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{{PBB|geneid=6524}}
{{PBB|geneid=6524}}
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]].<ref name="pmid8244402">{{cite journal | author = Wells RG, Mohandas TK, Hediger MA | title = Localization of the Na+/glucose cotransporter gene SGLT2 to human chromosome 16 close to the centromere | journal = Genomics | volume = 17 | issue = 3 | pages = 787–9 |date=September 1993 | pmid = 8244402 | doi = 10.1006/geno.1993.1411 | url = | issn = }}</ref>
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]].<ref name="pmid8244402">{{cite journal | vauthors = Wells RG, Mohandas TK, Hediger MA | title = Localization of the Na+/glucose cotransporter gene SGLT2 to human chromosome 16 close to the centromere | journal = Genomics | volume = 17 | issue = 3 | pages = 787–9 | date = Sep 1993 | pmid = 8244402 | doi = 10.1006/geno.1993.1411 }}</ref>


== Function ==
== Function ==
Line 8: Line 8:
== SGLT2 inhibitors for diabetes ==
== SGLT2 inhibitors for diabetes ==
{{Main|Gliflozin}}
{{Main|Gliflozin}}
SGLT2 inhibitors are called [[gliflozins]] and lead to a reduction in blood glucose levels. Therefore, SGLT2 inhibitors have potential use in the treatment of [[type II diabetes]]. As studied on [[canagliflozin]], a member of this class of drugs, gliflozins enhance glycemic control as well as reduce [[body weight]] and systolic and diastolic [[blood pressure]].<ref name="HaasEckstein2014">{{cite journal|last1=Haas|first1=B|last2=Eckstein|first2=N|last3=Pfeifer|first3=V|last4=Mayer|first4=P|last5=Hass|first5=M D S|title=Efficacy, safety and regulatory status of SGLT2 inhibitors: focus on canagliflozin|journal=Nutrition & Diabetes|volume=4|issue=11|year=2014|pages=e143|issn=2044-4052|doi=10.1038/nutd.2014.40}}</ref> The gliflozins canagliflozin, dapagliflozin, and empagliflozin may lead to [[ketoacidosis]].<ref>{{cite web|url=http://www.fda.gov/Drugs/DrugSafety/ucm446845.htm|title=FDA Drug Safety Communication: FDA warns that SGLT2 inhibitors for diabetes may result in a serious condition of too much acid in the blood|date=2015-05-15|publisher=[[Food and Drug Administration]], USA}}</ref> Other side effects of gliflozins include increased risk of (generally mild) [[urinary tract infection]]s, [[candidal vulvovaginitis]] and [[hypoglycemia]].<ref>{{cite web|url=http://www.diabetes.co.uk/diabetes-medication/sglt2-inhibitors.html|title=SGLT2 Inhibitors (Gliflozins)|publisher=[[Diabetes.co.uk]]|accessdate=2015-05-19}}</ref>
SGLT2 inhibitors are called [[gliflozins]] and lead to a reduction in blood glucose levels. Therefore, SGLT2 inhibitors have potential use in the treatment of [[type II diabetes]]. As studied on [[canagliflozin]], a member of this class of drugs, gliflozins enhance glycemic control as well as reduce [[body weight]] and systolic and diastolic [[blood pressure]].<ref name="HaasEckstein2014">{{cite journal | vauthors = Haas B, Eckstein N, Pfeifer V, Mayer P, Hass MD | title = Efficacy, safety and regulatory status of SGLT2 inhibitors: focus on canagliflozin | journal = Nutrition & Diabetes | volume = 4 | issue = 11 | pages = e143 | year = 2014 | pmid = 25365416 | doi = 10.1038/nutd.2014.40 }}</ref> The gliflozins canagliflozin, dapagliflozin, and empagliflozin may lead to [[ketoacidosis]].<ref>{{cite web|url=http://www.fda.gov/Drugs/DrugSafety/ucm446845.htm|title=FDA Drug Safety Communication: FDA warns that SGLT2 inhibitors for diabetes may result in a serious condition of too much acid in the blood|date=2015-05-15|publisher=[[Food and Drug Administration]], USA}}</ref> Other side effects of gliflozins include increased risk of (generally mild) [[urinary tract infection]]s, [[candidal vulvovaginitis]] and [[hypoglycemia]].<ref>{{cite web|url=http://www.diabetes.co.uk/diabetes-medication/sglt2-inhibitors.html|title=SGLT2 Inhibitors (Gliflozins)|publisher=[[Diabetes.co.uk]]|accessdate=2015-05-19}}</ref>


