Contribution of various substrates to total citric acid cycle flux and ]anaplerosis as determined by13C isotopomer analysis and O2 consumption in the heart

1996 ◽  
Vol 4 (1) ◽  
pp. 35-46 ◽  
Author(s):  
Craig R. Malloy ◽  
John G. Jones ◽  
F. Mark Jeffrey ◽  
Michael E. Jessen ◽  
A. Dean Sherry
1995 ◽  
Vol 270 (17) ◽  
pp. 10027-10036 ◽  
Author(s):  
Christine Des Rosiers ◽  
Lorella Di Donato ◽  
Blandine Comte ◽  
Annick Laplante ◽  
Caroline Marcoux ◽  
...  

2008 ◽  
Vol 283 (32) ◽  
pp. 21988-21996 ◽  
Author(s):  
Lili Yang ◽  
Takhar Kasumov ◽  
Rajan S. Kombu ◽  
Shu-Han Zhu ◽  
Andrea V. Cendrowski ◽  
...  

1978 ◽  
Vol 170 (2) ◽  
pp. 235-240 ◽  
Author(s):  
J. Kalervo Hiltunen ◽  
V. Pekka Jauhonen ◽  
Markku J. Savolainen ◽  
Ilmo E. Hassinen

The metabolic effects of pent-4-enoate were studied in beating and potassium-arrested perfused rat hearts. The addition of 0.8mm-pent-4-enoate to the fluid used to perfuse a potassium-arrested heart resulted in a 70% increase in the O2 consumption and a 66% decrease in the glycolytic flux as measured in terms of the de-tritiation of [3-3H]glucose, although the proportion of the O2 consumption attributable to glucose oxidation decreased from an initial 30% to 10%. The pent-4-enoate-induced increase in O2 consumption was only 15% in the beating heart. In the potassium-arrested heart, pent-4-enoate stimulated palmitate oxidation by more than 100% when measured in terms of the production of 14CO2 from [1-14C]palmitate, but in the beating heart palmitate oxidation was inhibited. Perfusion of the heart with pent-4-enoate had no effect on the proportion of pyruvate dehydrogenase found in the active form, in spite of large changes in the CoASH and acetyl-CoA concentrations and changes in their concentration ratios. The effects of pent-4-enoate on the cellular redox state were dependent on the ATP consumption of the heart. In the beating heart, pent-4-enoate caused a rapid mitochondrial NAD+ reduction that subsequently faded out, so that the final state was more oxidized than the initial state. The arrested heart, however, remained in a more reduced state than initially, even after the partial re-oxidation that followed the initial rapid NAD+ reduction. The ability of pent-4-enoate to increase or decrease fatty acid oxidation can be explained on the basis of the differential effects of pent-4-enoate on the concentration of citric acid-cycle intermediates under conditions of high or low ATP consumption of the myocardial cell. The proportion of the fatty acids in the fuel consumed by the heart is probably primarily determined by the regulatory mechanisms of glycolysis. When pent-4-enoate causes an increase in the citric acid-cycle intermediates, feedback inhibition of glycolysis results in an increase in the oxidation of fatty acids.


2008 ◽  
Vol 283 (32) ◽  
pp. 21978-21987 ◽  
Author(s):  
Lili Yang ◽  
Rajan S. Kombu ◽  
Takhar Kasumov ◽  
Shu-Han Zhu ◽  
Andrea V. Cendrowski ◽  
...  

1963 ◽  
Vol 42 (4) ◽  
pp. 480-484 ◽  
Author(s):  
B. Eckstein ◽  
R. Landsberg

ABSTRACT The succinic, malic and isocitric dehydrogenases in the ovary of immature and mature, normal and serum gonadotrophin injected rats were examined. The Qo2 of these enzymes were markedly enhanced in the gonadotrophin injected rats of both age groups, except in the case of succinic dehydrogenase in the ovary of the immature rats, where a slight non-significant decrease was noted. It is concluded that in the mature rat ovary, gonadotrophin administration stimulates the activity of all the examined dehydrogenases of the citric acid cycle, whereas in the immature rat ovary, at least the isocitric- and malic dehydrogenases are thus stimulated.


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