GLUT2 has high capacity for glucose but low affinity (high Km, ca. 15-20 mM) and thus functions as part of the "glucose sensor" in the pancreatic β-cells of rodents, though in human β-cells the role of GLUT2 seems to be a minor one. It is a very efficient carrier for glucose.
When the glucose concentration in the lumen of the small intestine goes above 30 mM, such as occurs in the fed-state, GLUT2 is up-regulated at the brush border membrane, enhancing the capacity of glucose transport. Basolateral GLUT2 in enterocytes also aids in the transport of fructose into the bloodstream through glucose-dependent cotransport.
In drug-treated diabetic pregnancies in which glucose levels in the woman are uncontrolled, neural tube and cardiac defects in the early-developing brain, spine, and heart depend upon functional GLUT2 carriers, and defects in the GLUT2 gene have been shown to be protective against such defects in rats. However, whilst a lack of GLUT2 adaptability 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, which 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.
^Gwyn W. Gould; Helen M. Thomas; Thomas J. Jess; Graeme I. Bell (May 1991). "Expression of human glucose transporters in Xenopus oocytes: kinetic characterization and substrate specificities of the erythrocyte, liver, and brain isoforms". Biochemistry. 30 (21): 5139–5145. doi:10.1021/bi00235a004.
^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". Molecular and Cellular Endocrinology. 237 (1-2): 49–57. PMID15869838. doi:10.1016/j.mce.2005.03.005.
^McCulloch LJ, van de Bunt M, Braun M, Frayn KN, Clark A, Gloyn AL (December 2011). "GLUT2 (SLC2A2) is not the principal glucose transporter in human pancreatic beta cells: implications for understanding genetic association signals at this locus". Molecular Genetics and Metabolism. 104 (4): 648–53. PMID21920790. doi:10.1016/j.ymgme.2011.08.026.
^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". Nature Genetics. 17 (3): 327–30. PMID9354799. doi:10.1038/ng1197-327.
^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". Human Genetics. 110 (1): 21–9. PMID11810292. doi:10.1007/s00439-001-0638-6.
^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. PMID17235524. doi:10.1007/s00125-006-0579-7.
^Thomson AB, Wild G (March 1997). "Adaptation of intestinal nutrient transport in health and disease. Part I". Digestive Diseases and Sciences. 42 (3): 453–69. PMID9073126. doi:10.1023/A:1018807120691.