The primary goal of this study was to investigate the effects of glucose in
fusion on surfactant phosphatidylcholine (PC) metabolic kinetics in the lun
gs. A new stable isotope tracer model was used in which [1,2-C-13(2)]acetat
e and uniformly labeled [U-C-13(16)]palmitate were infused in 12 normal ove
rnight-fasted pigs to quantify lung surfactant kinetics with or without glu
cose infusion (24 mg.kg(-1).min(-1)). With glucose infusion, the rate of su
rfactant PC incorporation from de novo synthesized palmitate increased from
the control value of 2.1 +/- 0.2 to 15.5 +/- 1.9 nmol PC-bound palmitate.h
(=1).g wet lung(-1) (P < 0.05), whereas the incorporation rate from plasma
preformed palmitate decreased from the control value of 20.9 +/- 1.9 to 11.
6 +/- 1.1 nmol palmitate.h(-1).g wet lung(-1) (P < 0.05). The palmitate com
position in lamellar body surfactant PC increased from the control value of
61.7 +/- 2.1% to 75.9 +/- 0.6% (P < 0.05). The surfactant PC secretion rat
e decreased from the control value of 239.0 +/- 26.1 to 81.9 +/- 5.3 nmol P
C-bound palmitate.h(-1).g wet lung(-1) (P < 0.05). We conclude that, wherea
s surfactant secretion was inhibited by glucose infusion, neither total sur
factant PC synthesis nor the surfactant PC pool size was significantly affe
cted due to an increased reliance on de novo synthesized fatty acids.