scholarly journals Plasma acylcarnitine profiling indicates increased fatty acid oxidation relative to tricarboxylic acid cycle capacity in young, healthy low birth weight men

2016 ◽  
Vol 4 (19) ◽  
pp. e12977 ◽  
Author(s):  
Amalie Ribel-Madsen ◽  
Rasmus Ribel-Madsen ◽  
Charlotte Brøns ◽  
Christopher B. Newgard ◽  
Allan A. Vaag ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Birth Weight ◽  
Low Birth Weight ◽  
Fatty Acid Oxidation ◽  
Tricarboxylic Acid Cycle ◽  
Tricarboxylic Acid ◽  
Acid Oxidation ◽  
Acid Cycle

scholarly journals Detection of myocardial medium‐chain fatty acid oxidation and tricarboxylic acid cycle activity with hyperpolarized [1– 13 C]octanoate

2020 ◽  
Vol 33 (3) ◽  
Author(s):  
Hikari A.I. Yoshihara ◽  
Jessica A.M. Bastiaansen ◽  
Magnus Karlsson ◽  
Mathilde H. Lerche ◽  
Arnaud Comment ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Tricarboxylic Acid Cycle ◽  
Tricarboxylic Acid ◽  
Chain Fatty Acid ◽  
Medium Chain Fatty Acid ◽  
Acid Oxidation ◽  
Acid Cycle ◽  
Medium Chain

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 Logical modelling reveals the PDC-PDK interaction as the regulatory switch driving metabolic flexibility at the cellular level

2019 ◽  
Vol 14 (1) ◽  
Author(s):  
Samar HK Tareen ◽  
Martina Kutmon ◽  
Ilja CW Arts ◽  
Theo M de Kok ◽  
Chris T Evelo ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Pyruvate Dehydrogenase ◽  
Tricarboxylic Acid Cycle ◽  
Pyruvate Dehydrogenase Complex ◽  
Tricarboxylic Acid ◽  
Cellular Level ◽  
Acid Oxidation ◽  
Metabolic Flexibility ◽  
Acid Cycle

Abstract Background Metabolic flexibility is the ability of an organism to switch between substrates for energy metabolism, in response to the changing nutritional state and needs of the organism. On the cellular level, metabolic flexibility revolves around the tricarboxylic acid cycle by switching acetyl coenzyme A production from glucose to fatty acids and vice versa. In this study, we modelled cellular metabolic flexibility by constructing a logical model connecting glycolysis, fatty acid oxidation, fatty acid synthesis and the tricarboxylic acid cycle, and then using network analysis to study the behaviours of the model. Results We observed that the substrate switching usually occurs through the inhibition of pyruvate dehydrogenase complex (PDC) by pyruvate dehydrogenase kinases (PDK), which moves the metabolism from glycolysis to fatty acid oxidation. Furthermore, we were able to verify four different regulatory models of PDK to contain known biological observations, leading to the biological plausibility of all four models across different cells and conditions. Conclusion These results suggest that the cellular metabolic flexibility depends upon the PDC-PDK regulatory interaction as a key regulatory switch for changing metabolic substrates.

Biochemical studies on ovine pregnancy toxaemia. I. Enzymic activities of liver and brain

1959 ◽  
Vol 10 (6) ◽  
pp. 854 ◽  
Author(s):  
CH Gallagher
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Tricarboxylic Acid Cycle ◽  
Liver Mitochondria ◽  
Tricarboxylic Acid ◽  
Acid Oxidation ◽  
Enzyme Preparations ◽  
Acid Cycle ◽  
Sheep Liver ◽  
Pregnancy Toxaemia

Enzymic activities in vitro of liver and brain tissue of sheep with pregnancy toxaemia were measured. Anaerobic glycolysis and oxidations of tricarboxylic acid cycle intermediates and related substrates were normal for both brain and liver enzyme preparations. Fatty acid oxidation by liver mitochondria was abnormal. Liver mitochondria from cases of pregnancy toxaemia were invariably incapable of oxidizing octanoate and palmitate, and frequently unable to oxidize propionate. The rate of propionate oxidation was low even when this substrate was oxidized. Butyrate oxidation was not much reduced by pregnancy toxaemia. Starvation of ewes in late pregnancy did not inactivate the fatty acid oxidation chains of liver mitochondria. Possible reasons for the failure of lipid metabolism are discussed. The dependence of sheep liver metabolism upon fatty acid oxidation is discussed. Insignificant amounts of glucose are absorbed from the alimentary canal in sheep and, even if absorbed, are not catabolized to supply acetyl coenzyme A for oxidation in the tricarboxylic acid cycle. Consequently sheep liver is prone to failure from interference with fatty acid oxidation. Pregnancy toxaemia is discussed in relevance to the disturbance of fatty acid metabolism which is thought to be of considerable significance in the disease.

