Jt. Barron et al., FATTY-ACID, TRICARBOXYLIC-ACID CYCLE METABOLITES, AND ENERGY-METABOLISM IN VASCULAR SMOOTH-MUSCLE, The American journal of physiology, 267(2), 1994, pp. 80000764-80000769
The influence of octanoate on O-2 consumption, tricarboxylic acid (TCA
) cycle intermediates, and high-energy phosphates was examined in inta
ct resting porcine carotid artery to investigate the role of fatty aci
d in energy metabolism and its integration with glucose metabolism in
vascular smooth muscle. Incubation of resting arteries with octanoate
(0.5 mM), which was previously shown to inhibit aerobic glycolysis (6)
, inhibited lactate production by 64% and increased Oz consumption by
30%. The increase in O-2 consumption with octanoate was approximately
equal to that calculated to account for the ATP production lost by inh
ibition of aerobic lactate production by octanoate. In glucose-free me
dium, the level of high-energy phosphate was reduced but was restored
when octanoate was included in the incubation medium. This was associa
ted with an increase in O-2 consumption. These results suggest that th
e energy requirements of resting carotid artery can be largely met by
the oxidative metabolism of fatty acid. Octanoate induced anaplerosis
of the TCA cycle, as indicated by a 70% increase in the level of citra
te. Extracellular glucose was necessary for octanoate-induced anaplero
sis, probably by providing the extra carbon via pyruvate carboxylation
, whereas a coupled transamination involving aspartate was a less impo
rtant anaplerotic mechanism.