Search results for SLC5A1

Showing 7 results out of 24

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Protein (5 results from a total of 11)

Identifier: R-HSA-5656381
Species: Homo sapiens
Compartment: plasma membrane
Primary external reference: UniProt: SLC5A1: P13866
Identifier: R-HSA-5656362
Species: Homo sapiens
Compartment: plasma membrane
Primary external reference: UniProt: SLC5A1: P13866
Identifier: R-HSA-5215942
Species: Homo sapiens
Compartment: plasma membrane
Primary external reference: UniProt: SLC5A12: Q1EHB4
Identifier: R-HSA-429589
Species: Homo sapiens
Compartment: plasma membrane
Primary external reference: UniProt: SLC5A11: Q8WWX8
Identifier: R-HSA-5216084
Species: Homo sapiens
Compartment: plasma membrane
Primary external reference: UniProt: SLC5A10: A0PJK1

Reaction (2 results from a total of 8)

Identifier: R-HSA-429613
Species: Homo sapiens
Compartment: plasma membrane, cytosol, extracellular region
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.
Identifier: R-HSA-9728150
Species: Homo sapiens
Compartment: plasma membrane, extracellular region
The human gene SLC5A2 encodes sodium/glucose cotransporter 2 (SGLT2). At the plasma membrane, it co-transports extracellular sodium ions and glucose into the cytosol. SLC5A2 is located in the early proximal tubule, and absorbs 80-90% of the glucose filtered by the kidney glomerulus. The majority of the remaining glucose is absorbed by sodium/glucose cotransporter 1 (SLC5A1, SGLT1) in more distal sections of the proximal tubule.

SLC5A2 inhibitors, collectively called 'gliflozins', inhibit SLC5A2 in proximal tubules of renal glomeruli, causing inhibition of glucose reabsorption, resulting in glycosuria in diabetics which in turn lowers plasma glucose levels (Katsuno et al. 2007, Pajor et al. 2008, Hummel et al. 2012, review - Chao 2014). Therefore, gliflozins can be used in the treatment of type II diabetes mellitus (T2DM); dapagliflozin (Zhang et al. 2010), ertugliflozin (Mascitti et al. 2011), canagliflozin (Liang et al. 2012), sotagliflozin (Zambrowicz et al. 2012), tofogliflozin (Grempler et al. 2012), tofogliflozin (Ohtake et al. 2012), and ipragliflozin (Imamura et al. 2012). Dapagliflozin was the first gliflozin approved for the treatment of T2DM. They are most often used as second- or third-line treatment of T2DM because other anti-diabetics have better safety records and are less expensive than gliflozins. They are good options for diabetics who fail with metformin monotherapy or in combination therapy, for example metformin plus gliflozin. The most common adverse effect of gliflozin treatment is genital infections.

Gliflozins have shown protective effects in heart failure. This is primarily due to haemodynamic effects, where gliflozins potently reduce intravascular volume through osmotic diuresis and natriuresis. Consequently, this may lead to a reduction in cardiac workload and improving left ventricular function (Lan et al. 2019, Chan et al. 2020).
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