Liver essential fatty acids desaturation

Poisson JP, Dupuy RP, Sarda P, Descomps B, Narce M, Rieu D, et al. Evidence that liver-microsomes of human neonates desaturate essential fatty-acids. Biochim Biophy Acta 1993 1167(2) 109-113. 

The metabolic pathways for synthesis of n-6 and n-3 families of polyunsaturated fatty acids from the essential fatty acids, linoleic acid (LA) (18 2 [n-6]) and a-linolenic acid (18 3 [n-3]), respectively, are showninFig. 2. Conversion of LA to arachidonic acid (AA) occurs via A6 desaturation to yield y-linolenic acid (GLA), then an elongation step to produce dihomo-y-linolenic acid (DHGL A) and A5 desaturation, to form AA. The A6 and A5 microsomal desaturases have been reported to utilize both NADH and NADPH as cofactors in vitro (Brenner 1977). Whether there is a more stringent pyridine nucleotide requirement in vivo is not known with certainty. Desaturase activities are especially abundant in the liver. 

The metabolic transformation of the C,s essential fatty acids to their longer chain fatty acid derivatives has been studied mainly in the liver and to some extent in the brain. Animals and tissues vary greatly in their efficiency of desaturation and chain elongation [18,414,415]. Thus young rats have a particularly active system whereas cats are unable to perform this metabolic reaction. The failure of the cat family to desaturate linoleic acid has been suggested to be a possible reason behind the cats evolution to carnivorous animals [416] (e.g. eating rats). Humans occupy an intermediate position. 

Diets deprived of essential fatty acids (EFA) enhance the A6 desaturation activity of rat liver or testis microsomes. Changes of fatty acid composition with decrease of linoleic and arachidonic acids and increase of oleic and 20 3 (o)9) acids are shown as early as 3 days after EFA deprivation (Table 1). The changes evoke a decrease of the double bond index saturated acid ratio from 2.2 to... 

Propylthiouracil-treated animals also showed a decrease in the percent of linoleic acid distribution in liver. In spite of the results obtained by different authors (Ellefson and Mason, 1964 Mitchel and Truchot, 1962 Kirkeby, 1972), the changes in the percent distribution of total fatty acids in plasma are small and unimportant (Table 3). The probable explanation for the low linoleic acid concentration in liver could be that the supply of essential fatty acids from the diet does not parallel the increase of lipid degradation (Kirkeby, 1972), thereby giving a relative linoleic acid deficiency despite the food intake. The changes on A6 and A9 desaturation activities are not apparently related with the modifications observed in the percent distribution of total fatty acids in liver. This fact could be explained considering that the composition of liver and plasma lipids is a result of a balance between dietary fat, lipid, and carbohydrate metabolism, lipolysis of tissue lipids, and endocrinological factors. 

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