Effects of Coenzyme A and Carnitine on Fatty Acid Oxidation by Rainbow Trout Mitochondria

1970 ◽  
Vol 27 (5) ◽  
pp. 857-864 ◽  
Author(s):  
E. Bilinski ◽  
R. E. E. Jonas
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Rainbow Trout ◽  
Fatty Acid Oxidation ◽  
Lateral Line ◽  
Coenzyme A ◽  
Maximal Activity ◽  
Salmo Gairdneri ◽  
Acid Oxidation ◽  
Mitochondrial Fractions

The effects of coenzyme A (CoA) and carnitine on the oxidation of 0.1 mM K-palmitate-1-14C and K-oleate-1-14C by mitochondrial fractions from lateral line muscle, white muscle, heart, liver, and kidney was studied in rainbow trout (Salmo gairdneri). CoA (0.01–0.10 mM) stimulated the oxidation of fatty acids by mitochondria from lateral line muscle and heart. With all the preparations of mitochondria, fatty acid oxidation was increased by addition of carnitine (1.0 mM) and in the presence of carnitine (1.0 mM), CoA (0.1–1.0 mM) gave a further increase in oxidative activity. Mitochondria from lateral line muscle and heart showed the same range of maximal activity (oxidized substrate at 15 C = 180–200 nmoles/mg N per hr), which was considerably above that found with mitochondria from other tissues. The results suggest similarities in the energy-supplying metabolism in lateral line muscle and heart of trout with respect to the utilization of fatty acids.

UTILIZATION OF LIPIDS BY FISH: I. FATTY ACID OXIDATION BY TISSUE SLICES FROM DARK AND WHITE MUSCLE OF RAINBOW TROUT (SALMO GAIRDNERII)

1963 ◽  
Vol 41 (1) ◽  
pp. 107-112 ◽  
Author(s):  
E. Bilinski
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Rainbow Trout ◽  
Fatty Acid Oxidation ◽  
White Muscle ◽  
Acid Oxidation ◽  
Muscular Tissue ◽  
Tissue Slices ◽  
Dark Muscle ◽  
Pronounced Difference

The ability of the muscular tissue of fish to oxidize fatty acids has been studied on rainbow trout (Salmo gairdnerii). The rate of oxidation of Na hexanoate-1-C14, K octanoate-1-C14, and K myristate-1-C14by tissue slices from the lateral dark muscle and from the dorsal white muscle was determined at 25 °C by measuring the formation of C14O2. This transformation can be demonstrated in both the white and dark muscle; however, quantitatively a very pronounced difference exists between the two tissues, the dark muscle being more active.

UTILIZATION OF LIPIDS BY FISH: I. FATTY ACID OXIDATION BY TISSUE SLICES FROM DARK AND WHITE MUSCLE OF RAINBOW TROUT (SALMO GAIRDNERII)

1963 ◽  
Vol 41 (1) ◽  
pp. 107-112 ◽  
Author(s):  
E. Bilinski
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Rainbow Trout ◽  
Fatty Acid Oxidation ◽  
White Muscle ◽  
Acid Oxidation ◽  
Muscular Tissue ◽  
Tissue Slices ◽  
Dark Muscle ◽  
Pronounced Difference

The ability of the muscular tissue of fish to oxidize fatty acids has been studied on rainbow trout (Salmo gairdnerii). The rate of oxidation of Na hexanoate-1-C14, K octanoate-1-C14, and K myristate-1-C14by tissue slices from the lateral dark muscle and from the dorsal white muscle was determined at 25 °C by measuring the formation of C14O2. This transformation can be demonstrated in both the white and dark muscle; however, quantitatively a very pronounced difference exists between the two tissues, the dark muscle being more active.

UTILIZATION OF LIPIDS BY FISH: II. FATTY ACID OXIDATION BY A PARTICULATE FRACTION FROM LATERAL LINE MUSCLE

1964 ◽  
Vol 42 (3) ◽  
pp. 345-352 ◽  
Author(s):  
E. Bilinski ◽  
R. E. E. Jonas
Keyword(s):  
Fatty Acid ◽  
Rainbow Trout ◽  
Fatty Acid Oxidation ◽  
Lateral Line ◽  
Sockeye Salmon ◽  
Tricarboxylic Acid Cycle ◽  
Tricarboxylic Acid ◽  
Acid Oxidation ◽  
Acid Cycle ◽  
Tricarboxylic Acid Cycle Intermediates