Effect of experimental dysthyroidism on the enzymatic character of the diaphragm

1984 ◽  
Vol 56 (1) ◽  
pp. 117-121 ◽  
Author(s):  
C. D. Ianuzzo ◽  
V. Chen ◽  
P. O'Brien ◽  
T. G. Keens
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Fiber Type ◽  
Tricarboxylic Acid Cycle ◽  
Minute Ventilation ◽  
Tricarboxylic Acid ◽  
Albino Rats ◽  
Acid Oxidation ◽  
Fiber Types ◽  
Acid Cycle

This study examined the effects of long-term experimental dysthyroidism on the enzymatic character of the costal diaphragm and selected respiratory parameters. Costal diaphragms from thyroidectomized (TX), euthyroid (EU), and hyperthyroid (HT) male albino rats were used. HT was induced by subcutaneous injections of triiodothyronine on alternate days for 6 wk. Minute ventilation was greater for the HT (70%) compared with the TX rats. The enzymatic potentials of glycolysis (28%), tricarboxylic acid cycle (30%), and fatty acid oxidation (16%) were significantly increased in the HT diaphragms, whereas the potentials were lower by a similar relative extent in the TX diaphragms. The proportion of alkali-labile fibers were greater in the TX and lower in the HT diaphragm. The shifts in heart and muscle lactate dehydrogenase isoenzyme activities were consistent with the fiber type changes. These findings show that dysthyroidism modifies the overall enzymatic capacity of the diaphragm (i.e., glycolysis, tricarboxylic acid cycle, and fatty acid oxidation) along with the proportion of alkali-labile to alkali-stable fiber types. These enzymatic changes are similar to those resulting from exercise training, tracheal banding, streptozotocin diabetes, and emphysema.

A new correction factor for use in tracer estimations of plasma fatty acid oxidation

1995 ◽  
Vol 269 (4) ◽  
pp. E649-E656 ◽  
Author(s):  
L. S. Sidossis ◽  
A. R. Coggan ◽  
A. Gastaldelli ◽  
R. R. Wolfe
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Correction Factor ◽  
Tricarboxylic Acid Cycle ◽  
Tricarboxylic Acid ◽  
Acid Oxidation ◽  
Plasma Fatty Acid ◽  
Oxidation Rates ◽  
Breath Co2 ◽  
Isotopic Measurements

The purpose of this study was to acquire a new correction factor for use in tracer estimations of plasma fatty acid oxidation that would fully account for label fixation during the infusion of fatty acid tracers. Thus volunteers were infused with 13C-labeled fatty acids and [1-14C]acetate in the basal state, during hyperinsulinemia-hyperglycemia (clamp), and during 1 h of cycling exercise. The fractional recovery of acetate label (i.e., the acetate correction factor) was 0.56 +/- 0.02, 0.50 +/- 0.03, and 0.80 +/- 0.03 in the basal state and during the clamp and exercise, respectively. Isotopically determined plasma fatty acid oxidation rates (mumol.kg-1.min-1) were 1.7 +/- 0.2, 0.8 +/- 0.2, and 6.4 +/- 0.5 (no correction); 2.1 +/- 0.2, 1.0 +/- 0.2, and 6.7 +/- 0.5 (bicarbonate correction); and 3.1 +/- 0.2, 1.5 +/- 0.2, and 8.2 +/- 0.4 (acetate correction). We conclude that use of the acetate correction factor in place of the bicarbonate correction factor should improve the accuracy of isotopic measurements of plasma fatty acid oxidation, because it accounts for label fixation that might occur at any step between the entrance of labeled acetyl-CoA into the tricarboxylic acid cycle until the recovery of label in breath CO2.

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