Essential fatty acid requirements in pregnancy and lactation with special reference to brain development.
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Biomedical subjects
Publications and source records attributed to A G Hassam.
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Essential fatty acid (EFA) restriction has been found to inhibit the action of vitamin D on the active transport of calcium in the intestine. This inhibition suggests EFAs are involved in facilitating the active transport of calcium across the mucosal membrane.
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Radioactivity from orally administered radiolabeled dihomo-gamma-linolenic acid (20 : 3 omega 6) was recovered from the liver, plasma and brain lipid fractions. After administration the fatty acid was metabolized to arachidonic acid, the 22 carbon chain length fatty acid, and was also beta-oxidized. However, 22 hr after administration of [1-14C] 20 : 3 between one-third and one-half of the recovered radioactivity was still associated with dihomo-gamma-linolenic acid in the liver and plasma lipid fractions. Orally administered dihomo-gamma-linolenic acid is incorporated into lipid fractions and is, therefore, available in the metabolic pool for PGE1 synthesis.
1. Rats were fed on either a diet deficient in essential fatty acid (EFA) or one supplemented with dihomo-gamma-linolenic acid (20:3,n-6) at levels that represented 0.25, 0.5, 1.0 and 2.0% of the dietary energy. 2. Supplementation of the diet of EFA-deficient animals with 20:3,n-6 reversed most of the fatty acid changes induced in the liver phospholipid fraction. 3 The EFA potency of 20:3,n-6 was found to be similar to that of gamma-linolenic acid (18:3,n-6) which has been shown to be higher than that of linoleic acid (18:2,n-6).
The view expressed by Cuthbertson that essential fatty acid needs of human infants have been overestimated is contested. In our view Cuthbertson's assessment of essential fatty acid requirements of infants is too low because 1) consideration of the omega3 fatty acids is omitted; 2) the biological value of long-chain essential fatty acids is wrongly assessed; and 3) the significance of variations in composition of random human milk samples is misunderstood.
Essential fatty acids not only control blood lipid levels, but are the precursors of prostaglandins responsible for regulation of platelet aggregation. Dietary deficiency of essential fatty acids may play an important role in the development of coronary heart disease, particularly during the early growth period.
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1. Essential fatty acid-deficient rats were fed gamma-linolenic acid (18: 3omega6) at 2% dietary energy and alpha-linolenic acid (18: 3omega3) at 0, 1-6, 2-8 and 4-0% of the dietary energy. 2. 18: 3omega3 at 1-6% apparently inhibits the synthesis of the C20 and C22 omega6 long-chain polyunsaturated fatty acids (omega6 LC-PUFA) metabolized from 18: 3omega6. 3. However, increasing the dietary levels of 18: 3omega3 from 1-6 to 4-0% has no further influence. 4. The results suggest that dietary 18: 3omega6 is an efficent precursor for the omega6 LC-PUFA synthesis even in the presence of 18: 3omega3.
Female rats were weaned and fed a semipurified diet lacking in essential fatty acids. After 160 days, the deficient diet was supplemented with varying amounts of gamma-linolenic acid. Changes in body weight and feed efficiency were measured. Total liver phospholipid fatty acids were also analyzed. Supplementation with gamma-linolenic acid to the deficient diet for 7 days led to improvements in body weight and feed efficiency of the deficient rats. The liver phospholipid fatty acid composition returned to a normal pattern. There was a reduction of 5,8,11-eicosatrienoic acid and an increase in the arachidonic acid. Thus, there was a fall in the triene: tetraene ratio with increasing dietary supplementation of gamma-linolenic acid. The essential fatty acid potency, the minimum dietary requirement for this fatty acid, and the widely accepted levels of the minimum requirements of dietary essential fatty acids are discussed.
In vivo administration of 1-14C-linoleic acid to domestic cats demonstrated that these animals are unable to convert this essential fatty acid to its physiologically active metabolities. This experiment confirms the absence of both the delta6 and delta8 desaturases in the cat, and suggests that this species has a dietary requirement for polyunsaturated fatty acids of animal origin.
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