2003
DOI: 10.1002/jcb.10631
|View full text |Cite
|
Sign up to set email alerts
|

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

Abstract: 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/microg total RNA) relative to that in the kidney (3E + 4 molecules/microg total RNA). Surprisingly, we observed that the expression of SGLT1 in human heart was unexpectedly high (3.4E + 5 molecules/microg total RNA), … Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1

Citation Types

10
142
2
1

Year Published

2006
2006
2024
2024

Publication Types

Select...
7
2

Relationship

0
9

Authors

Journals

citations
Cited by 189 publications
(155 citation statements)
references
References 20 publications
10
142
2
1
Order By: Relevance
“…1,[5][6][7] This concept is based on mRNA and transport studies in isolated nephron segments and membrane vesicles from various tissue zones of rat and rabbit kidneys. 6 -14 Real-time PCR suggested SGLT2 mRNA expression in many human tissues, 15 but, because of the lack of good antibodies (Ab), the implication for extrarenal protein expression of SGLT2 is unclear. Another low-affinity Na ϩ -D-glucose co-transporter named NaGLT1 was cloned from rat, 2 which has no amino acid sequence similarity to transporters of the SGLT family and does not transport D-galactose, as has been described for SGLT2.…”
mentioning
confidence: 99%
“…1,[5][6][7] This concept is based on mRNA and transport studies in isolated nephron segments and membrane vesicles from various tissue zones of rat and rabbit kidneys. 6 -14 Real-time PCR suggested SGLT2 mRNA expression in many human tissues, 15 but, because of the lack of good antibodies (Ab), the implication for extrarenal protein expression of SGLT2 is unclear. Another low-affinity Na ϩ -D-glucose co-transporter named NaGLT1 was cloned from rat, 2 which has no amino acid sequence similarity to transporters of the SGLT family and does not transport D-galactose, as has been described for SGLT2.…”
mentioning
confidence: 99%
“…Two major SGLT transporters exist in the kidneys, SGLT1 and SGLT2, which differ in their affinity, substrate specificity, and tissue expression. Whereas SGLT1 is more widely expressed and is found in the small intestine, the distal (S2, S3) segments of the renal proximal tubule, and in cardiomyocytes, 1,2 SGLT2 is expressed only in the apical brush border of the S1 and S2 portion of the proximal renal tubule. SGLT1 is a high-affinity (K 0.5 ϭ 0.…”
mentioning
confidence: 99%
“…4,5 Familial renal glucosuria describes patients with a rare mutation in the solute carrier family 5, member 2 (SLC5A2) gene that encodes for a 75-kD sodium-glucose cotransporter 2 (SGLT2). Patients with this disorder manifest a variable degree of glucosuria, depending on the type of mutation and the number of alleles affected; massive glucosuria of 169 g/1.73 m 2 per d has been reported, 6 yet most of them remain euglycemic and have no other major health sequela. 7 Given the apparent benign nature of loss of function of SGLT2 and its restricted renal expression, it follows that SGLT inhibition might be a valuable treatment for diabetes to enhance renal glucose excretion and thereby improve glycemic control.…”
mentioning
confidence: 99%
“…In addition, the newer compounds are more selective for SGLT2 than SGLT1, thus minimizing potential side effects associated with the broad tissue distribution of SGLT1. Besides intestine and kidney, SGLT1 is found in other organs and tissues, including blood-brain barrier and heart (Zhou et al, 2003;Elfeber et al, 2004;Tazawa et al, 2005). In diabetic animal models, inhibition of SGLT2 produces glucosuria, followed by a normalization of blood glucose levels and a consequent improve-ment in insulin resistance and renal damage (Asano et al, 2004;Katsuno et al, 2007).…”
mentioning
confidence: 99%