Titlebook: Cardiac Energy Metabolism in Health and Disease; Gary D. Lopaschuk,Naranjan S. Dhalla Book 2014 Springer Science+Business Media New York 2

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arrhythmic

Lipoproteins: A Source of Cardiac Lipidshesized in the liver and they obtain their mature form following interaction with enzymes that are present in the circulation. Lipoprotein-derived fatty acids are released by lipoprotein lipase and are then taken up by cardiomyocytes either passively or via fatty acid receptors, such as CD36. Uptake

JUST

Role of Lipoprotein Lipase in Fatty Acid Delivery to the Heartnagement predisposes the patient to heart failure, which is the leading cause of diabetes related deaths. One instigator for this cardiac dysfunction is change in fuel utilization by the heart. Thus, following diabetes, when cardiac glucose utilization is impaired, the heart undergoes metabolic tran

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Control of Myocardial Fatty Acid Uptakel carbohydrate (glucose, lactate) uptake have been unraveled in detail in the 1990s, insight into fatty acid uptake originates from more recent studies. Fatty acid movement across the sarcolemma is facilitated by membrane-associated proteins, specifically CD36, membrane-associated fatty acid-binding

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泥沼

泥沼

Relationship Between Substrate Metabolism and Cardiac Efficiencysm with efficient ATP generation and utilization. As ATP is primarily derived from mitochondrial oxidative phosphorylation, myocardial oxygen consumption (MVO.) can be used to measure the rate of energy expenditure of the heart. Although cardiac efficiency is an ambiguous term, it commonly embraces

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The Myocardial Creatine Kinase System in the Normal, Ischaemic and Failing Heartnd energy utilising ATPases. It acts as an energy storage and transport mechanism and maintains favourable local ATP/ADP ratios, thereby supporting further energy production and high levels of free energy from ATP hydrolysis. Down-regulation of CK activity and myocardial creatine levels is a univers