Abstract

Fatty acid compositions of intestinal cell phospholipids were compared in six groups of rats fed miscellaneous dietary oils (corn, rapeseed, peanut, hydrogenated palm, hydrogenated coconut, and salmon oils). Diets were representative of different supplies of essential polyunsaturated fatty acids (n-6 and n-3). Epithelial cells were isolated according to a gradient descending from the villus tip to the crypt base, and fatty acid compositions in total cell phospholipids were reported relative to the level of differentiation. The standard differentiation pattern of linoleic acid was profiled after computer processing of the data. The amount of linoleic acid in the phospholipids of crypt stem cells represented about 50% of the maximum amount found in mature villus cells. A minimum linoleic acid threshold of 6–7% of total fatty acids in the crypt stem cells was necessary to reach a maximum level of 13–15% in the upper villus cells. Hydrogenated coconut and salmon oils did not meet this minimum requirement. When diets supplied sufficient amounts of n-6 fatty acids, arachidonic acid accretion paralleled that of linoleic acid so that 20:4n-6 contents rose up to 20–26% of total fatty acids in mature cells. Dietary deficiency in total polyunsaturated fatty acids (hydrogenated vegetable oils) and a relative excess of n-3 fatty acids (salmon oil) induced major alterations of the accretion profile of arachidonic acid. Concomitantly, eicosatrienoic acid appeared in both hydrogenated vegetable oil groups, while n-3 fatty acids dramatically increased in salmon oil-fed rats. In all groups the sum of total dimethylacetals (representative of total plasmalogens in cell phospholipids) decreased as stem cells were translocated toward the villus base. These data indicate that enterocyte differentiation involves an increasing incorporation of n-6 fatty acids, which is controlled by the diet. The main physiological features directly concerned are membrane biogenesis, remodelling, and functions on the one hand, and intestinal metabolism of eicosanoids on the other hand.

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