Dihomo-gamma-linolenic acid (DGLA) is a 20-carbon omega-6 with 3 double bonds (20:3n6) derived from the essential linolenic acid. LA is metabolized to GLA, which is rapidly elongated to DGLA. There are only trace amounts of DGLA found in organ meats, otherwise it must be synthesized from GLA. The inability to convert precursor fatty acids to DGLA is associated with various pathologic and physiologic conditions such as aging, diabetes, alcoholism, atopic dermatitis, rheumatoid arthritis, cancer, and cardiovascular disease.
DGLA is a precursor to prostaglandin PGE1, which inhibits platelet aggregation and inflammation, produces vasodilation, inhibits cholesterol biosynthesis and thrombus formation, regulates immune responses and reduces blood pressure. It is also involved in inhibiting the formation of pro-inflammatory compounds from AA. PGE1 can also inhibit growth and differentiation of cancer cells. Although the mechanism of DGLA in cancer has not yet been identified, the potential benefits are being studied. DGLA-enriched oils and fermented DGLA oil supplements are being developed with excellent safety profiles and studied in a variety of clinical conditions.
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Decreased intake of the essential LA, or inefficient metabolism of the omega-6 fatty acids can lead to decreased production of DGLA. Lack of vitamin or mineral cofactors, or SNPs in the elongase and desaturase enzymes can contribute to lower DGLA levels either from production to DGLA or increased metabolism to AA.
It should also be emphasized that smoking, alcohol, and systemic inflammation can slow the elongase enzyme and conversion to DGLA. Due to the anti-inflammatory and beneficial effects of DGLA, low levels have significant clinical associations such as diabetes, alcoholism, atopic dermatitis, rheumatoid arthritis, cancer, and cardiovascular disease. Decreased levels are associated with increased total mortality in patients with acute cardiac events and decompensated heart failure.
Supplementation with DGLA or GLA, as well as high dietary intake of the essential LA, can lead to higher DGLA levels.
Lack of vitamin and mineral cofactors, or SNPs in the enzyme which converts DGLA downstream to arachidonic acid, may also contribute to elevations.
Higher DGLA levels are mainly beneficial due to its anti-inflammatory role. Although there is some concern regarding DGLA being converted to its pro-inflammatory metabolite, arachidonic acid, the conversion is generally limited. The reason for this limitation is that inflammatory arachidonic acid-derived lipid mediators (eicosanoids) are made via several pathways two of which are cyclooxygenase (COX) and lipoxygenase (LOX).
The synthesis of AA eicosanoids is dependent on DGLA since DGLA competes with AA for COX and LOX. When DGLA is in excess, it inhibits the synthesis of AA-derived eicosanoids due to its higher affinity for the COX and LOX enzymes.
High levels of DGLA are associated with elevated body mass index, waist circumference, body fat percentage, and other obesity-related parameters. It should be noted that some of these clinical associations are related to increased overall intake of omega-6 fatty acids. But insulin itself can downregulate the enzyme delta-5-desaturase which synthesizes AA from DGLA. Therefore, obesity and insulin resistance can affect delta-5-desaturase resulting in higher DGLA levels.
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