Action of carnitine on long chain fatty acid oxidation by liver

1959 ◽  
Vol 197 (2) ◽  
pp. 297-304 ◽  
Author(s):  
Irving B. Fritz

The addition of dl-carnitine to various types of particulate liver preparations resulted in augmented oxidation of labeled palmitate and stearate. In contrast, carnitine exerted little if any effects upon the degradation of octanoate or laurate. The oxidation of palmityl-1-C14 CoA by liver particulates was not affected by the presence of carnitine, suggesting that carnitine action is at a stage prior to the formation of this intermediate. Since carnitine addition consistently induced an increase in long chain fatty acid oxidation by slices and by subcellular particulates but did not enhance fatty acid degradation by various soluble systems, it was concluded that an intracellular structure is probably required for carnitine action. A carnitine effect on the long chain fatty acid activating enzyme could not be demonstrated. It was concluded tentatively that the site of carnitine action is independent of direct influence on the known enzymes required for fatty acid oxidation. Palmitic acid oxidation by particulate preparations was inhibited by added serum albumin or calcium, and this inhibition was in large part relieved by the addition of carnitine.

1960 ◽  
Vol 198 (1) ◽  
pp. 39-44 ◽  
Author(s):  
Irving B. Fritz ◽  
Eli Kaplan

Palmitic acid-1-C14 oxidation by hemidiaphragms was measured in tissues from fed and starved normal and alloxanized rats. Muscle from normal rats starved for 3 days or longer showed an enhanced conversion of added palmitate to C14O2, while fasting for 1 or 2 days had little effect on fatty acid degradation by diaphragms from normal rats. Tissues from fed or starved alloxan diabetic animals had an augmented oxidation of labeled palmitate. The addition of glucose to the medium spared fatty acid oxidation by diaphragms from starved or diabetic rats but did not influence palmitate degradation by tissues from normal fed rats. The presence of insulin increased the glucose sparing action on long-chain fatty acid oxidation but was without effect on palmitate oxidation in the absence of added glucose. The conversion of C14-octanoic acid to C14O2 by muscle was not influenced by previous starvation nor by addition of glucose to the medium. Glucose-U-C14 and glucose-1-C14 conversion to C14O2 and glycogen were essentially the same in diaphragms from fed and starved animals.


Cell Reports ◽  
2018 ◽  
Vol 23 (11) ◽  
pp. 3300-3311 ◽  
Author(s):  
Linford J.B. Briant ◽  
Michael S. Dodd ◽  
Margarita V. Chibalina ◽  
Nils J.G. Rorsman ◽  
Paul R.V. Johnson ◽  
...  

1990 ◽  
Vol 258 (1) ◽  
pp. H51-H56 ◽  
Author(s):  
S. E. Litwin ◽  
T. E. Raya ◽  
R. G. Gay ◽  
J. B. Bedotto ◽  
J. J. Bahl ◽  
...  

This study was designed to determine the changes in the heart that result from inhibition of long-chain fatty acid oxidation with 2-tetradecylglycidic acid (TDGA). Male Sprague-Dawley rats (n = 64) were treated with TDGA (20 mg.kg-1.day-1) or a comparable volume of vehicle by gavage feeding for 7 or 21 days. In conscious rats TDGA produced no changes in heart rate, left ventricular systolic or end-diastolic pressures, left ventricular pressure development (dP/dt), or the time constant of left ventricular relaxation. Left ventricular developed pressure was not changed at 21 days. TDGA increased left ventricular weight, left ventricular weight-to-body weight ratio, and total heart weight-to-body weight ratio. Left ventricular endocardial and epicardial myocyte volumes were increased by 53 and 65%, respectively. Myocardial triglyceride content was increased threefold. Left ventricular chamber stiffness constants between end-diastolic pressures of 0 and 30 mmHg were increased, and left ventricular end-diastolic volumes at operating end-diastolic pressures were decreased at both 7 and 21 days. The myocardial stiffness constant was also increased at 7 and 21 days. Thus inhibition of long-chain fatty acid oxidation with TDGA increased left ventricular mass and altered left ventricular chamber and muscle stiffness without changing left ventricular relaxation or systolic function. We conclude that inhibition of long-chain fatty acid oxidation produced an unusual model of left ventricular hypertrophy and diastolic dysfunction characterized by abnormalities of passive-elastic properties but preserved relaxation.


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