Glucose transport by class I GLUTs Authored: Jassal, B, 2009-07-10 Edited: Jassal, B, 2009-07-10 Pubmed10227690 Pubmed10987651 Pubmed1756912 Pubmed1918382 Pubmed2656669 Pubmed3170580 Pubmed3399500 Pubmed3839598 Reactome Database ID Release 43428825 Reactome, http://www.reactome.org ReactomeREACT_19335 Reviewed: He, L, 2009-08-24 The class I facilitative glucose transporters contain GLUT1-4. As well as glucose, these proteins can transport other hexoses such as fructose, galactose and glucosamine. GLUT1 was cloned from a HepG2 cell line (Mueckler M et al, 1985). GLUT1 is expressed by SLC2A1 mainly in brain and erythrocytes but is also expressed at lower levels in many other tissues containing endothelial and epithelial barriers. Defects in SLC2A1 are the cause of autosomal dominant GLUT1 deficiency syndrome which results in impaired glucose transport across the brain tissue barrier and is characterized by infantile seizures, delayed development and acquired microcephaly (Klepper J et al, 1999).<br><br>GLUT2 is expressed by SLC2A2 and is a low affinity glucose transporter (Fukumoto H et al, 1988). It is expressed mainly in the kidney, liver and pancreatic beta-cells. In beta-cells, it functions as a glucose-sensor for insulin secretion and in the liver, it allows for bi-directional glucose transport. In this reaction, it is shown to mediate the influx of glucose. In the next reaction, it is shown to be mediating efflux of glucose. Defects in SLC2A2 are the cause of Fanconi-Bickel syndrome (FBS). It is characterized by hepatorenal glycogen accumulation, proximal renal tubular dysfunction, and impaired utilization of glucose and galactose (Burwinkel B et al, 1999).<br><br>SLC2A3 encodes GLUT3 which is mainly expressed in the brain but also in a wide range of tissues. If has a high affinity for glucose and can also transport other sugars (Kayano T et al, 1988). GLUT4, encoded by SLC2A4, is an insulin-responsive glucose transporter found in heart, skeletal muscle, brain and adipose tissue. Due to its sensitivity to insulin, it may play a role in diabetes. In a non-insulin condition, GLUT4 is localized in intracellular GLUT4-containing vesicles. On insulin stimulation, GLUT4 translocates to the plasma membrane where it can increase glucose transport 10-20-fold (Fukumoto H et al, 1989). Defects in SLC2A4 may be a cause of non-insulin-dependent diabetes mellitus (NIDDM) (Kusari J et al, 1991; Choi WH et al, 1991).