction of total fatty acids.
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