Regulation of and intervention into the oxidative pentose phosphate pathway and adenine nucleotide metabolism in the heart

Zimmer, Heinz‐Gerd

doi:10.1007/978-1-4613-1279-6_14

Cited by 10 publications

(13 citation statements)

References 43 publications

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“…ATP content in the remote, noninfarcted area of the heart was higher in the D-ribose-treated rats, and the elevation in left ventricular end-diastolic pressure that occurred was not as pronounced. This suggests that D-ribose administration preserves adenine nucleotide synthesis in the remote, noninfarcted zones and allows better overall cardiac function following a regional infarction (4,42).…”

Section: D-ribose In Cardiac Hypertrophy and Cardiomyopathymentioning

confidence: 97%

“…In addition, it indicates that exogenous supplementation can overcome the limitation. DRibose infusion enhances the functional parameter dP/dtlll<lx in catheter-instrumented rats receiving isoproterenol (4,30). Furthermore, in conjunction with adenine or inosine, D-ribose supplementation prevents the ATP depletion that occurs with isoproterenol administration (38,39).…”

Section: D-ribose In Cardiac Hypertrophy and Cardiomyopathymentioning

confidence: 97%

“…As a result, the activity of the enzymes that control the hexose monophosphate shunt: glucose 6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase (Fig. 2) are low in terminally differentiated cardiac cells (4).…”

Section: Hexose Monophosphate Shunt and Nucleotide Salvage Pathways Imentioning

confidence: 99%

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D-Ribose as a Supplement for Cardiac Energy Metabolism

Pauly

Pepine

2000

J Cardiovasc Pharmacol Ther

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Metabolic support for the heart has been an attractive concept since the pioneering work of Sodi-Pallares et al. four decades ago.* Recently, interest has increased in the use of over-the-counter supplements and naturally occurring nutriceuticals for enhancement of cardiac and skeletal muscle performance. These include amino acids such as creatine, L-carnitine, and L-arginine, as well as vitamins and cofactors such as alpha-tocopherol and coenzyme Q. Like these other molecules, D-ribose is a naturally occurring compound. It is the sugar moiety of ATP and has also received interest as a metabolic supplement for the heart. The general hypothesis is that under certain pathologic cardiac conditions, nucleotides (particularly ATP, ADP, and AMP) are degraded and lost from the heart. The heart's ability to resynthesize ATP is then limited by the supply of D-ribose, which is a necessary component of the adenine nucleotide structure. In support of this hypothesis, recent reports have used D-ribose to increase tolerance to myocardial ischemia. Its use in patients with stable coronary artery disease improves time to exercise-induced angina and electrocardiographic changes. In conjunction with thallium imaging or dobutamine stress echocardiography, D-ribose supplementation has been used to enhance detection of hibernating myocardium. In this article, we review the biochemical basis for using supplemental D-ribose as metabolic support for the heart and discuss the experimental evidence for its benefit.

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Section: D-ribose In Cardiac Hypertrophy and Cardiomyopathymentioning

confidence: 97%

Section: D-ribose In Cardiac Hypertrophy and Cardiomyopathymentioning

confidence: 97%

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D-Ribose as a Supplement for Cardiac Energy Metabolism

Pauly

Pepine

2000

J Cardiovasc Pharmacol Ther

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“…It has been shown that induction of cardiac hypertrophy results in an upregulation of glucose-6-P dehydrogenase which is believed to be the ratedetermining enzyme in the pentose phosphate pathway [114]. It is tempting to speculate that this may result in an enhanced availability of carbohydrate intermediates such as xylulose-5-phosphate, that are thought to act as signalling molecules involved in glucose sensing.…”

Section: Glucose Sensing In the Heartmentioning

confidence: 99%

Transcriptional regulation of metabolic processes: implications for cardiac metabolism

