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Influence of dietary long‐chain PUFA on premature baboon lung FA and dipalmitoyl PC composition
Author(s) -
Chao Angela Chueh,
Ziadeh Bassem I.,
Diau GuanYeu,
Wijendran Vasuki,
SarkadiNagy Eszter,
Hsieh Andrea T.,
Nathanielsz Peter W.,
Brenna J. Thomas
Publication year - 2003
Publication title -
lipids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.601
H-Index - 120
eISSN - 1558-9307
pISSN - 0024-4201
DOI - 10.1007/s11745-003-1079-8
Subject(s) - baboon , composition (language) , lung , pulmonary surfactant , docosahexaenoic acid , lipidology , polyunsaturated fatty acid , medicine , phospholipid , breast milk , arachidonic acid , endocrinology , chemistry , zoology , clinical chemistry , fatty acid , biology , biochemistry , philosophy , linguistics , membrane , enzyme
Abstract One of the major survival challenges of premature birth is production of lung surfactant. The lipid component of surfactant, dipalmitoyl PC (DPPC), increases in concentration in the period before normal term birth via a net shift in FA composition away from unsaturates. We investigated the influence of dietary DHA and arachidonic acid (AA) on lung FA composition and DPPC concentration in term and preterm baboons. Pregnant animals/neonates were randomized to one of four groups: breast‐fed (B), term formula‐fed (T − ), preterm formulafed (P − ), and preterm fed formula supplemented with DHA‐AA (P + ). Breast milk contained 0.68%wt DHA and the P + group formula contained 0.61%wt DHA. In the preterm groups (P − and P + ), pregnant females received a course of antenatal corticosteroids. At the adjusted age of 4 wk, neonate lung tissue was harvested, and FA composition and DPPC were analyzed. Palmitate was ∼28%wt of lung total FA and no significant differences were found among the four treatment groups. In contrast, DPPC in the B group lung tissue was significantly greater than DPPC in the unsupplemented groups, but not compared with the P + group. The B and P + groups were not significantly different in DHA and AA, but were different compared with the unsupplemented (T, P − ) groups. These results indicate that LCP supplementation increases lung DHA and AA, without compromising overall lung 16∶0 or DPPC. The shift in FA composition toward greater unsaturation in the groups consuming LCP supported improved surfactant lipid concentration in preterm neonate lungs.