Sodium/glucose cotransporter 2

SLC5A2
Identifiers
Aliases	SGLT2solute carrier family 5 member 2
External IDs	GeneCards: [1]
Orthologs Species Human Mouse Entrez n/a n/a Ensembl n/a n/a UniProt n a n/a RefSeq (mRNA) n/a n/a RefSeq (protein) n/a n/a Location (UCSC) n/a n/a PubMed search n/a n/a
Wikidata
View/Edit Human

The sodium/glucose cotransporter 2 (SGLT2) is a protein that in humans is encoded by the SLC5A2 (solute carrier family 5 (sodium/glucose cotransporter)) gene.

Function

SGLT2 is a member of the sodium glucose cotransporter family, which are sodium-dependent glucose transport proteins. SGLT2 is the major cotransporter involved in glucose reabsorption in the kidney. SGLT2 is located in the early proximal tubule, and is responsible for reabsorption of 80-90% of the glucose filtered by the kidney glomerulus. Most of the remaining glucose absorption is by sodium/glucose cotransporter 1 (SGLT1) in more distal sections of the proximal tubule.

SGLT2 inhibitors for diabetes

Main article: SGLT2 inhibitor

SGLT2 inhibitors are also called gliflozins or flozins. They lead to a reduction in blood glucose levels, and therefore have potential use in the treatment of type 2 diabetes. Gliflozins enhance glycemic control as well as reduce body weight and systolic and diastolic blood pressure. The gliflozins canagliflozin, dapagliflozin, and empagliflozin may lead to euglycemic ketoacidosis. Other side effects of gliflozins include increased risk of Fournier gangrene

Clinical significance

Mutations in this gene are also associated with renal glycosuria.

See also

• SGLT Family
• Discovery and development of gliflozins
• Phlorizin — a competitive inhibitor of SGLT1 and SGLT2

Further reading

• van den Heuvel LP, Assink K, Willemsen M, Monnens L (Dec 2002). "Autosomal recessive renal glucosuria attributable to a mutation in the sodium glucose cotransporter (SGLT2)". Human Genetics. 111 (6): 544–7. doi:10.1007/s00439-002-0820-5. PMID 12436245. S2CID 28089635.
• Santer R, Kinner M, Lassen CL, Schneppenheim R, Eggert P, Bald M, Brodehl J, Daschner M, Ehrich JH, Kemper M, Li Volti S, Neuhaus T, Skovby F, Swift PG, Schaub J, Klaerke D (Nov 2003). "Molecular analysis of the SGLT2 gene in patients with renal glucosuria". Journal of the American Society of Nephrology. 14 (11): 2873–82. doi:10.1097/01.asn.0000092790.89332.d2. PMID 14569097.
• Wells RG, Pajor AM, Kanai Y, Turk E, Wright EM, Hediger MA (Sep 1992). "Cloning of a human kidney cDNA with similarity to the sodium-glucose cotransporter". The American Journal of Physiology. 263 (3 Pt 2): F459-65. doi:10.1152/ajprenal.1992.263.3.F459. PMID 1415574.
• Calado J, Sznajer Y, Metzger D, Rita A, Hogan MC, Kattamis A, Scharf M, Tasic V, Greil J, Brinkert F, Kemper MJ, Santer R (Dec 2008). "Twenty-one additional cases of familial renal glucosuria: absence of genetic heterogeneity, high prevalence of private mutations and further evidence of volume depletion". Nephrology, Dialysis, Transplantation. 23 (12): 3874–9. doi:10.1093/ndt/gfn386. PMID 18622023.
• Calado J, Soto K, Clemente C, Correia P, Rueff J (Feb 2004). "Novel compound heterozygous mutations in SLC5A2 are responsible for autosomal recessive renal glucosuria". Human Genetics. 114 (3): 314–6. doi:10.1007/s00439-003-1054-x. PMID 14614622. S2CID 23741937.
• Magen D, Sprecher E, Zelikovic I, Skorecki K (Jan 2005). "A novel missense mutation in SLC5A2 encoding SGLT2 underlies autosomal-recessive renal glucosuria and aminoaciduria". Kidney International. 67 (1): 34–41. doi:10.1111/j.1523-1755.2005.00053.x. PMID 15610225.
• Castaneda F, Burse A, Boland W, Kinne RK (2007). "Thioglycosides as inhibitors of hSGLT1 and hSGLT2: potential therapeutic agents for the control of hyperglycemia in diabetes". International Journal of Medical Sciences. 4 (3): 131–9. doi:10.7150/ijms.4.131. PMC 1868657. PMID 17505558.