Brain metabolism of alpha-linolenic acid during development.

To date, experimental models for evaluation of the relative contribution of conversion of 18:3n-3 to 22:6n-3 in brain, particularly during crucial stages of rapid brain growth, have limitations that preclude a definitive resolution of the relative contribution of conversion in brain per se compared with dependence on extracerebral sources of 22:6n-3. Clearly, brain in the neonatal period has substantial capacity for delta 6- and delta 5-desaturation that equals or surpasses that of immature liver. Furthermore, activity in brain is much less susceptible than that in liver to dietary fluctuations. Studies with cultured cells of neural origin provide valuable insight into relative contributions of alternate pathways and into molecular mechanisms of regulation of desaturation and chain elongation but obviously have limitations when trying to extrapolate this to the intact animal. Some investigators have concluded that 22:6n-3 for brain phospholipids may be derived primarily from liver and dietary sources; at the same time, brain has the capacity for formation of 22:6n-3 should 18:3n-3 be the primary dietary component of the n-3 family. Whereas 18:3n-3 itself appears not to be essential for esterification to brain membrane phospholipids, 22:6n-3 is clearly a vital and quantitatively significant component. Potentially, brain can convert 18:3n-3 to more polyunsaturated derivates during the growth period when the products are most needed and other sources such as diet or conversion by liver may be restrictive.