== Clinical significance ==
== Clinical significance ==


Mutations in this gene are also associated with [[renal glucosuria]].<ref name="pmid16518345">{{cite journal | author = Calado J, Loeffler J, Sakallioglu O, Gok F, Lhotta K, Barata J, Rueff J | title = Familial renal glucosuria: SLC5A2 mutation analysis and evidence of salt-wasting | journal = Kidney Int. | volume = 69 | issue = 5 | pages = 852–5 |date=March 2006 | pmid = 16518345 | doi = 10.1038/sj.ki.5000194 | url = | issn = }}</ref>
Mutations in this gene are also associated with [[renal glucosuria]].<ref name="pmid16518345">{{cite journal | vauthors = Calado J, Loeffler J, Sakallioglu O, Gok F, Lhotta K, Barata J, Rueff J | title = Familial renal glucosuria: SLC5A2 mutation analysis and evidence of salt-wasting | journal = Kidney International | volume = 69 | issue = 5 | pages = 852–5 | date = Mar 2006 | pmid = 16518345 | doi = 10.1038/sj.ki.5000194 }}</ref>


== Model organisms ==
== Model organisms ==
Line 68: Line 68:
| colspan=2; style="text-align: center;" | All tests and analysis from<ref name="mgp_reference">{{cite journal | doi = 10.1111/j.1755-3768.2010.4142.x | title = The Sanger Mouse Genetics Programme: High throughput characterisation of knockout mice | year = 2010 | author = Gerdin AK | journal = Acta Ophthalmologica | volume = 88 | pages = 925–7 }}</ref><ref>[http://www.sanger.ac.uk/mouseportal/ Mouse Resources Portal], Wellcome Trust Sanger Institute.</ref>
| colspan=2; style="text-align: center;" | All tests and analysis from<ref name="mgp_reference">{{cite journal | doi = 10.1111/j.1755-3768.2010.4142.x | title = The Sanger Mouse Genetics Programme: High throughput characterisation of knockout mice | year = 2010 | author = Gerdin AK | journal = Acta Ophthalmologica | volume = 88 | pages = 925–7 }}</ref><ref>[http://www.sanger.ac.uk/mouseportal/ Mouse Resources Portal], Wellcome Trust Sanger Institute.</ref>
|}
|}
[[Model organism]]s have been used in the study of SLC5A2 function. A conditional [[knockout mouse]] line, called ''Slc5a2<sup>tm1a(KOMP)Wtsi</sup>''<ref name="allele_ref">{{cite web |url=http://www.knockoutmouse.org/martsearch/search?query=Slc5a2 |title=International Knockout Mouse Consortium}}</ref><ref name="mgi_allele_ref">{{cite web |url=http://www.informatics.jax.org/searchtool/Search.do?query=MGI:4363573 |title=Mouse Genome Informatics}}</ref> was generated as part of the [[International Knockout Mouse Consortium]] program — a high-throughput mutagenesis project to generate and distribute animal models of disease to interested scientists.<ref name="pmid21677750">{{Cite journal
[[Model organism]]s have been used in the study of SLC5A2 function. A conditional [[knockout mouse]] line, called ''Slc5a2<sup>tm1a(KOMP)Wtsi</sup>''<ref name="allele_ref">{{cite web |url=http://www.knockoutmouse.org/martsearch/search?query=Slc5a2 |title=International Knockout Mouse Consortium}}</ref><ref name="mgi_allele_ref">{{cite web |url=http://www.informatics.jax.org/searchtool/Search.do?query=MGI:4363573 |title=Mouse Genome Informatics}}</ref> was generated as part of the [[International Knockout Mouse Consortium]] program — a high-throughput mutagenesis project to generate and distribute animal models of disease to interested scientists.