3-Mercaptopropionic acid, a potent inhibitor of fatty acid oxidation in rat heart mitochondria.

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.

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EFFECTS OF CORTISOL ON CULTURED RAT HEART CELLS

The Journal of Cell Biology ◽

10.1083/jcb.57.1.109 ◽

1973 ◽

Vol 57 (1) ◽

pp. 109-116 ◽

Cited By ~ 10

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.

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Effects of rapeseed oil on fatty acid oxidation and lipid levels in rat heart and liver

Lipids ◽

10.1007/bf02532884 ◽

1976 ◽

Vol 11 (9) ◽

pp. 670-675 ◽

Cited By ~ 9

Author(s):

M. Galli Kienle ◽

G. Cighetti ◽

C. Spagnuolo ◽

C. Galli

Keyword(s):

Fatty Acid ◽

Fatty Acid Oxidation ◽

Rat Heart ◽

Rapeseed Oil ◽

Acid Oxidation ◽

Lipid Levels

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Fatty Acid Oxidation and Mitochondrial Morphology Changes as Key Modulators of the Affinity for ADP in Rat Heart Mitochondria

Cells ◽

10.3390/cells9020340 ◽

2020 ◽

Vol 9 (2) ◽

pp. 340 ◽

Cited By ~ 1

Author(s):

Adolfas Toleikis ◽

Sonata Trumbeckaite ◽

Julius Liobikas ◽

Neringa Pauziene ◽

Lolita Kursvietiene ◽

...

Keyword(s):

Fatty Acids ◽

Fatty Acid ◽

Fatty Acid Oxidation ◽

Adenosine Diphosphate ◽

Acid Oxidation ◽

Mitochondrial Morphology ◽

Rat Heart Mitochondria ◽

Induced Changes ◽

Kinetics Of ◽

Cardiac Fibers

Fatty acids are the main respiratory substrates important for cardiac function, and their oxidation is altered during various chronic disorders. We investigated the mechanism of fatty acid–oxidation-induced changes and their relations with mitochondrial morphology and ADP/ATP carrier conformation on the kinetics of the regulation of mitochondrial respiration in rat skinned cardiac fibers. Saturated and unsaturated, activated and not activated, long and medium chain, fatty acids similarly decreased the apparent KmADP. Addition of 5% dextran T-70 to mimic the oncotic pressure of the cellular cytoplasm markedly increased the low apparent KmADP value of mitochondria in cardiac fibers respiring on palmitoyl-l-carnitine or octanoyl-l-carnitine, but did not affect the high apparent KmADP of mitochondria respiring on pyruvate and malate. Electron microscopy revealed that palmitoyl-l-carnitine oxidation-induced changes in the mitochondrial ultrastructure (preventable by dextran) are similar to those induced by carboxyatractyloside. Our data suggest that a fatty acid oxidation-induced conformational change of the adenosine diphosphate (ADP)/adenosine triphosphate (ATP) carrier (M-state to C-state, condensed to orthodox mitochondria) may affect the oxidative phosphorylation affinity for ADP.

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