Oxidative energy metabolism in equine tendon cells

1997 ◽  
Vol 62 (2) ◽  
pp. 93-97 ◽  
Author(s):  
H.L Birch ◽  
G.A Rutter ◽  
A.E Goodship
Keyword(s):  
Energy Metabolism ◽  
Oxidative Energy Metabolism ◽  
Tendon Cells

scholarly journals Metabolic Profiling of Hearts Exposed to Sevoflurane and Propofol Reveals Distinct Regulation of Fatty Acid and Glucose Oxidation

2010 ◽  
Vol 113 (3) ◽  
pp. 541-551 ◽  
Author(s):  
Lianguo Wang ◽  
Kerry W. S. Ko ◽  
Eliana Lucchinetti ◽  
Liyan Zhang ◽  
Heinz Troxler ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Energy Metabolism ◽  
Lipid Rafts ◽  
Metabolic Profiling ◽  
Glucose Oxidation ◽  
Molecular Mechanisms ◽  
Glucose Transporter ◽  
Left Ventricular ◽  
Glucose Transporter 4 ◽  
Oxidative Energy Metabolism

Background Myocardial energy metabolism is a strong predictor of postoperative cardiac function. This study profiled the metabolites and metabolic changes in the myocardium exposed to sevoflurane, propofol, and Intralipid and investigated the underlying molecular mechanisms. Methods Sevoflurane (2 vol%) and propofol (10 and 100 microM) in the formulation of 1% Diprivan (AstraZeneca Inc., Mississauga, ON, Canada) were compared for their effects on oxidative energy metabolism and contractility in the isolated working rat heart model. Intralipid served as a control. Substrate flux through the major pathways for adenosine triphosphate generation in the heart, that is, fatty acid and glucose oxidation, was measured using [H]palmitate and [C]glucose. Biochemical analyses of nucleotides, acyl-CoAs, ceramides, and 32 acylcarnitine species were used to profile individual metabolites. Lipid rafts were isolated and used for Western blotting of the plasma membrane transporters CD36 and glucose transporter 4. Results Metabolic profiling of the hearts exposed to sevoflurane and propofol revealed distinct regulation of fatty acid and glucose oxidation. Sevoflurane selectively decreased fatty acid oxidation, which was closely related to a marked reduction in left ventricular work. In contrast, propofol at 100 microM but not 10 microM increased glucose oxidation without affecting cardiac work. Sevoflurane decreased fatty acid transporter CD36 in lipid rafts/caveolae, whereas high propofol increased pyruvate dehydrogenase activity without affecting glucose transporter 4, providing mechanisms for the fuel shifts in energy metabolism. Propofol increased ceramide formation, and Intralipid increased hydroxy acylcarnitine species. Conclusions Anesthetics and their solvents elicit distinct metabolic profiles in the myocardium, which may have clinical implications for the already jeopardized diseased heart.

scholarly journals Aspartoacylase Supports Oxidative Energy Metabolism during Myelination

2012 ◽  
Vol 32 (9) ◽  
pp. 1725-1736 ◽  
Author(s):  
Jeremy S Francis ◽  
Louise Strande ◽  
Vladamir Markov ◽  
Paola Leone
Keyword(s):  
Energy Metabolism ◽  
Postnatal Development ◽  
Strong Association ◽  
Canavan Disease ◽  
Lipid Synthesis ◽  
Systematic Analysis ◽  
Early Postnatal Development ◽  
Neuronal Viability ◽  
Oxidative Energy Metabolism ◽  
The Brain

The inherited leukodystrophy Canavan disease arises due to a loss of the ability to catabolize N-acetylaspartic acid (NAA) in the brain and constitutes a major point of focus for efforts to define NAA function. Accumulation of noncatabolized NAA is diagnostic for Canavan disease, but contrasts with the abnormally low NAA associated with compromised neuronal integrity in a broad spectrum of other clinical conditions. Experimental evidence for NAA function supports a role in white matter lipid synthesis, but does not explain how both elevated and lowered NAA can be associated with pathology in the brain. We have undertaken a systematic analysis of postnatal development in a mouse model of Canavan disease that delineates development and pathology by identifying markers of oxidative stress preceding oligodendrocyte loss and dysmyelination. These data suggest a role for NAA in the maintenance of metabolic integrity in oligodendrocytes that may be of relevance to the strong association between NAA and neuronal viability. N-acetylaspartic acid is proposed here to support lipid synthesis and energy metabolism via the provision of substrate for both cellular processes during early postnatal development.

scholarly journals Mitochondrial oxidative energy metabolism in guanethidine-induced sympathectomized ducklings

2014 ◽  
Vol 33 (01) ◽  
pp. 91-97
Author(s):  
Younes Filali-Zegzouti ◽  
Jean-Louis Rouanet ◽  
Toufiq Fechtali ◽  
Damien Roussel
Keyword(s):  
Energy Metabolism ◽  
Oxidative Energy Metabolism

Evidence that levels of malate dehydrogenase and fumarase are increased by cAMP in rat myotubes

1984 ◽  
Vol 247 (1) ◽  
pp. C33-C38 ◽  
Author(s):  
J. C. Lawrence ◽  
W. J. Salsgiver
Keyword(s):  
Energy Metabolism ◽  
Malate Dehydrogenase ◽  
Potential Role ◽  
Primary Cultures ◽  
Phosphodiesterase Inhibitors ◽  
Dibutyryl Camp ◽  
Rat Skeletal Muscle ◽  
Oxidative Energy Metabolism ◽  
Enzymes Of Energy Metabolism

We have investigated the potential role of adenosine 3',5'-cyclic monophosphate (cAMP) in controlling levels of enzymes of energy metabolism in primary cultures of rat skeletal muscle cells. Incubating myotubes with cholera toxin or forskolin (2 persistent activators of adenylate cyclase) significantly increased the levels of two enzymes of oxidative metabolism, fumarase and malate dehydrogenase. These enzymes were also increased (1.5- to 2.0-fold) by phosphodiesterase inhibitors (caffeine, theophylline, theobromine, 3-isobutyl-1-methylxanthine, papaverine, MJ 1988, Ro 20–1724, or SQ 20009) and the cAMP derivatives: 8-bromo-cAMP or dibutyryl cAMP. In contrast two enzymes of glycolytic metabolism, lactate dehydrogenase and pyruvate kinase, were not consistently affected by these agents. The results presented provide strong evidence that an increase in cAMP can lead to an increase in certain enzymes of oxidative energy metabolism.

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