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solute carrier family 2 (facilitated glucose transporter), member 2
Identifiers
Symbol SLC2A2
Alt. symbols GLUT2
Entrez 6514
HUGO 11006
OMIM 138160
RefSeq NM_000340
UniProt P11168
Other data
Locus Chr. 3 q26.2-q27

Glucose transporter 2 (GLUT2) also known as solute carrier family 2 (facilitated glucose transporter), member 2 (SLC2A2) is a transmembrane carrier protein that enables passive glucose movement across cell membranes. It is the principal transporter for transfer of glucose between liver and blood, and for renal glucose reabsorption. In humans, this protein is encoded by the SLC2A2 gene.[1][2]

Contents

Tissue distribution

GLUT2 is found in cellular membranes of:

Function

GLUT2 has high capacity but low affinity (high Km, ca. 5 mM) part of "the glucose sensor" in pancreatic β-cells. It is a very efficient carrier for glucose.[4][5]

GLUT2 also carries glucosamine.[6]

Clinical significance

Defects in the SLC2A2 gene are associated with a particular type of glycogen storage disease called Fanconi-Bickel syndrome.[7]

It has been proposed by genetics researchers in neonatal and maternal-fetal medicine at Harvard University Medical School and Beth-Israel Deaconess Hospital Medical Center, that this creates a problem for drug treated diabetic pregnancies in which glucose levels in the woman are uncontrolled, exposing her fetus to the possibility of neural tube and cardiac defects in the early-developing brain, spine, and heart.[8] However, whilst a lack of GLUT2 adaptability[9] is negative, it is important to remember the fact that the main result of untreated gestational diabetes appears to cause babies to be of above average size and that may well be an advantage that is managed very well with a healthy GLUT2 status.

Maintaining a regulated osmotic balance of sugar concentration between the blood circulation and the interstitial spaces is critical in some cases of edema including cerebral edema.

GLUT2 appears to be particularly important to osmoregulation, and preventing edema induced stroke[1] or coma, especially when blood glucose concentration is above average.[10] GLUT2 could reasonably referred to as the "diabetic glucose transporter" or a "stress hyperglycemia glucose transporter".

See also

References

  1. ^ Froguel P, Zouali H, Sun F, Velho G, Fukumoto H, Passa P, Cohen D (July 1991). "CA repeat polymorphism in the glucose transporter GLUT 2 gene". Nucleic Acids Res. 19 (13): 3754. doi:10.1093/nar/19.13.3754-a. PMID 1852621.  
  2. ^ Uldry M, Thorens B (2004). "The SLC2 family of facilitated hexose and polyol transporters". Pflugers Arch 447 (5): 480–489. doi:10.1007/s00424-003-1085-0. PMID 12750891.  
  3. ^ Freitas HS, Schaan BD, Seraphim PM, Nunes MT, Machado UF (June 2005). "Acute and short-term insulin-induced molecular adaptations of GLUT2 gene expression in the renal cortex of diabetic rats". Mol. Cell. Endocrinol. 237 (1-2): 49–57. doi:10.1016/j.mce.2005.03.005. PMID 15869838.  
  4. ^ Guillam MT, Hümmler E, Schaerer E, Yeh JI, Birnbaum MJ, Beermann F, Schmidt A, Dériaz N, Thorens B, Wu JY (November 1997). "Early diabetes and abnormal postnatal pancreatic islet development in mice lacking Glut-2". Nat. Genet. 17 (3): 327–30. doi:10.1038/ng1197-327. PMID 9354799.  
  5. ^ Efrat S (November 1997). "Making sense of glucose sensing". Nat. Genet. 17 (3): 249–50. doi:10.1038/ng1197-249. PMID 9354775.  
  6. ^ Uldry M, Ibberson M, Hosokawa M, Thorens B (July 2002). "GLUT2 is a high affinity glucosamine transporter". FEBS Lett. 524 (1-3): 199–203. doi:10.1016/S0014-5793(02)03058-2. PMID 12135767.  
  7. ^ Santer R, Groth S, Kinner M, Dombrowski A, Berry GT, Brodehl J, Leonard JV, Moses S, Norgren S, Skovby F, Schneppenheim R, Steinmann B, Schaub J (January 2002). "The mutation spectrum of the facilitative glucose transporter gene SLC2A2 (GLUT2) in patients with Fanconi-Bickel syndrome". Hum. Genet. 110 (1): 21–9. doi:10.1007/s00439-001-0638-6. PMID 11810292.  
  8. ^ Li R, Thorens B, Loeken MR (March 2007). "Expression of the gene encoding the high-Km glucose transporter 2 by the early postimplantation mouse embryo is essential for neural tube defects associated with diabetic embryopathy". Diabetologia 50 (3): 682–9. doi:10.1007/s00125-006-0579-7. PMID 17235524.  
  9. ^ Thomson AB, Wild G (March 1997). "Adaptation of intestinal nutrient transport in health and disease. Part I". Dig. Dis. Sci. 42 (3): 453–69. doi:10.1023/A:1018807120691. PMID 9073126.  
  10. ^ Stolarczyk E, Le Gall M, Even P, Houllier A, Serradas P, Brot-Laroche E, Leturque A (2007). "Loss of sugar detection by GLUT2 affects glucose homeostasis in mice". PLoS ONE 2 (12): e1288. doi:10.1371/journal.pone.0001288. PMID 18074013.  

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