ABSTRACT
Asim K. Dutta-Roy*, Fiona M. Campbell, Samson Taffesse, and Margaret J. Gordon
Receptor Research Laboratory, Rowett Research Institute, Aberdeen, Scotland, U.K.
Linoleic acid, (LA, 18:2n-6) and α-linolenic acid (ALA, 18:3n-3) are the two main dietary essential fatty acids (EFA) (1). LA and ALA are not interconvertible, but they can be further elongated and desaturated by the same enzyme systems to n-6 and n-3 long-chain polyunsaturated fatty acids (LCPUFA) in the body (2). LA and ALA are primarily present in the diet in vegetable oils, whereas preformed LCPUFA may also be consumed in foods of animal origin. The importance of LCPUFA has been related to their structural action, their specific interaction with membrane proteins or their ability to serve as precursors of second messenger systems (3-5). Therefore, both LA and ALA must be converted to their further metabolites to exert the full range of biological actions. Among LCPUFA, arachidonic acid (AA, 20:4n-6) and docosahexaenoic acid (DHA, 22:6n-3) are found in high concentrations in the structural lipids of central nervous system as well as other mammalian tissues (6,7). The first and rate-determining step in LCPUFA synthesis is ∆6-desaturation. The ∆6-desaturation step is therefore critical for full utilization of dietary LA and ALA in the body. The formation of γ-linolenic acid (GLA), the immediate ∆6-desaturated metabolite of LA, is reported to be reduced in a number of diseases (6-8), indicating an abnormality in EFA metabolism in the body. In such conditions, dietary supplementation of GLA could be useful as a means of by-passing the rate-limiting ∆6-desaturation step to maintain optimum LCPUFA levels in the body.
