The effect of dihomogammalinolenic acid on platelet aggregation and prostaglandin release, erythrocyte membrane fatty acids and serum lipids: Evidence for defects in PGE₁ synthesis and Δ⁵-desaturase activity in insulin-dependent diabetics

The effect of dihomogammalinolenic acid (DHLA) administration on platelet aggregation and prostaglandin production, erythrocyte fatty acid composition and serum lipids was compared in healthy subjects and insulin-dependent diabetics (IDDs). In healthy subjects, DHLA caused a significant inhibition of ADP-induced platelet aggregation and an increase in platelet PGE₁ release; IDDs did not show these changes. There were no differences, however, in platelet thromboxane A₂ (TXA₂) or PGE₂ release between healthy subjects and IDDs before and after DHLA. Following DHLA, the arachidonic acid content of erythrocytes increased in healthy subjects; this increase was not observed in IDDs. DHLA induced a significant fall in serum non-esterified fatty acid concentrations in both groups without altering either cholesterol or triglyceride concentrations. These data show for the first time that (a) IDD platelets may have a specific defect of PGE₁ synthesis quite distinct from the Δ⁵- and Δ⁶-desaturase defects known to be associated with experimental diabetes; this defect may contribute to platelet hyper-aggregability in diabetes; and (b) DHLA has a potent antilipolytic effect in vivo; and (c) erythrocytes from IDDs may have a Δ⁶-desaturase defect.