Postnatal hepatic fatty acid oxidative capacity of preterm pigs receiving TPN does not differ from that of term pigs and is not affected by supplemental arachidonic and docosahexaenoic acids.
To improve pediatric care of preterm infants, a better understanding of the metabolic processes associated with immaturity is needed. To this end, preterm and term pigs were delivered and administered either a control, a low-PUFA [0.3 and 0.6% of total lipids as docosahexaenoic acid (DHA) and arachidonic acid (AA), respectively], or a high-PUFA (5 and 11% of total lipids as DHA and AA, respectively) parenteral solution. Hepatic oxidative capacity and carnitine palmitoyltransferase (CPT) mRNA and activity in the presence or absence of malonyl-CoA were determined after 6 d. Oxidation of [1-(14)C]-palmitate or [1-(14)C]-glucose was similar in liver homogenates isolated from preterm and term pigs receiving the control solution. Oxidative capacity for either substrate did not differ with parenteral solution in preterm pigs, whereas in term pigs, glucose oxidation was 64% greater when the high-PUFA solution was administered relative to the control (P < 0.05). In preterm pigs, CPT I mRNA determined after 6 d of parenteral feeding were 1.5-fold greater (P < 0.05) than newborn estimates irrespective of solution administered, whereas CPT I mRNA were only greater for term pigs receiving the low- and high-PUFA solutions (66 and 115%, respectively; P < 0.05) relative to newborn estimates. Malonyl-CoA-sensitive CPT activity did not differ between preterm and term pigs or parenteral solution. Postnatal adaptations demonstrated by parenterally fed term neonates are present following preterm birth and are not improved by the provision of DHA and AA to parenteral solutions.
Campbell
Jenny A
JA
Departments of Animal Sciences, The Ohio State University, Columbus, OH 43210, USA. jenny.campbell@ucdenver.edu
Martin
Jessica E
JE
Melendez
Krizia
K
Stout
Michael B
MB
Lyvers-Peffer
Pasha A
PA
D000818:Animals; D000831:Animals, Newborn; D016718:Arachidonic Acid / Q000494:pharmacology*; D004281:Docosahexaenoic Acids / Q000494:pharmacology*; D005227:Fatty Acids / Q000378:metabolism*; D005260:Female; D008099:Liver / Q000378:metabolism*; D023421:Models, Animal; D010084:Oxidation-Reduction; D010289:Parenteral Nutrition, Total; D011247:Pregnancy; D047928:Premature Birth; D013552:Swine
D005227:Fatty Acids; D004281:Docosahexaenoic Acids; D016718:Arachidonic Acid