• DOI:10.1002/jcb.10631
• Corpus ID: 21908010

Human cardiomyocytes express high level of Na+/glucose cotransporter 1 (SGLT1)

@article{Zhou2003HumanCE,
  title={Human cardiomyocytes express high level of Na+/glucose cotransporter 1 (SGLT1)},
  author={Lubing Zhou and Ellen V. Cryan and Michael R. D'Andrea and Stanley M. Belkowski and Bruce R. Conway and Keith T. Demarest},
  journal={Journal of Cellular Biochemistry},
  year={2003},
  volume={90}
}

• Lubing Zhou, E. Cryan, +3 authors K. Demarest
• Published 1 October 2003
• Biology
• Journal of Cellular Biochemistry

We have quantitatively measured gene expression for the sodium‐dependent glucose cotransporters 1 and 2 (SGLT1 and SGLT2) in 23 human tissues using the method of real time PCR. As predicted, our results revealed that the expression of SGLT1 was very high in the small intestine (1.2E + 6 molecules/μg total RNA) relative to that in the kidney (3E + 4 molecules/μg total RNA). Surprisingly, we observed that the expression of SGLT1 in human heart was unexpectedly high (3.4E + 5 molecules/μg total RNA), approximately 10‐fold higher than that observed in kidney tissue. DNA sequencing confirmed that the PCR amplified fragment was indeed the human SGLT1 gene. Moreover, in situ hybridization studies using a digoxigenin (DIG)‐labeled antisense cRNA probe corresponding to human SGLT1 cDNA confirm that human cardiomyocytes express SGLT1 mRNA. In contrast, the expression of SGLT2 in human tissues appears to be ubiquitous, with levels ranging from 6.7E + 4 molecules/μg total RNA (in skeletal muscle) to 3.2E + 6 molecules/μg total RNA (in kidney), levels 10–100‐fold higher than the expression of SGLT1 in the same tissues. Our finding that human cardiomyocytes express high levels of SGLT1 RNA suggests that SGLT1 may have a functional role in cardiac glucose transport. Since several SGLT inhibitors are currently in development as potential anti‐diabetic agents, it may be important to assess the functional consequences of inhibition of SGLT1 in the heart. J. Cell. Biochem. 90: 339–346, 2003. © 2003 Wiley‐Liss, Inc.