<ref name="pmid21677750">{{cite journal | vauthors = Skarnes WC, Rosen B, West AP, Koutsourakis M, Bushell W, Iyer V, Mujica AO, Thomas M, Harrow J, Cox T, Jackson D, Severin J, Biggs P, Fu J, Nefedov M, de Jong PJ, Stewart AF, Bradley A | title = A conditional knockout resource for the genome-wide study of mouse gene function | journal = Nature | volume = 474 | issue = 7351 | pages = 337–42 | date = Jun 2011 | pmid = 21677750 | pmc = 3572410 | doi = 10.1038/nature10163 }}</ref><ref name="mouse_library">{{cite journal | vauthors = Dolgin E | title = Mouse library set to be knockout | journal = Nature | volume = 474 | issue = 7351 | pages = 262–3 | date = Jun 2011 | pmid = 21677718 | doi = 10.1038/474262a }}</ref><ref name="mouse_for_all_reasons">{{cite journal | vauthors = Collins FS, Rossant J, Wurst W | title = A mouse for all reasons | journal = Cell | volume = 128 | issue = 1 | pages = 9–13 | date = Jan 2007 | pmid = 17218247 | doi = 10.1016/j.cell.2006.12.018 }}</ref>
| last1 = Skarnes |first1 =W. C.
| doi = 10.1038/nature10163
| last2 = Rosen | first2 = B.
| last3 = West | first3 = A. P.
| last4 = Koutsourakis | first4 = M.
| last5 = Bushell | first5 = W.
| last6 = Iyer | first6 = V.
| last7 = Mujica | first7 = A. O.
| last8 = Thomas | first8 = M.
| last9 = Harrow | first9 = J.
| last10 = Cox | first10 = T.
| last11 = Jackson | first11 = D.
| last12 = Severin | first12 = J.
| last13 = Biggs | first13 = P.
| last14 = Fu | first14 = J.
| last15 = Nefedov | first15 = M.
| last16 = De Jong | first16 = P. J.
| last17 = Stewart | first17 = A. F.
| last18 = Bradley | first18 = A.
| title = A conditional knockout resource for the genome-wide study of mouse gene function
| journal = Nature
| volume = 474
| issue = 7351
| pages = 337–342
| year = 2011
| pmid = 21677750
| pmc =3572410
}}</ref><ref name="mouse_library">{{cite journal | doi = 10.1038/474262a | title = Mouse library set to be knockout | year = 2011 | author = Dolgin E | journal = Nature | volume = 474 | issue = 7351 | pages = 262–3 | pmid = 21677718 }}</ref><ref name="mouse_for_all_reasons">{{cite journal | doi = 10.1016/j.cell.2006.12.018 | title = A Mouse for All Reasons | year = 2007 | journal = Cell | volume = 128 | pages = 9–13 | pmid = 17218247 |author=Collins FS, Rossant J, Wurst W| issue = 1 }}</ref>


Male and female animals underwent a standardized [[phenotypic screen]] to determine the effects of deletion.<ref name="mgp_reference" /><ref name="pmid21722353">{{cite journal| author=van der Weyden L, White JK, Adams DJ, Logan DW| title=The mouse genetics toolkit: revealing function and mechanism. | journal=Genome Biol | year= 2011 | volume= 12 | issue= 6 | pages= 224 | pmid=21722353 | doi=10.1186/gb-2011-12-6-224 | pmc=3218837}}</ref> Twenty two tests were carried out on homozygous [[mutant]] mice and one significant abnormality was observed: males displayed increased drinking behaviour.<ref name="mgp_reference" />
Male and female animals underwent a standardized [[phenotypic screen]] to determine the effects of deletion.<ref name="mgp_reference" /><ref name="pmid21722353">{{cite journal | vauthors = van der Weyden L, White JK, Adams DJ, Logan DW | title = The mouse genetics toolkit: revealing function and mechanism | journal = Genome Biology | volume = 12 | issue = 6 | pages = 224 | year = 2011 | pmid = 21722353 | pmc = 3218837 | doi = 10.1186/gb-2011-12-6-224 }}</ref> Twenty two tests were carried out on homozygous [[mutant]] mice and one significant abnormality was observed: males displayed increased drinking behaviour.<ref name="mgp_reference" />


