scholarly journals The temporal relationship between glycogen phosphorylase and activation of the pyruvate dehydrogenase complex during adrenaline infusion in resting canine skeletal muscle

2002 ◽  
Vol 545 (1) ◽  
pp. 297-304 ◽  
Author(s):  
Paul A. Roberts ◽  
Susan J. G. Loxham ◽  
Simon M. Poucher ◽  
Dumitru Constantin‐Teodosiu ◽  
Paul L. Greenhaff
Keyword(s):  
Skeletal Muscle ◽  
Pyruvate Dehydrogenase ◽  
Glycogen Phosphorylase ◽  
Temporal Relationship ◽  
Pyruvate Dehydrogenase Complex ◽  
Adrenaline Infusion ◽  
Dehydrogenase Complex

scholarly journals Exercise Training Increases the Activity of Pyruvate Dehydrogenase Complex in Skeletal Muscle of Diabetic Rats.

2002 ◽  
Vol 49 (5) ◽  
pp. 547-554 ◽  
Author(s):  
NAOYA NAKAI ◽  
YUTAKA MIYAZAKI ◽  
YUZO SATO ◽  
YOSHIHARU OSHIDA ◽  
MASARU NAGASAKI ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Exercise Training ◽  
Pyruvate Dehydrogenase ◽  
Pyruvate Dehydrogenase Complex ◽  
Diabetic Rats ◽  
Dehydrogenase Complex

scholarly journals Tissue-specific pyruvate dehydrogenase complex deficiency causes cardiac hypertrophy and sudden death of weaned male mice

2008 ◽  
Vol 295 (3) ◽  
pp. H946-H952 ◽  
Author(s):  
Sukhdeep Sidhu ◽  
Ashish Gangasani ◽  
Lioubov G. Korotchkina ◽  
Gen Suzuki ◽  
James A. Fallavollita ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Mouse Model ◽  
Pyruvate Dehydrogenase ◽  
Pyruvate Dehydrogenase Complex ◽  
Left Ventricular ◽  
Oxidative Decarboxylation ◽  
Male Mice ◽  
Wild Type ◽  
Α Subunit ◽  
Dehydrogenase Complex

Pyruvate dehydrogenase complex (PDC) plays an important role in energy homeostasis in the heart by catalyzing the oxidative decarboxylation of pyruvate derived primarily from glucose and lactate. Because various pathophysiological states can markedly alter cardiac glucose metabolism and PDC has been shown to be altered in response to chronic ischemia, cardiac physiology of a mouse model with knockout of the α-subunit of the pyruvate dehydrogenase component of PDC in heart/skeletal muscle (H/SM-PDCKO) was investigated. H/SM-PDCKO mice did not show embryonic lethality and grew normally during the preweaning period. Heart and skeletal muscle of homozygous male mice had very low PDC activity (∼5% of wild-type), and PDC activity in these tissues from heterozygous females was ∼50%. Male mice did not survive for >7 days after weaning on a rodent chow diet. However, they survived on a high-fat diet and developed left ventricular hypertrophy and reduced left ventricular systolic function compared with wild-type male mice. The changes in the heterozygote female mice were of lesser severity. The deficiency of PDC in H/SM-PDCKO male mice greatly compromises the ability of the heart to oxidize glucose for the generation of energy (and hence cardiac function) and results in cardiac pathological changes. This mouse model demonstrates the importance of glucose oxidation in cardiac energetics and function under basal conditions.

