The
eicosanoid metabolites of DGLA are: • Series-1
thromboxanes (thromboxanes with 1 double-bond), via the
COX-1 and COX-2 pathways. • Series-1
prostanoids, via the COX-1 and COX-2 pathways. • A 15-hydroxyl derivative that blocks the transformation of
arachidonic acid to
leukotrienes. All of these effects are anti-inflammatory. This is in marked contrast with the analogous metabolites of
arachidonic acid (AA), which are the series-2 thromboxanes and prostanoids and the series-4 leukotrienes. In addition to yielding anti-inflammatory eicosanoids, DGLA
competes with AA for COX and lipoxygenase, inhibiting the production of AA's eicosanoids. However, DGLA is converted to AA by
Δ5 desaturase (
FADS1).
FADS1 and
ELOVL5 are differently expressed among tissues and cell types. For example, human neutrophils contain
ELOVL5 but not
FADS1. is a rich source of γ-linolenic acid (GLA)—the dietary precursor to DGLA. Supplementing dietary GLA increases serum DGLA as well as serum AA levels. Cosupplementation of GLA and
EPA (20:5 n−3) increases serum DGLA while also decreasing increasing AA levels by blocking Δ5-desaturase activity. Leukotriene synthesis in neutrophils is consequently lowered. Cosupplementation of GLA with botanical n-3 fatty acids also result in improved conversion from GLA to DGLA and reduced conversion from DGLA to AA. == See also ==