==See also==
== See also ==


* [[SGLT]] Family
* [[SGLT]] Family
* [[Discovery and development of gliflozins]]
* [[Discovery and development of gliflozins]]


==References==
== References ==
{{reflist}}
{{reflist}}


==Further reading==
== Further reading ==
{{refbegin | 2}}
{{refbegin | 2}}
*{{cite journal |author=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=Hum. Genet. |volume=111 |issue= 6 |pages= 544–7 |year= 2002 |pmid= 12436245 |doi= 10.1007/s00439-002-0820-5 }}
* {{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 }}
*{{cite journal |author=Santer R, Kinner M, Lassen CL, ''et al.'' |title=Molecular analysis of the SGLT2 gene in patients with renal glucosuria. |journal=J. Am. Soc. Nephrol. |volume=14 |issue= 11 |pages= 2873–82 |year= 2003 |pmid= 14569097 |doi= 10.1097/01.asn.0000092790.89332.d2}}
* {{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 }}
*{{cite journal |author=Wells RG, Pajor AM, Kanai Y, ''et al.'' |title=Cloning of a human kidney cDNA with similarity to the sodium-glucose cotransporter. |journal=Am. J. Physiol. |volume=263 |issue= 3 Pt 2 |pages= F459-65 |year= 1992 |pmid= 1415574 |doi= }}
* {{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 = }}
*{{cite journal |author=Calado J, Sznajer Y, Metzger D, ''et al.'' |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=Nephrol. Dial. Transplant. |volume=23 |issue= 12 |pages= 3874–9 |year= 2008 |pmid= 18622023 |doi= 10.1093/ndt/gfn386 }}
* {{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 }}
*{{cite journal |author=Calado J, Soto K, Clemente C, ''et al.'' |title=Novel compound heterozygous mutations in SLC5A2 are responsible for autosomal recessive renal glucosuria. |journal=Hum. Genet. |volume=114 |issue= 3 |pages= 314–6 |year= 2004 |pmid= 14614622 |doi= 10.1007/s00439-003-1054-x }}
* {{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 }}
*{{cite journal |author=Ota T, Suzuki Y, Nishikawa T, ''et al.'' |title=Complete sequencing and characterization of 21,243 full-length human cDNAs. |journal=Nat. Genet. |volume=36 |issue= 1 |pages= 40–5 |year= 2004 |pmid= 14702039 |doi= 10.1038/ng1285 }}
* {{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 }}
*{{cite journal |author=Strausberg RL, Feingold EA, Grouse LH, ''et al.'' |title=Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=99 |issue= 26 |pages= 16899–903 |year= 2002 |pmid= 12477932 |doi= 10.1073/pnas.242603899 |pmc=139241}}
* {{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 }}
*{{cite journal |author=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 Int. |volume=67 |issue= 1 |pages= 34–41 |year= 2005 |pmid= 15610225 |doi= 10.1111/j.1523-1755.2005.00053.x }}
*{{cite journal |author=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=Int J Med Sci |volume=4 |issue= 3 |pages= 131–9 |year= 2007 |pmid= 17505558 |doi= 10.7150/ijms.4.131|pmc=1868657}}
{{refend}}
{{refend}}


Revision as of 05:59, 29 August 2015

Template:PBB 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.[1]

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.[2]

SGLT2 inhibitors for diabetes

Main article: Gliflozin

SGLT2 inhibitors are called gliflozins and lead to a reduction in blood glucose levels. Therefore, SGLT2 inhibitors have potential use in the treatment of type II diabetes. As studied on canagliflozin, a member of this class of drugs, gliflozins enhance glycemic control as well as reduce body weight and systolic and diastolic blood pressure.[3] The gliflozins canagliflozin, dapagliflozin, and empagliflozin may lead to ketoacidosis.[4] Other side effects of gliflozins include increased risk of (generally mild) urinary tract infections, candidal vulvovaginitis and hypoglycemia.[5]

