DIETARY SUPPLEMENTATION WITH GAMMA-LINOLENIC ACID ALTERS FATTY-ACID CONTENT AND EICOSANOID PRODUCTION IN HEALTHY HUMANS

To understand the in vivo metabolism of dietary gamma-linolenic acid ( GLA), we supplemented the diets of 29 volunteers with GLA in doses of 1.5-6.0 g/d. Twenty-four subjects ate controlled eucaloric diets consi sting of 25% fat; the remaining subjects maintained their typical West ern diets. GLA and dihomo-gamma-linolenic acid (DGLA) increased in ser um lipids of subjects supplemented with 3.0 and 6.0 g/d; serum arachid onic acid increased in all subjects. GLA supplementation with 3.0 and 6.0 g/d also resulted in an enrichment of DGLA in neutrophil phospholi pids but no change in GLA or AA levels, Before supplementation, DGLA w as associated primarily with phosphatidylethanolamine (PE) of neutroph il glycerolipids, and DGLA increased significantly in PE and neutral l ipids after GLA supplementation. Extending the supplementation to 12 w k did not consistently change the magnitude of increase in either seru m or neutrophil lipids in subjects receiving 3.0 g/d. After GLA supple mentation, A23187-stimulated neutrophils released significantly more D GLA, but AA release did not change. Neutrophils obtained from subjects after 3 wk of supplementation with 3.0 g/d GLA synthesized less leuko triene B-4 (P < 0.05) and platelet-activating factor. Together, these data reveal that DGLA, the elongase product of GLA, but not AA accumul ates in neutrophil glycerolipids after GLA supplementation. The increa se in DGLA relative to AA within inflammatory cells such as the neutro phil may attenuate the biosynthesis of AA metabolites and may represen t a mechanism by which dietary GLA exerts an anti-inflammatory effect.