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{{Short description|Protein-coding gene in the species Homo sapiens}}<br />
{{Infobox gene}}<br />
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The '''sodium/glucose cotransporter 2''' (SGLT2) is a [[protein]] that in humans is encoded by the {{gene|SLC5A2}} (solute carrier family 5 (sodium/glucose cotransporter)) [[gene]].<br />
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== Function ==<br />
SGLT2 is a member of the [[sodium-glucose transport proteins|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 (kidney)|glomerulus]]. Most of the remaining glucose absorption is by [[sodium/glucose cotransporter 1]] (SGLT1) in more distal sections of the proximal tubule.<br />
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== SGLT2 inhibitors for diabetes ==<br />
{{Main|SGLT2 inhibitor}}<br />
[[SGLT2 inhibitor]]s 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 [[Human body weight|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<br />
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== Clinical significance ==<br />
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Mutations in this gene are also associated with [[renal glycosuria]].<br />
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== See also ==<br />
* [[SGLT]] Family<br />
* [[Discovery and development of gliflozins]]<br />
* [[Phlorizin]] — a competitive inhibitor of [[SLC5A1|SGLT1]] and [[SGLT2]]<br />
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== References ==<br />
{{reflist|33em}}<br />
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== Further reading ==<br />
{{refbegin|33em}}<br />
* {{cite journal | vauthors = van den Heuvel LP, Assink K, Willemsen M, Monnens L | title = Autosomal recessive renal glucosuria attributable to a mutation in the sodium glucose cotransporter (SGLT2) | journal = Human Genetics | volume = 111 | issue = 6 | pages = 544–7 | date = Dec 2002 | pmid = 12436245 | doi = 10.1007/s00439-002-0820-5 | s2cid = 28089635 }}<br />
* {{cite journal | vauthors = 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 | title = Molecular analysis of the SGLT2 gene in patients with renal glucosuria | journal = Journal of the American Society of Nephrology | volume = 14 | issue = 11 | pages = 2873–82 | date = Nov 2003 | pmid = 14569097 | doi = 10.1097/01.asn.0000092790.89332.d2 | doi-access = free }}<br />
* {{cite journal | vauthors = Wells RG, Pajor AM, Kanai Y, Turk E, Wright EM, Hediger MA | title = Cloning of a human kidney cDNA with similarity to the sodium-glucose cotransporter | journal = The American Journal of Physiology | volume = 263 | issue = 3 Pt 2 | pages = F459-65 | date = Sep 1992 | pmid = 1415574 | doi = 10.1152/ajprenal.1992.263.3.F459}}<br />
* {{cite journal | vauthors = Calado J, Sznajer Y, Metzger D, Rita A, Hogan MC, Kattamis A, Scharf M, Tasic V, Greil J, Brinkert F, Kemper MJ, Santer R | title = Twenty-one additional cases of familial renal glucosuria: absence of genetic heterogeneity, high prevalence of private mutations and further evidence of volume depletion | journal = Nephrology, Dialysis, Transplantation | volume = 23 | issue = 12 | pages = 3874–9 | date = Dec 2008 | pmid = 18622023 | doi = 10.1093/ndt/gfn386 | doi-access = free }}<br />
* {{cite journal | vauthors = Calado J, Soto K, Clemente C, Correia P, Rueff J | title = Novel compound heterozygous mutations in SLC5A2 are responsible for autosomal recessive renal glucosuria | journal = Human Genetics | volume = 114 | issue = 3 | pages = 314–6 | date = Feb 2004 | pmid = 14614622 | doi = 10.1007/s00439-003-1054-x | s2cid = 23741937 }}<br />
* {{cite journal | vauthors = Magen D, Sprecher E, Zelikovic I, Skorecki K | title = A novel missense mutation in SLC5A2 encoding SGLT2 underlies autosomal-recessive renal glucosuria and aminoaciduria | journal = Kidney International | volume = 67 | issue = 1 | pages = 34–41 | date = Jan 2005 | pmid = 15610225 | doi = 10.1111/j.1523-1755.2005.00053.x | doi-access = free }}<br />
* {{cite journal | vauthors = Castaneda F, Burse A, Boland W, Kinne RK | title = Thioglycosides as inhibitors of hSGLT1 and hSGLT2: potential therapeutic agents for the control of hyperglycemia in diabetes | journal = International Journal of Medical Sciences | volume = 4 | issue = 3 | pages = 131–9 | year = 2007 | pmid = 17505558 | pmc = 1868657 | doi = 10.7150/ijms.4.131 }}<br />
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{{Solute carrier family|bg|bg0}}<br />
{{Sodium-glucose transporter modulators}}<br />
{{二次利用|date=18 December 2023}}<br />
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[[Category:Solute carrier family]]<br />
[[Category:Genes mutated in mice]]</div>FuzzyBot