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PGEI, a potent stimulator young fat girls of adenylate cyclase. inhibits young fat girls phospholipase activity in human platelets [59]. Impairment of PGE production may allow increased phospholipase activity and increased synthesis of proinflammatory young fat girls PGs and Us. Analogous situations exist in cystic fibrosis (60] and Crohn disease [61], in which increased 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 would produce a distortion of PG/ LT synthesis rather than 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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