The online version of this article (doi:10.1186/1475-2840-11-63) contains supplementary material, which is available to authorized users.
The authors declare that they have no competing interests.
LAF conceived the study, assisted in the design, execution and interpretation of experiments, and drafted the manuscript. MA, MP and AK assisted in performing experiments. PH provided guidance in experimental design, performed data analysis and interpretation, and assisted in writing and editing the manuscript. All authors read and approved the final manuscript.
The heart derives energy from a wide variety of substrates including fatty acids, carbohydrates, ketones, and amino acids. The healthy heart generates up to 30% of its ATP from glucose. Under conditions of cardiac injury or stress, the heart relies even more heavily on glucose as a source of fuel. Glucose is transported into the heart by members of the family of facilitative glucose transporters (GLUTs). While research examining the transport of glucose into the heart has primarily focused on the roles of the classical glucose transporters GLUT1 and GLUT4, little is known about the functions of more newly identified GLUT isoforms in the myocardium.
In this study the presence and relative RNA message abundance of each of the known GLUT isoforms was determined in left ventricular tissue from two commonly used inbred laboratory mouse strains (C57BL/6J and FVB/NJ) by quantitative real time PCR. Relative message abundance was also determined in GLUT4 null mice and in murine models of dilated and hypertrophic cardiomyopathy.
GLUT4, GLUT1, and GLUT8 were found to be the most abundant GLUT transcripts in the normal heart, while GLUT3, GLUT10, and GLUT12 are present at relatively lower levels. Assessment of relative GLUT expression in left ventricular myocardium from mice with dilated cardiomyopathy revealed increased expression of GLUT1 with reduced levels of GLUT4, GLUT8, and GLUT12. Compensatory increase in the expression of GLUT12 was observed in genetically altered mice lacking GLUT4.
Glucose transporter expression varies significantly among murine models of cardiac dysfunction and involves several of the class III GLUT isoforms. Understanding how these more newly identified GLUT isoforms contribute to regulating myocardial glucose transport will enhance our comprehension of the normal physiology and pathophysiology of the heart.
Additional file 1: Figure S1.Detection of GLUT mRNAs in the left ventricle of FVB/NJ mice. A) PCR was employed to identify each known murine member of the facilitative glucose transporter family in the left ventricle of 10-week-old male FVB/NJ mice. GLUTs-1, -3, -4, -6, -8, -10, and −12 were amplified using cDNA derived from the left ventricular myocardium. The identity of each GLUT amplicon was confirmed by sequencing. A faint band for GLUT5 was detected in some but not all of the left ventricles analyzed. GLUTs-2 and −9 were not present in the left ventricle of male C57BL/6J mice. Representative images are shown (n = 3). B) The specificity of the primers used to amplify GLUTs-2 and −9 were confirmed using cDNA derived from liver and intestine, respectively. The specificity of the primers for each GLUT amplicon was confirmed by sequencing. (JPEG 35 KB)12933_2012_484_MOESM1_ESM.jpeg
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- GLUT4, GLUT1, and GLUT8 are the dominant GLUT transcripts expressed in the murine left ventricle
Paul W Hruz
- BioMed Central
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