Clinical significance

Mutations in this gene are also associated with renal glucosuria.[6]

Model organisms

Model organisms have been used in the study of SLC5A2 function. A conditional knockout mouse line, called Slc5a2tm1a(KOMP)Wtsi[12][13] was generated as part of the International Knockout Mouse Consortium program — a high-throughput mutagenesis project to generate and distribute animal models of disease to interested scientists.[14][15][16]

Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion.[10][17] Twenty two tests were carried out on homozygous mutant mice and one significant abnormality was observed: males displayed increased drinking behaviour.[10]

See also

References

  1. ^ Wells RG, Mohandas TK, Hediger MA (Sep 1993). "Localization of the Na+/glucose cotransporter gene SGLT2 to human chromosome 16 close to the centromere". Genomics. 17 (3): 787–9. doi:10.1006/geno.1993.1411. PMID 8244402.
  2. ^ "Entrez Gene: solute carrier family 5 (sodium/glucose cotransporter)".
  3. ^ Haas B, Eckstein N, Pfeifer V, Mayer P, Hass MD (2014). "Efficacy, safety and regulatory status of SGLT2 inhibitors: focus on canagliflozin". Nutrition & Diabetes. 4 (11): e143. doi:10.1038/nutd.2014.40. PMID 25365416.
  4. ^ "FDA Drug Safety Communication: FDA warns that SGLT2 inhibitors for diabetes may result in a serious condition of too much acid in the blood". Food and Drug Administration, USA. 2015-05-15.
  5. ^ "SGLT2 Inhibitors (Gliflozins)". Diabetes.co.uk. Retrieved 2015-05-19.
  6. ^ Calado J, Loeffler J, Sakallioglu O, Gok F, Lhotta K, Barata J, Rueff J (Mar 2006). "Familial renal glucosuria: SLC5A2 mutation analysis and evidence of salt-wasting". Kidney International. 69 (5): 852–5. doi:10.1038/sj.ki.5000194. PMID 16518345.
  7. ^ "Indirect calorimetry data for Slc5a2". Wellcome Trust Sanger Institute.
  8. ^ "Salmonella infection data for Slc5a2". Wellcome Trust Sanger Institute.
  9. ^ "Citrobacter infection data for Slc5a2". Wellcome Trust Sanger Institute.
  10. ^ a b c Gerdin AK (2010). "The Sanger Mouse Genetics Programme: High throughput characterisation of knockout mice". Acta Ophthalmologica. 88: 925–7. doi:10.1111/j.1755-3768.2010.4142.x.
  11. ^ Mouse Resources Portal, Wellcome Trust Sanger Institute.
  12. ^ "International Knockout Mouse Consortium".
  13. ^ "Mouse Genome Informatics".
  14. ^ Skarnes WC, Rosen B, West AP, Koutsourakis M, Bushell W, Iyer V, Mujica AO, Thomas M, Harrow J, Cox T, Jackson D, Severin J, Biggs P, Fu J, Nefedov M, de Jong PJ, Stewart AF, Bradley A (Jun 2011). "A conditional knockout resource for the genome-wide study of mouse gene function". Nature. 474 (7351): 337–42. doi:10.1038/nature10163. PMC 3572410. PMID 21677750.
  15. ^ Dolgin E (Jun 2011). "Mouse library set to be knockout". Nature. 474 (7351): 262–3. doi:10.1038/474262a. PMID 21677718.
  16. ^ Collins FS, Rossant J, Wurst W (Jan 2007). "A mouse for all reasons". Cell. 128 (1): 9–13. doi:10.1016/j.cell.2006.12.018. PMID 17218247.
  17. ^ van der Weyden L, White JK, Adams DJ, Logan DW (2011). "The mouse genetics toolkit: revealing function and mechanism". Genome Biology. 12 (6): 224. doi:10.1186/gb-2011-12-6-224. PMC 3218837. PMID 21722353.{{cite journal}}: CS1 maint: unflagged free DOI (link)

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.
  • 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. 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.
  • 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.
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