FATTY-ACID, TRICARBOXYLIC-ACID CYCLE METABOLITES, AND ENERGY-METABOLISM IN VASCULAR SMOOTH-MUSCLE

Citation
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
Citations number
29
Categorie Soggetti
Physiology
ISSN journal
00029513
Volume
267
Issue
2
Year of publication
1994
Part
2
Pages
80000764 - 80000769
Database
ISI
SICI code
0002-9513(1994)267:2<80000764:FTCMAE>2.0.ZU;2-E
Abstract
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.