The fatty acid oxidizing system present in lateral line muscle of rainbow trout (Salmo gairdnerii) and sockeye salmon (Oncorhynchus nerka) was studied by using subcellular particles, having the sedimentation characteristics of mitochondria. The rate of oxidation of K-myristate-1-C14, K-octanoate-1-C14, and Na-hexanoate-1-C14 was determined at 25 °C by measuring the formation of C14O2. Oxidation was stimulated by adenosine triphosphate Mg++, coenzyme A and tricarboxylic acid cycle intermediates, but not by cytochrome c. It was optimum at pH 7.5–8.5.The data are consistent with the assumption that in the lateral line muscle fatty acid oxidation takes place through the known mechanism involving CoA derivatives.

scholarly journals Mitochondrial Fission Governed by Drp1 Regulates Exogenous Fatty Acid Usage and Storage in Hela Cells

Metabolites ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 322
Author(s):  
Jae-Eun Song ◽  
Tiago C. Alves ◽  
Bernardo Stutz ◽  
Matija Šestan-Peša ◽  
Nicole Kilian ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Lipid Droplets ◽  
Mitochondrial Fission ◽  
Acid Oxidation ◽  
Mitochondrial Morphology ◽  
Mitochondrial Fatty Acid Oxidation ◽  
Mitochondrial Fatty Acid ◽  
And Storage

In the presence of high abundance of exogenous fatty acids, cells either store fatty acids in lipid droplets or oxidize them in mitochondria. In this study, we aimed to explore a novel and direct role of mitochondrial fission in lipid homeostasis in HeLa cells. We observed the association between mitochondrial morphology and lipid droplet accumulation in response to high exogenous fatty acids. We inhibited mitochondrial fission by silencing dynamin-related protein 1(DRP1) and observed the shift in fatty acid storage-usage balance. Inhibition of mitochondrial fission resulted in an increase in fatty acid content of lipid droplets and a decrease in mitochondrial fatty acid oxidation. Next, we overexpressed carnitine palmitoyltransferase-1 (CPT1), a key mitochondrial protein in fatty acid oxidation, to further examine the relationship between mitochondrial fatty acid usage and mitochondrial morphology. Mitochondrial fission plays a role in distributing exogenous fatty acids. CPT1A controlled the respiratory rate of mitochondrial fatty acid oxidation but did not cause a shift in the distribution of fatty acids between mitochondria and lipid droplets. Our data reveals a novel function for mitochondrial fission in balancing exogenous fatty acids between usage and storage, assigning a role for mitochondrial dynamics in control of intracellular fuel utilization and partitioning.

Meal composition affects postprandial fatty acid oxidation

1993 ◽  
Vol 264 (6) ◽  
pp. R1065-R1070 ◽  
Author(s):  
D. M. Surina ◽  
W. Langhans ◽  
R. Pauli ◽  
C. Wenk
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Nutrient Utilization ◽  
Whole Body ◽  
Acid Oxidation ◽  
Plasma Ffa ◽  
Hepatic Fatty Acid Oxidation ◽  
Beta Hydroxybutyrate ◽  
Chain Fatty Acids

The influence of macronutrient content of a meal on postprandial fatty acid oxidation was investigated in 13 Caucasian males after consumption of a high-fat (HF) breakfast (33% carbohydrate, 52% fat, 15% protein) and after an equicaloric high-carbohydrate (HC) breakfast (78% carbohydrate, 6% fat, 15% protein). The HF breakfast contained short- and medium-chain fatty acids, as well as long-chain fatty acids. Respiratory quotient (RQ) and plasma beta-hydroxybutyrate (BHB) were measured during the 3 h after the meal as indicators of whole body substrate oxidation and hepatic fatty acid oxidation, respectively. Plasma levels of free fatty acids (FFA), triglycerides, glucose, insulin, and lactate were also determined because of their relationship to nutrient utilization. RQ was significantly lower and plasma BHB was higher after the HF breakfast than after the HC breakfast, implying that more fat is burned in general and specifically in the liver after an HF meal. As expected, plasma FFA and triglycerides were higher after the HF meal, and insulin and lactate were higher after the HC meal. In sum, oxidation of ingested fat occurred in response to a single HF meal.

scholarly journals Effect of Medium-Chain Fatty Acids-Containing Dietary Oil on Hepatic Fatty Acid Oxidation Enzyme Activity in Rats.

2002 ◽  
Vol 51 (10) ◽  
pp. 621-626 ◽  
Author(s):  
Hisami SHINOHARA ◽  
Hatsumi SHIMADA ◽  
Osamu NOGUCHI ◽  
Fumie KUBOTA ◽  
Toshiaki AOYAMA
Keyword(s):  
Fatty Acids ◽  
Enzyme Activity ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Acid Oxidation ◽  
Medium Chain ◽  
Fatty Acid Oxidation Enzyme ◽  
Hepatic Fatty Acid Oxidation ◽  
Dietary Oil ◽  
Oxidation Enzyme

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 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
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