Regulation of myocardial glucose uptake and transport during ischemia and energetic stress
Autor: | Lawrence H. Young, Raymond R. Russell, Michael J. Caplan, Jian-Ming Ren, Gerald I. Shulman, Raynald Bergeron, Albert J. Sinusas, Renfu Yin |
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Rok vydání: | 1999 |
Předmět: |
medicine.medical_specialty
Monosaccharide Transport Proteins Glucose uptake Myocardial Ischemia Ischemia Muscle Proteins Coronary artery disease Internal medicine medicine Animals Humans Exercise Pressure overload Glucose Transporter Type 1 Glucose Transporter Type 4 biology business.industry Myocardium Adenylate Kinase Glucose transporter Biological Transport medicine.disease Adenosine Adenosine Monophosphate Oxidative Stress Glucose Endocrinology biology.protein GLUT1 Cardiology and Cardiovascular Medicine business GLUT4 medicine.drug |
Zdroj: | The American Journal of Cardiology. 83:25-30 |
ISSN: | 0002-9149 |
DOI: | 10.1016/s0002-9149(99)00253-2 |
Popis: | Myocardial glucose utilization increases in response to the energetic stress imposed on the heart by exercise, pressure overload, and myocardial ischemia. Recruitment of glucose transport proteins is the cellular mechanism by which the heart increases glucose transport for subsequent metabolism. Moderate regional ischemia leads to the translocation of both glucose transporters, GLUT4 and GLUT1, to the sarcolemma in vivo. Myocardial ischemia also stimulates 5'-adenosine monophosphate-activated protein kinase, which may be a fuel gauge in the heart and other tissues signaling the need to turn on energy-generating metabolic pathways. Pharmacologic stimulation of this kinase increases cardiac glucose uptake and transporter translocation, suggesting that it may play an important role in augmenting glucose entry in the setting of ischemic or energetic stress. Thus, recent work has provided insight into the cellular and molecular mechanisms responsible for glucose uptake during energetic stress, which may lead to new approaches to the treatment of patients with coronary artery disease. |
Databáze: | OpenAIRE |
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