Dihomo-γ-linolenic acid

Dihomo-γ-Linolenic Acid

Fig. 1 – Dihomo-γ-Linolenic Acid

Molecular weight: 306.48276 [g/mol]

Molecular formula: C20H34O2

IUPAC name: (8Z,11Z,14Z)-icosa-8,11,14-trienoic acid

CAS registry number: 1783-84-2

PubChem: 5280581

Some synonyms:

  • DGLA
  • bishomo-γ-linolenic acid
  • 8,11,14-eicosatrienoic acid
  • 8,11,14-all-cis-eicosatrienoic acid
  • cis-8,11,14-eicosatrienoic acid
  • 20:3n-6

Dihomo-γ-linolenic acid (18 carbon atoms) is a polyunsaturated fatty acid (PUFA) with three cis double bounds (the first one from the methyl end is in n-6 or omega-6 (ω-6) so in shorthand 20:3n-6) member of sub-group called very long chain fatty acids (from 20 carbon atoms onwards).
It is produced from γ-linolenic acid in an elongation reaction catalyzed by an elongase (it catalyzes the addition of two carbon atoms from glucose metabolism to lengthen the fatty acid chain); it may be further desaturated in very limited amount to the essential fatty acid arachidonic acid, in a reaction catalyzed by the rate limiting Δ5-desaturase.
Dihomo-γ-linolenic acid is a minor component of animal phospholipids but, depending on the cell type, is the precursor of prostaglandin of 1-series (PGE1), in a reaction catalyzed by ciclooxygenase 1 (COX-1), and/or is metabolized by the 15-lipoxygenase (15-LOX) into 15-(S)-hydroxy-8,11,13-eicosatrienoic acid (15-HETrE) (in several cell types, including neutrophils, macrophage/monocytes and epidermal cells).

PGEis associated with:

  • retarding platelet aggregation and so, in turn, inhibition of thrombus formation;
  • lowering blood pressure;
  • inhibition of cancer cell growth;
  • in vitro inhibition of vascular smooth muscle cell proliferation, a hallmark of the atherogenic process, because associated with atherosclerotic plaque development.

15-HETrE is capable of:

  • suppress inflammation also by inhibiting the formation of proinflammatory arachidonic acid-derived 5-lipoxygenase metabolites, e.g., LTC4 and LTB4;
  • suppres cell growth, particularly epithelial cells.

Furthermore, clinical efficacy of dihomo-γ-linolenic acid is due to the fact that it can’t be converted to leukotrienes, competing with arachidonic acid for COX-1, can suppress the formation of PGE2 and finally is modestly metabolized into arachidonic acid, thus limiting further the formation of PGE2.
On the other hand dihomo-γ-linolenic acid appear to be related to the risk of development diabetes because of the composition of cholesterol ester: the risk increases when esters are rich in saturated fatty acidspalmitoleic acidγ-linolenic acid and dihomo-γ-linolenic acid and low in linoleic acid.


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