SLC5As, NAGLT1 cotransport Glc and Na+ from extracellular region to cytosol

Stable Identifier
Reaction [transition]
Homo sapiens
Co-transport (influx) of glucose and Na+ ions by SLC5As, NAGLT1
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The human gene SLC5A2 encodes a sodium-dependent glucose transporter, SGLT2 (Wells et al. 1992). SLC5A2 is expressed in many tissues but primarily in the kidney, specifically the renal proximal tubules (S1 and S2 segments). It is a low affinity, high capacity transporter of glucose across the apical membrane, with co-transport of Na+ ions in a 1:1 ratio. Unlike SGLT1, it doesn't transport galactose. SLC5A2 is the main transporter of glucose in the kidney, responsible for approximately 98% of glucose reabsorption (remainder by SGLT1). Defects in SLC5A2 are the cause of renal glucosuria (GLYS1), an autosomal recessive renal tubular disorder (Calado et al. 2004). A separate sodium dependent glucose transporter NAGLT1, was identified in the multifacilitator superfamily (MFS) and could be a transporter of glucose in kidney proximal tubules. Its rat orthologue, Naglt1, has been shown to mediate tubular reabsorption of glucose (Horiba et al. 2003). By similarity, SLC5A1, 4 and 9 are predicted proteins that transport glucose in a Na+-dependent manner.
Literature References
PubMed ID Title Journal Year
1415574 Cloning of a human kidney cDNA with similarity to the sodium-glucose cotransporter

Hediger, MA, Turk, E, Pajor, AM, Wright, EM, Kanai, Y, Wells, RG

Am J Physiol 1992
12590146 Cloning and characterization of a novel Na+-dependent glucose transporter (NaGLT1) in rat kidney

Takeuchi, D, Masuda, S, Inui, K, Horiba, N, Takeuchi, A, Okuda, M

J. Biol. Chem. 2003
14614622 Novel compound heterozygous mutations in SLC5A2 are responsible for autosomal recessive renal glucosuria

Rueff, J, Clemente, C, Soto, K, Correia, P, Calado, J

Hum Genet 2004
Catalyst Activity

glucose:sodium symporter activity of SLC5As, NAGLT1 [plasma membrane]

Orthologous Events
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