Polyunsaturated fatty acids in the low-birth-weight infant.
The essentiality of certain PUFAs is related to their capability to be incorporated into lipids and to act as precursor in the formation of prostaglandins. Via phospholipids the EFA's influence the physico-chemical characteristics of biomembranes. EFAs are metabolized differently from nonessential PUFAs. While the nonessential fatty acids are metabolized rapidly, the organism tends to conserve the stores of EFAs. Inhibitions and competitions among the EFAs of the three series (oleic, linoleic, and alpha-linolenic) have been demonstrated. Apparently, for any given chain length the more unsaturated fatty acid has a greater affinity for the enzyme system responsible for further elongation and desaturation. EFAs are also necessary for the proper utilization of the saturated fatty acids. Vitamin E and pyridoxine seem to be involved in EFA metabolism. Normal growth of infants is dependent upon an adequate supply of EFA. The human fetus, like the adult, is unable to synthesize the EFAs, which must therefore be derived from the maternal circulation and pass through the placenta. In the fetus, increased concentration of the polyenoic fatty acids with advanced gestational age may result from increased activity of the fetomaternal unit by preferential transfer of these FAs. Enzymatic activity in the placenta or the fetus may also be responsible for desaturation and elongation of these EFAs. Several clinical manifestations have been ascribed in the human infant to prolonged EFA deficiency; however, none of these findings was noted in a group of sick newborn infants with very rapid onset of deficiency. Platelet dysfunction, decreased prostaglandin biosynthesis and turnover and altered pulmonary surfactant are among the effects of EFA deficiency on infants. Supplementation of the EFAs by the diet, parenterally or by the inunction of oil rich in linoleic acid, were reported to alleviate the symptoms of EFA deficiency. The minimal estimated requirement of linoleic acid is 1% of calories and 4% is an optimal intake. Most diets, including human breast milk, infant formulas and parenteral fat emulsions, far exceed the optimal intake of linoleic acid. Relatively little is known about the possible effects of high levels of linoleate in the diet; however, early studies suggest an adverse effect on platelet function, prostaglandin biosynthesis, pulmonary gas exchange and immune function.
D000328:Adult; D000818:Animals; D005228:Fatty Acids, Essential / Q000172:deficiency / Q000378:metabolism* / Q000627:therapeutic use; D005231:Fatty Acids, Unsaturated / Q000037:antagonists & inhibitors / Q000096:biosynthesis / Q000378:metabolism*; D005260:Female; D005333:Fetus / Q000378:metabolism; D006128:Growth; D006801:Humans; D007227:Infant Nutritional Physiological Phenomena; D007230:Infant, Low Birth Weight; D007231:Infant, Newborn; D008041:Linoleic Acids / Q000009:adverse effects / Q000378:metabolism; D008055:Lipids / Q000096:biosynthesis; D008431:Maternal-Fetal Exchange; D009751:Nutritional Requirements; D010743:Phospholipids / Q000378:metabolism; D011247:Pregnancy; D011453:Prostaglandins / Q000378:metabolism; D013329:Structure-Activity Relationship
D005228:Fatty Acids, Essential; D005231:Fatty Acids, Unsaturated; D008041:Linoleic Acids; D008055:Lipids; D010743:Phospholipids; D011453:Prostaglandins