Journal
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM
Volume 303, Issue 3, Pages E308-E321Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpendo.00054.2012
Keywords
nicotinamide adenine dinucleotide; sirtuin-1; sirtuin-3; poly(ADP-ribose) polymerase; COOH-terminal binding protein
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Funding
- National Institutes of Health [R24 HD-050837, P30 AR-058878-02]
- UCSD/UCLA Diabetes and Endocrinology Research Center [P30 DK-063491]
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White AT, Schenk S. NAD(+)/NADH and skeletal muscle mitochondrial adaptations to exercise. Am J Physiol Endocrinol Metab 303: E308-E321, 2012. First published March 27, 2012; doi: 10.1152/ajpendo. 00054.2012.-The pyridine nucleotides, NAD(+) and NADH, are coenzymes that provide oxidoreductive power for the generation of ATP by mitochondria. In skeletal muscle, exercise perturbs the levels of NAD(+), NADH, and consequently, the NAD(+)/NADH ratio, and initial research in this area focused on the contribution of redox control to ATP production. More recently, numerous signaling pathways that are sensitive to perturbations in NAD(+)(H) have come to the fore, as has an appreciation for the potential importance of compartmentation of NAD(+)(H) metabolism and its subsequent effects on various signaling pathways. These pathways, which include the sirtuin (SIRT) proteins SIRT1 and SIRT3, the poly(ADP-ribose) polymerase (PARP) proteins PARP1 and PARP2, and COOH-terminal binding protein (CtBP), are of particular interest because they potentially link changes in cellular redox state to both immediate, metabolic-related changes and transcriptional adaptations to exercise. In this review, we discuss what is known, and not known, about the contribution of NAD(+)(H) metabolism and these aforementioned proteins to mitochondrial adaptations to acute and chronic endurance exercise.
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