Additive effects of hyperinsulinemia and ischemia on myocardial GLUT1 and GLUT4 translocation in vivo
- PMID: 9815873
- DOI: 10.1161/01.cir.98.20.2180
Additive effects of hyperinsulinemia and ischemia on myocardial GLUT1 and GLUT4 translocation in vivo
Abstract
Background: Myocardial ischemia increases glucose uptake through the translocation of GLUT1 and GLUT4 from an intracellular compartment to the sarcolemma. The present study was performed to determine whether hyperinsulinemia causes translocation of myocardial GLUT1 as well as GLUT4 in vivo and whether there are additive effects of insulin and ischemia on GLUT1 and GLUT4 translocation. METHODS ADN RESULTS: Myocardial glucose uptake and transporter distribution were assessed by arteriovenous measurements, cell fractionation, and immunofluorescence. In fasted anesthetized dogs, hyperinsulinemia increased myocardial glucose extraction 3-fold (P<0.01) and the sarcolemmal content of GLUT4 by 90% and GLUT1 by 50% (P<0.05 for both) compared with saline infusion. In subsequent experiments, glucose uptake and transporter distribution were determined in ischemic and nonischemic regions of hearts from hyperinsulinemic animals during regional myocardial ischemia. Glucose uptake was 50% greater in the ischemic region (P<0.05). This was associated with a 20% increase in sarcolemmal GLUT1 and a 60% increase in sarcolemmal GLUT4 contents in the ischemic region (P<0.05 for both).
Conclusions: Insulin stimulates myocardial glucose utilization through translocation of GLUT1 as well as GLUT4. Insulin and ischemia have additive effects to increase in vivo glucose utilization and augment glucose transporter translocation. We conclude that recruitment of both GLUT1 and GLUT4 contributes to increased myocardial glucose uptake during moderate reductions in coronary blood flow under insulin-stimulated conditions.
Similar articles
-
Increased sarcolemmal glucose transporter abundance in myocardial ischemia.Am J Cardiol. 1997 Aug 4;80(3A):77A-84A. doi: 10.1016/s0002-9149(97)00460-8. Am J Cardiol. 1997. PMID: 9293958
-
Myocardial glucose transporter GLUT1: translocation induced by insulin and ischemia.J Mol Cell Cardiol. 1999 Jul;31(7):1337-44. doi: 10.1006/jmcc.1999.0965. J Mol Cell Cardiol. 1999. PMID: 10403751
-
Ischemia induces translocation of the insulin-responsive glucose transporter GLUT4 to the plasma membrane of cardiac myocytes.Circulation. 1994 Feb;89(2):793-8. doi: 10.1161/01.cir.89.2.793. Circulation. 1994. PMID: 8313568
-
Regulation of myocardial glucose uptake and transport during ischemia and energetic stress.Am J Cardiol. 1999 Jun 17;83(12A):25H-30H. doi: 10.1016/s0002-9149(99)00253-2. Am J Cardiol. 1999. PMID: 10750583 Review.
-
Insulin-induced redistribution of GLUT4 glucose carriers in the muscle fiber. In search of GLUT4 trafficking pathways.Diabetes. 1996 Jan;45 Suppl 1:S70-81. doi: 10.2337/diab.45.1.s70. Diabetes. 1996. PMID: 8529804 Review.
Cited by
-
Absence of glucose transporter 4 diminishes electrical activity of mouse hearts during hypoxia.Exp Physiol. 2013 Mar;98(3):746-57. doi: 10.1113/expphysiol.2012.070235. Epub 2012 Nov 23. Exp Physiol. 2013. PMID: 23180812 Free PMC article.
-
Comparative Analysis of CTRP-Mediated Effects on Cardiomyocyte Glucose Metabolism: Cross Talk between AMPK and Akt Signaling Pathway.Cells. 2021 Apr 14;10(4):905. doi: 10.3390/cells10040905. Cells. 2021. PMID: 33919975 Free PMC article.
-
Cellular and molecular regulation of cardiac glucose transport.J Nucl Cardiol. 2000 May-Jun;7(3):267-76. doi: 10.1016/s1071-3581(00)70016-x. J Nucl Cardiol. 2000. PMID: 10888399 Review. No abstract available.
-
Role of differential signaling pathways and oxidative stress in diabetic cardiomyopathy.Curr Cardiol Rev. 2010 Nov;6(4):280-90. doi: 10.2174/157340310793566145. Curr Cardiol Rev. 2010. PMID: 22043204 Free PMC article.
-
Diabetic cardiomyopathy: ongoing controversies in 2012.Herz. 2012 Dec;37(8):880-6. doi: 10.1007/s00059-012-3720-z. Herz. 2012. PMID: 23223771
Publication types
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources
Miscellaneous