Bilsen¹,

Vusse²,

Reneman³

1998

Pfl�gers Archiv European Journal of Physiology

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Under normal conditions the oxidation of fatty acids and glucose covers, respectively, approximately 65% and 30% of the energy demand of the beating heart. Evidence is accumulating that various pathophysiological conditions are associated with overt changes in cardiac energy metabolism. For instance, in diabetes cardiac energy conversion relies even more on fatty acid than on glucose oxidation. In contrast, during cardiac hypertrophy the opposite takes place, i. e. the utilization of carbohydrates increases at the expense of lipids. The mechanisms responsible for and the significance of these metabolic adaptations are largely unknown. A growing body of evidence indicates that these metabolic adaptations are brought about, at least in part, through adjustments in the rate of transcription of genes encoding proteins involved in substrate transport and metabolism. There are reasons to believe that the transcriptional regulation of these "metabolic genes" is subject to modulation by metabolites per se, i.e. by oxygen, glucose and fatty acids. In this review the concept of metabolic remodelling as an important facet of cardiac adaptation to chronic pathophysiological conditions is introduced and the putative roles of metabolites in transcriptional regulation in the heart are considered.

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“…Not all processes requiring ATP are controlled by the nonlethal range of ATP fluctuations. In contrast to ATP, the status of the entire redox network or its components can vary markedly as part of normal cell hmction (Gilbert, 1984;Ziegler, 1985;Prinz et al, 1997;Meister, 1994Meister, ,1995Chen et al, 1995;Wong et al, 1995;Sen and Packer 1996;Zimmer, 1996;Nakamura et al, 1997;Anderson, 1998;Cotgreave and Gerdes, 1998;DiSimplicio et al, 1998;Roy and Packer, 1998;Arrigo, 1999;Atalay and Sen, 1999;Sen, 1999).…”

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confidence: 96%

Redox Control of Protein Degradation

Lockwood

2000

Antioxidants & Redox Signaling

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This review summarizes evidence that most of cell protein degradation is maintained by pathways transferring energy from glucose to reduction of enzymic and nonenzymic proteins (redox-responsive). In contrast, a major subcomponent of proteolysis is simultaneously independent of the cell redox network (redox-unresponsive). Thus far, direct and indirect redox-responsive proteolytic effector mechanisms characterized by various investigators include: several classes of proteases, some peptide protease inhibitors, substrate conjugation systems, substrate redox and folding status, cytoskeletal-membrane kinesis, metal homeostasis, and others. The present focus involves redox control of sulfhydryl proteases and proteolytic pathways of mammalian muscle; however, other mechanisms, cell types, and species are also surveyed. The diversity of redox-responsive catabolic mechanisms reveals that the machinery of protein turnover evolved with fundamental dependencies upon the cell redox network, as observed in many species. The net redox status of a reversible proteolytic effector mechanism represents the balance between combined oxidative inactivating influences versus reductive activating influences. Similar to other proteins, redox-responsive proteolytic effectors appear to be oxidized by mixed disulfide formation, nitrosation, reactive oxygen species, and associations or reactions with metal ions and various pro-oxidative metabolites. Systems reducing the proteolytic machinery include major redox enzyme chains, such as thioredoxins or glutaredoxins, and perhaps various reductive metabolites, including glutathione and dihydrolipoic acid. Much of mammalian intracellular protein degradation is reversibly responsive to noninjurious experimental intervention in the reductive energy supply-demand balance. Proteolysis is reversibly inhibited by diamide or dehydroascorbic acid; and such antiproteolytic actions are strongly dependent on the cell glucose supply. However, gross redox-responsive proteolysis is not accompanied by ATP depletion or vice versa. Redox-responsive proteolysis includes Golgi-endoplasmic reticulum degradation, lysosomal degradation, and some amount of extravesicular degradation, all comprising more than half of total cell proteolysis. Speculatively, redox-dependent proteolysis exhibits features expected of a controlling influence coordinating distinct proteolytic processes under some intracellular conditions.

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Regulation of and intervention into the oxidative pentose phosphate pathway and adenine nucleotide metabolism in the heart

Cited by 10 publications

References 43 publications

D-Ribose as a Supplement for Cardiac Energy Metabolism

D-Ribose as a Supplement for Cardiac Energy Metabolism

Transcriptional regulation of metabolic processes: implications for cardiac metabolism

Redox Control of Protein Degradation

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