Enhancement of Fatty Acid Oxidation and Medium-Chain Fatty Acyl Coenzyme A Synthetase by Adenine Nucleotides in Rat Heart Homogenates

1971 ◽  
Vol 60 (1) ◽  
pp. 77-81 ◽  
Author(s):  
V. Gene Erwin ◽  
A. Duane Anderson ◽  
Grethe Jurgensen Eide
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Rat Heart ◽  
Coenzyme A ◽  
Adenine Nucleotides ◽  
Fatty Acyl ◽  
Acid Oxidation ◽  
Medium Chain ◽  
Acyl Coenzyme A

scholarly journals Mouse Cardiac Acyl Coenzyme A Synthetase 1 Deficiency Impairs Fatty Acid Oxidation and Induces Cardiac Hypertrophy

2011 ◽  
Vol 31 (6) ◽  
pp. 1252-1262 ◽  
Author(s):  
J. M. Ellis ◽  
S. M. Mentock ◽  
M. A. DePetrillo ◽  
T. R. Koves ◽  
S. Sen ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Cardiac Hypertrophy ◽  
Fatty Acid Oxidation ◽  
Coenzyme A ◽  
Acid Oxidation ◽  
Acyl Coenzyme A

Carnitine effects on palmitate-1-C14 conversion to CO2 and glycerides by various tissues

1964 ◽  
Vol 206 (6) ◽  
pp. 1217-1222 ◽  
Author(s):  
Irving B. Fritz
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Rat Heart ◽  
Liver Microsomes ◽  
Tissue Homogenate ◽  
Acid Oxidation ◽  
Acid Oxidase ◽  
Palmitate Oxidation ◽  
Glyceride Synthesis ◽  
Low Concentrations

Carnitine increased oxidation of palmitate-1-C14 by rat heart and liver preparations, but decreased palmitate incorporation into glycerides. To determine which of the effects was derivative and which was primary, experiments were repeated using tissues whose rates of fatty acid oxidation had been depressed by Amytal poisoning. Under these conditions, carnitine inhibition of fatty acid conversion to glycerides was abolished. Similarly, low concentrations of carnitine were found to enhance palmitate oxidation without influencing palmitate esterification. Isolated liver microsomes which synthesized glycerides without oxidizing fatty acids showed no response to carnitine under all conditions tried. The inability of carnitine to alter glyceride formation in experiments described may signify that acyl-CoA generation from CoA and acylcarnitine is specifically directed toward the fatty acid oxidase system rather than to glyceride synthesis. It was also shown that, under conditions optimal for demonstration of carnitine augmentation of fatty acid oxidation by rat heart preparations, carnitine increased palmitate oxidation by a variety of other tissue homogenate preparations.

scholarly journals EFFECTS OF CORTISOL ON CULTURED RAT HEART CELLS

1973 ◽  
Vol 57 (1) ◽  
pp. 109-116 ◽  
Author(s):  
J. V. Anastasia ◽  
R. L. McCarl
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Free Fatty Acids ◽  
Fatty Acid Oxidation ◽  
Growth Medium ◽  
Rat Heart ◽  
Acid Oxidation ◽  
Heart Cells ◽  
Atp Production ◽  
Rat Heart Cells

This paper reports the determination of the ability of rat heart cells in culture to release [14C]palmitate from its triglyceride and to oxidize this fatty acid and free [14C]palmitate to 14CO2 when the cells are actively beating and when they stop beating after aging in culture. In addition, the levels of glucose, glycogen, and ATP were determined to relate the concentration of these metabolites with beating and with cessation of beating. When young rat heart cells in culture are actively beating, they oxidize free fatty acids at a rate parallel with cellular ATP production. Both fatty acid oxidation and ATP production remain constant while the cells continue to beat. Furthermore, glucose is removed from the growth medium by the cells and stored as glycogen. When cultured cells stop beating, a decrease is seen in their ability to oxidize free fatty acids and to release them from their corresponding triglycerides. Concomitant with decreased fatty acid oxidation is a decrease in cellular levels of ATP until beating ceases. Midway between initiation of cultures and cessation of beating the cells begin to mobilize the stored glycogen. When the growth medium is supplemented with cortisol acetate and given to cultures which have ceased to beat, reinitiation of beating occurs. Furthermore, all decreases previously observed in ATP levels, fatty acid oxidation, and esterase activity are restored.

scholarly journals Recent Advances in the Pathophysiology of Fatty Acid Oxidation Defects: Secondary Alterations of Bioenergetics and Mitochondrial Calcium Homeostasis Caused by the Accumulating Fatty Acids

2020 ◽  
Vol 11 ◽  
Author(s):  
Alexandre Umpierrez Amaral ◽  
Moacir Wajner
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Calcium Homeostasis ◽  
Acid Oxidation ◽  
Cultured Fibroblasts ◽  
Medium Chain ◽  
Chain Acyl ◽  
Energy Deprivation ◽  
Long Chain

Deficiencies of medium-chain acyl-CoA dehydrogenase, mitochondrial trifunctional protein, isolated long-chain 3-hydroxyacyl-CoA dehydrogenase, and very long-chain acyl-CoA dehydrogenase activities are considered the most frequent fatty acid oxidation defects (FAOD). They are biochemically characterized by the accumulation of medium-chain, long-chain hydroxyl, and long-chain fatty acids and derivatives, respectively, in tissues and biological fluids of the affected patients. Clinical manifestations commonly include hypoglycemia, cardiomyopathy, and recurrent rhabdomyolysis. Although the pathogenesis of these diseases is still poorly understood, energy deprivation secondary to blockage of fatty acid degradation seems to play an important role. However, recent evidence indicates that the predominant fatty acids accumulating in these disorders disrupt mitochondrial functions and are involved in their pathophysiology, possibly explaining the lactic acidosis, mitochondrial morphological alterations, and altered mitochondrial biochemical parameters found in tissues and cultured fibroblasts from some affected patients and also in animal models of these diseases. In this review, we will update the present knowledge on disturbances of mitochondrial bioenergetics, calcium homeostasis, uncoupling of oxidative phosphorylation, and mitochondrial permeability transition induction provoked by the major fatty acids accumulating in prevalent FAOD. It is emphasized that further in vivo studies carried out in tissues from affected patients and from animal genetic models of these disorders are necessary to confirm the present evidence mostly achieved from in vitro experiments.

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