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of gestation, n = 4)

n = 4)

old, n = 6)

16:0/16:0

992± 156

1004±81

538± 121

16:0/18:1

2007±250

2240±173

2353±496

16:0/18:2

466 ± 52

1259±139

2202±273

16:0/20:4

1402± 98

1784±38

1062±219

16:0/22:6

431±110

953 ± 82

614 ± 512

18:0/18:2

308 ± 56

443 ± 68

1239±252

18:0/20:4

1298±288

953 ± 89

448±403

18:0/22:6

115 ± 31

210 ± 50

221±267

aMolecular species were analyzed by reverse-phase HPLC and quantified by postcolumn fluorescence detection with 1,6-diphenyl-1,3,5-hexatriene. Concentrations expressed as mean ± SD.

aMolecular species were analyzed by reverse-phase HPLC and quantified by postcolumn fluorescence detection with 1,6-diphenyl-1,3,5-hexatriene. Concentrations expressed as mean ± SD.

their fed litter mates, even in the total absence of enteral nutrition.

In contrast, immature fetal lung PC also contains a high concentration of PC16:0/18:1 but becomes more, rather than less, saturated with progression of gestation due to increased synthesis of the disatu-rated species PC16:0/16:0 and PC16:0/14:0. PC16:0/ 16:0 is a major component of pulmonary surfactant that acts to oppose surface tension forces in the lungs and prevent alveolar collapse. Infants who are born preterm with immature surfactant are at high risk of death and disability caused by neonatal respiratory distress syndrome. In contrast to fetal liver, the phospholipid composition of fetal lung is only marginally affected by the changes to lipid nutrition in utero. Nevertheless, some nutritional influence is evident, even though PUFA-containing species are minor components of lung PC. Comparison of PC compositions in prenatal human lung shows a postnatal increase in the content of PC16:0/18:2, which reflects the increased dietary supply of 18:2n-6. The situation in developing lung reflects that of most other tissues in the body, in which dietary lipid modulation causes relatively modest changes to the specificity of phospholipid compositions. Such subtle alterations to membrane composition, however, can exert profound effects on cellular function.

Finally, adult brain PE contains approximately 50% of 22:6n-3 species, enriched in neuronal synapses and possibly involved in synaptic transmission. Failure to acquire sufficient 22:6n-3 in brain PE during neuronal differentiation in early development can lead to permanent suboptimal neurological function. Many of the changes to maternal lipid metabolism in pregnancy represent adaptations to ensure adequate supply of PUFA to the developing fetal brain. Increased synthesis and secretion of PC16:0/22:6 in livers of pregnant rats and guinea pigs correlates with the period in fetal brain growth of maximal accumulation rate of 22:6n-3 into brain PE. Once incorporated into brain or retinal PE, 22:6n-3 is retained throughout life, even in periods of prolonged nutritional deprivation. Infants who are born preterm and with inadequate reserves of 22:6n-3 are recognized to be in danger of nutritional deficiency if fed milk formula lacking preformed long-chain PUFA. For instance, 22:6n-3 content of brain PE was decreased in infants fed such formula and who had died suddenly from sudden infant death syndrome. For this reason, supplementation of preterm infant milk formula with preformed PUFA has been recommended by the European Society for Pediatric Gastroenterology and Nutrition.

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