Myocardial Energy Metabolism

Lh, Opie

doi:10.1159/000395454

Cited by 28 publications

(12 citation statements)

References 21 publications

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“…AMP, ADP, and inorganic phosphate are the positive effectors for PFK-1, which accelerates glycolytic flux when ATP level drops. On the other hand, ATP, proton and fructose 1,6-bisphosphate can inhibit PFK-1 activity (166, 219). Citrate, generated by TCA cycle as well as long chain fatty acids is a negative regulator of PFK-1, thus, linking mitochondrial oxidative metabolism to glycolysis (63, 92).…”

Section: Glucose Metabolism In the Heartmentioning

confidence: 99%

“…Fructose 2,6-bisphosphate can activate PFK-1 even in the presence of ATP by increasing the affinity of the enzyme for fructose 6-phosphate and by decreasing the inhibitory effects of ATP on PFK-1 (219). Conditions that stimulate glycolysis, such as insulin, adrenergic stimulation can increase the activity of PFK-2 (166, 219). Phosphorylation by AMPK causes PFK-2 activation, which serves as an essential mechanism to promote glycolysis in ischemia heart (143).…”

Section: Glucose Metabolism In the Heartmentioning

confidence: 99%

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Glucose Transporters in Cardiac Metabolism and Hypertrophy

Shao

Tian

2015

Comprehensive Physiology

206

173

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The heart is adapted to utilize all classes of substrates to meet the high-energy demand, and it tightly regulates its substrate utilization in response to environmental changes. Although fatty acids are known as the predominant fuel for the adult heart at resting stage, the heart switches its substrate preference toward glucose during stress conditions such as ischemia and pathological hypertrophy. Notably, increasing evidence suggests that the loss of metabolic flexibility associated with increased reliance on glucose utilization contribute to the development of cardiac dysfunction. The changes in glucose metabolism in hypertrophied hearts include altered glucose transport and increased glycolysis. Despite the role of glucose as an energy source, changes in other nonenergy producing pathways related to glucose metabolism, such as hexosamine biosynthetic pathway and pentose phosphate pathway, are also observed in the diseased hearts. This article summarizes the current knowledge regarding the regulation of glucose transporter expression and translocation in the heart during physiological and pathological conditions. It also discusses the signaling mechanisms governing glucose uptake in cardiomyocytes, as well as the changes of cardiac glucose metabolism under disease conditions.

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Section: Glucose Metabolism In the Heartmentioning

confidence: 99%

Section: Glucose Metabolism In the Heartmentioning

confidence: 99%

Glucose Transporters in Cardiac Metabolism and Hypertrophy

Shao

Tian

2015

Comprehensive Physiology

206

173

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“…Switching from free fatty acid to lactate can result in a reduction of O 2 consumption, because lactate is a more efficient fuel and may account for a Ϸ10% reduction of MV O 2 . 103,104 In conscious dogs, the stimulation of free fatty acid uptake by lipid infusion caused…”

Section: Regulation Of O 2 Consumption In Vivomentioning

confidence: 99%

Role of Endothelium-Derived Nitric Oxide in the Regulation of Cardiac Oxygen Metabolism

Trochu

Bouhour

Kaley

et al. 2000

Circulation Research

149

100

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Endothelium-derived NO is considered to be primarily an important determinant of vascular tone and platelet activity; however, the modulation of myocardial metabolism by NO may be one of its most important roles. This modulation may be critical for the regulation of tissue metabolism. Several physiological processes act in concert to make endothelial NO synthase-derived NO potentially important in the regulation of mitochondrial respiration in cardiac tissue, including (1) the nature of the capillary network in the myocardium, (2) the diffusion distance for NO, (3) the low toxicity of NO at physiological (nanomolar) concentrations, (4) the fact that low PO(2) in tissue facilitates the action of NO on cytochrome oxidase, and (5) the formation of oxygen free radicals. A decrease in NO production is involved in the pathophysiological modifications that occur in heart failure and diabetes, disease states associated with altered cardiac metabolism that contributes to the evolution of the disease process. In contrast, several drugs (eg, angiotensin-converting enzyme inhibitors, amlodipine, and statins) can restore or maintain endogenous production of NO by endothelial cells, and this mechanism may explain part of their therapeutic efficiency. Thus, the purpose of this review is to critically evaluate the role of NO in the control of mitochondrial respiration, with special emphasis on its effect on cardiac metabolism.

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“…Glycogen levels are closely related to myocardial function after CPB. 16,[18][19][20][21][22] Gradinac and colleagues 10 gave GIK solution postoperatively to patients requiring balloon pump support. They observed that the mean cardiac index increased and the requirement for mechanical and pharmacological support decreased.…”

Section: Discussionmentioning

confidence: 99%

“…Preoperative pulmonary capillary wedge pressure (mm Hg) 18 During resection of the mitral valve apparatus, biopsy samples (0.5 to 1 g) of papillary muscle were obtained and stored in liquid nitrogen. The glycogen content of these samples was measured biochemically.…”

Section: Introductionmentioning

confidence: 99%

Benefits of Glucose-Insulin-Potassium before Mitral Valve Replacement

Tünerir¹,

Aslan²,

Işıksoy

et al. 1998

Asian Cardiovasc Thorac Ann

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Of 30 consecutive patients undergoing mitral valve replacement, 15 were randomly assigned to receive pretreatment with glucose-insulin-potassium, while the other 15 received the same volume of normal saline. The characteristics of both groups were similar and all patients were in New York Heart Association functional class III or IV. Papillary muscle samples were obtained at the time of surgery and analyzed for glycogen both biochemically and histochemically. The clinical course was monitored closely during the first 24 hours after surgery. The treated patients had significantly higher glycogen levels (mean, 43 ± 13.54 µmol·g -1 ) in their heart muscle samples compared to the controls (mean, 22 ± 10.39 µmol·g -1 ). The treated patients required less pharmacological inotropic support and they had fewer ventricular arrhythmias and more favorable cardiac output and systemic vascular resistance. However, there was no difference in postoperative pulmonary capillary wedge pressure or mortality between the 2 groups. It was concluded that pretreatment with glucose-insulin-potassium had a significant myocardial protective effect in patients in advanced functional class undergoing mitral valve replacement.

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Myocardial Energy Metabolism

Cited by 28 publications

References 21 publications

Glucose Transporters in Cardiac Metabolism and Hypertrophy

Glucose Transporters in Cardiac Metabolism and Hypertrophy

Role of Endothelium-Derived Nitric Oxide in the Regulation of Cardiac Oxygen Metabolism

Benefits of Glucose-Insulin-Potassium before Mitral Valve Replacement

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