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American Journal of Clinical Nutrition, Vol 46, 570-576, Copyright © 1987 by The American Society for Clinical Nutrition, Inc
ORIGINAL RESEARCH COMMUNICATIONS |
KS Bjerve, S Fischer and K Alme
Department of Clinical Chemistry, University Hospital, Trondheim, Norway.
Treatment of human alpha-linolenic acid deficiency (ALAD) with ethyl linolenate is reported. The patient's scaly dermatitis nearly disappeared after 5-d supplementation with 0.1 mL ethyl linolenate. Pretreatment content of various n-3 fatty acids in RBC was 0-15% of healthy controls. After 14 d of supplementation, cholesterol and triglycerides were reduced by 70% of pretreatment values, 22:5n-3 and 22:6n-3 increased three- to fourfold while 18:3n-3 and 20:5n-3 remained low, indicating a rapid elongation and desaturation of 18:3n-3 in ALAD. Urinary excretion of PGI2-M was approximately 10 times higher than in healthy control subjects, while PGI3-M excretion was low. Linolenate supplementation increased PGI2-M excretion twofold, while PGI3-M remained near detection limit. Platelet capacity to synthesize TXA2, and urinary excretion of TXB2+3-M were nearly unaffected by supplementation. The results confirm that the minimal daily requirement of alpha-linolenic acid is 0.2-0.3% of total energy.
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