Effect of sepsis on activity of pyruvate dehydrogenase complex in skeletal muscle and liver

1986 ◽  
Vol 250 (6) ◽  
pp. E634-E640 ◽  
Author(s):  
T. C. Vary ◽  
J. H. Siegel ◽  
T. Nakatani ◽  
T. Sato ◽  
H. Aoyama
Keyword(s):  
Skeletal Muscle ◽  
Pyruvate Dehydrogenase ◽  
Concentration Ratio ◽  
Coenzyme A ◽  
Pyruvate Dehydrogenase Complex ◽  
Sterile Inflammation ◽  
Active Complex ◽  
Small Abscess ◽  
Dehydrogenase Complex ◽  
Large Abscess

The effect of chronic sepsis on the concentration of active pyruvate dehydrogenase complex has been investigated in liver and skeletal muscle of normal, sterile inflammatory, and chronic septic (small and large abscess) animals. Hyperdynamic sepsis was induced by the intraperitoneal introduction of a rat fecal-agar pellet of known size and bacterial composition (Escherichia coli + Bacteroides fragilis). Total pyruvate dehydrogenase complex activity was not altered in either liver or skeletal muscle in any of the conditions studied. In hepatic tissue, sterile inflammation increased the proportion of active complex 2.5-fold compared with control. The same increase in the concentration of active complex was observed in animals with a small abscess. When the abscess size was increased (large abscess), the concentration of active complex was decreased relative to sterile inflammatory or small abscess septic animals. In contrast to liver, sterile inflammation did not alter the proportion of active complex in skeletal muscle. Sepsis (either small or large septic abscess) resulted in threefold decrease in the concentration of active complex relative to control or sterile inflammatory animals. Changes in the concentration of active complex did not appear to be dependent on the ATP/ADP concentration ratio or tissue pyruvate levels but were consistent with changes in the acetyl-coenzyme A-to-coenzyme A concentration ratio. The mechanism responsible for altered concentration of active complex may be mediated through changes in the activity of the pyruvate dehydrogenase kinase, secondary to alterations in the effector concentration ratios.

Insulin-induced activation of pyruvate dehydrogenase complex in skeletal muscle of diabetic rats

Metabolism ◽  
1993 ◽  
Vol 42 (5) ◽  
pp. 615-623 ◽  
Author(s):  
Pamela W. Feldhoff ◽  
Jame Arnold ◽  
Brett Oesterling ◽  
Thomas C. Vary
Keyword(s):  
Skeletal Muscle ◽  
Pyruvate Dehydrogenase ◽  
Pyruvate Dehydrogenase Complex ◽  
Diabetic Rats ◽  
Dehydrogenase Complex

scholarly journals Pyruvate dehydrogenase activities during the fed-to-starved transition and on re-feeding after acute or prolonged starvation

1989 ◽  
Vol 258 (2) ◽  
pp. 529-533 ◽  
Author(s):  
M J Holness ◽  
M C Sugden
Keyword(s):  
Acute Phase ◽  
Pyruvate Dehydrogenase ◽  
Temporal Relationship ◽  
Pyruvate Dehydrogenase Complex ◽  
Hepatic Glycogen ◽  
Dietary Carbohydrate ◽  
Glycogen Depletion ◽  
Prolonged Starvation ◽  
Complex Activities ◽  
Dehydrogenase Complex

We investigated the temporal relationship between hepatic glycogen depletion and cardiac and hepatic PDH (pyruvate dehydrogenase complex) activities during the acute phase of starvation. There was a striking correlation between the decline in hepatic glycogen and PDH inactivation during the first 10 h of starvation. Re-feeding after 6 h starvation was associated with complete re-activation of PDH in liver and re-activation to approx. 75% of the fed value in heart, whereas in rats previously starved for 24-48 h re-activation was delayed in liver and diminished in heart. The results are discussed with reference to the fate of dietary carbohydrate after re-feeding.

Mechanism responsible for inactivation of skeletal muscle pyruvate dehydrogenase complex in starvation and diabetes

Diabetes ◽  
1999 ◽  
Vol 48 (8) ◽  
pp. 1593-1599 ◽  
Author(s):  
P. Wu ◽  
K. Inskeep ◽  
M. M. Bowker-Kinley ◽  
K. M. Popov ◽  
R. A. Harris
Keyword(s):  
Skeletal Muscle ◽  
Pyruvate Dehydrogenase ◽  
Pyruvate Dehydrogenase Complex ◽  
Dehydrogenase Complex
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