Parallel activation of mitochondrial oxidative metabolism with increased cardiac energy expenditure is not dependent on fatty acid oxidation in pigs.

Parallel activation of mitochondrial oxidative metabolism with increased cardiac energy expenditure is not dependent on fatty acid oxidation in pigs. Research Abstract Details 

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Parallel activation of mitochondrial oxidative metabolism with increased cardiac energy expenditure is not dependent on fatty acid oxidation in pigs. Abstract Text:

Lufang Zhou,Marco E Cabrera,Hazel Huang,Celvie L Yuan,Duda K Monika,Naveen Sharma,Fang Bian,William C Stanley,

Steady state concentrations of ATP and ADP in vivo are similar at low and high cardiac workloads; however, the mechanisms that regulate the activation of substrate metabolism and oxidative phosphorylation that supports this stability are poorly understood. We tested the hypotheses that (1) there is parallel activation of mitochondrial and cytosolic dehydrogenases in the transition from low to high workload, which increases NADH/NAD+ ratio in both compartments, and (2) this response does not require an increase in fatty acid oxidation (FAO). Anaesthetized pigs were subjected to either sham treatment, or an abrupt increase in cardiac workload for 5 min with dobutamine infusion and aortic constriction. Myocardial oxygen consumption and FAO were increased 3- and 2-fold, respectively, but ATP and ADP concentrations did not change. NADH-generating pathways were rapidly activated in both the cytosol and mitochondria, as seen in a 40% depletion in glycogen stores, a 3.6-fold activation of pyruvate dehydrogenase, and a 50% increase in tissue NADH/NAD+. Simulations from a multicompartmental computational model of cardiac energy metabolism predicted that parallel activation of glycolysis and mitochondrial metabolism results in an increase in the NADH/NAD+ ratio in both cytosol and mitochondria. FAO was blocked by 75% in a third group of pigs, and a similar increase in and the NAHD/NAD+ ratio was observed. In conclusion, in the transition to a high cardiac workload there is rapid parallel activation of substrate oxidation that results in an increase in the NADH/NAD+ ratio.

Parallel activation of mitochondrial oxidative metabolism with increased cardiac energy expenditure is not dependent on fatty acid oxidation in pigs. Publishing Authors By Initials

L Zhou,ME Cabrera,H Huang,CL Yuan,DK Monika,N Sharma,F Bian,WC Stanley,

For similar circulatory and respiratory physiology: cardiovascular physiology: cardiovascular physiologic phenomena: hemodynamics: ventricular pressure research abstracts see: circulatory and respiratory physiology: cardiovascular physiology: cardiovascular physiologic phenomena: hemodynamics: ventricular pressure research

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Parallel activation of mitochondrial oxidative metabolism with increased cardiac energy expenditure is not dependent on fatty acid oxidation in pigs. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: The Journal of physiology

VOLUME: 579

Page Numbers: 811-21

Journal Abbreviation: J. Physiol. (Lond.)

ISSN: 0022-3751

DAY: 21

MONTH: 12

YEAR: 2006

Parallel activation of mitochondrial oxidative metabolism with increased cardiac energy expenditure is not dependent on fatty acid oxidation in pigs. Information

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LANGUAGE: eng

NlmUniqueID: 266262

Parallel activation of mitochondrial oxidative metabolism with increased cardiac energy expenditure is not dependent on fatty acid oxidation in pigs. Keywords Mesh Terms:

KEYWORDS: Ventricular Pressure

MESH TERMS: physiology

Chemical & Substance for Abstract: Parallel activation of mitochondrial oxidative metabolism with increased cardiac energy expenditure is not dependent on fatty acid oxidation in pigs. Information

Substance Name: Adenosine Diphosphate

Registry Number: 58-64-0

Grant and Affiliation Information for Parallel activation of mitochondrial oxidative metabolism with increased cardiac energy expenditure is not dependent on fatty acid oxidation in pigs.

AFFILIATION: Department of Biomedical Engineering, Case Western Reserve University, Cleveland, OH 44106, USA.

Country: England

AGENCY: United States NHLBI

GRANT: HL074237

ACRONYM: HL

MEDLINETA: J Physiol

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