Metabolism of long-chain polyunsaturated fatty acids derived from 18:2ω−6 and 18:3ω−3 by chain elongation – desaturation is essential for synthesis of complex structural lipids, leukotrienes, thromboxanes, and prostaglandins. These essential fatty acids are required for normal function in developing tissues and appropriate maturation of a wide variety of physiological processes. During development, fetal accretion of long-chain metabolites of ω−6 and ω−3 fatty acids may result from maternal or placental synthesis and transfer or, alternatively, from the metabolism of 18:2ω−6 and 18:3ω−3 to longer chain homologues by the fetus. After birth the infant must synthesize or be fed the very long chain polyunsaturated fatty acids of C20 and C22 type derived from 18:2ω−6 and 18:3ω−3.Metabolism of ω−6 and ω−3 fatty acids utilizes the same enzyme system and is competitive. When levels of dietary ω−3 and ω−6 C18 fatty acids are altered, the levels of metabolites of these precursor fatty acids change in specific brain membranes, influencing membrane lipid dependent functions. For example, a diet unbalanced in very long chain ω−3 and ω−6 fatty acids may increase brain membrane ω−3 fatty acid content when 20:5ω−3 is fed, while decreasing membrane fatty acid content of the ω−6 series of competing fatty acids. As 20:4ω−6 is quantitatively and qualitatively important to brain phospholipid, significant reduction in brain levels of 20:4ω−6 may be less than optimal. The impact of these compositional changes on brain function is not yet clear.The authors in this symposium address how this general area of essential fatty acid metabolism is relevant to the evolution of man, growth and development of fish, function of the retina and neural tissue, cognitive development of infants, and infant nutrition.
Opposing effects of methylmercury and n‐3 long‐chain polyunsaturated fatty acids on adult rat brain essential fatty acids
