Quantitative relationships between dietary linoleate and prostaglandin (eicosanoid) biosynthesis.
Essential fatty acid deficiency consistently depresses eicosanoid (prostaglandin E2, F2, and I2 and thromboxane) biosynthesis independent of sampling protocols. Tissue fatty acid analyses support the hypothesis that the decrease is due in part to depression of arachidonate and accumulation of eicosatrienoate (n-9). Research on the alteration of eicosanoid biosynthesis by dietary linoleate supplementation is reviewed extensively. Responses of whole blood, lung, liver and heart eicosanoid synthesis to feeding eight concentrations of dietary linoleate between 0 and 27 energy percent are reported. It is concluded that stimulation, depression and no change in eicosanoid production could be equally well documented as a response to linoleate supplementation. Evidence for the obvious mechanism that alterations in precursor fatty acid composition are a possible explanation is fragmentary and inconsistent. The appropriate sampling techniques appear not to be established at this time and most likely are species, gender and tissue specific.
D000818:Animals; D004041:Dietary Fats / Q000378:metabolism*; D005228:Fatty Acids, Essential / Q000378:metabolism; D006801:Humans; D007700:Kinetics; D019787:Linoleic Acid; D008041:Linoleic Acids / Q000378:metabolism*; D010743:Phospholipids / Q000096:biosynthesis / Q000097:blood; D011453:Prostaglandins / Q000096:biosynthesis*; D013931:Thromboxanes / Q000096:biosynthesis* / Q000097:blood
D004041:Dietary Fats; D005228:Fatty Acids, Essential; D008041:Linoleic Acids; D010743:Phospholipids; D011453:Prostaglandins; D013931:Thromboxanes; D019787:Linoleic Acid