Introduction of MFSD4B
Sodium-dependent glucose transporter 1 (SGLT1), also known as MFSD4B, belongs to the SGLT family encoded by the MFSD4B gene predominantly expressed in the small intestine. The SGLT family consists of several isoforms that actively transport sugar through the cell membrane, and this process combines with sodium transport. SGLT1 is mainly expressed in the gastrointestinal tract and is mainly responsible for the absorption of glucose and galactose by the intestinal tract. In addition, MFSD4B is also present in the proximal straight tube of the kidney, which helps to absorb plasma glucose filtered from the blood. Under low glucose conditions, the expression of MFSD4B in the small intestine is down-regulated, mRNA expression level is also reduced, and MFSD4B function is impaired as well. Under dietary conditions, pancreatic MFSD4B mRNA did not change, indicating MFSD4B has different regulatory mechanisms in different tissues.
|Basic Information of MFSD4B|
|Protein Name||Sodium-dependent glucose transporter 1|
|Aliases||Major facilitator superfamily domain-containing protein 4B, SGLT1|
|Organism||Homo sapiens (Human)|
Function of MFSD4B Membrane Protein
Glucose transport across mammalian cell membranes is mediated either by facilitative glucose transporter (GLUT) or by SGLT1 (MFSD4B) and other SGLTs. The GLUT-mediated pathway is accomplished by passive diffusion of glucose. In contrast, MFSD4B-mediated transport is driven by sodium and glucose gradients, thus allowing glucose to move against its concentration gradient. In addition, MFSD4B is associated with detergent-resistant membrane microdomains. By disrupting these detergent-resistant membrane microdomains with methyl-β-cyclodextrin, the abundance of MFSD4B proteins in these microdomains is reduced and paralleled by a decrease of sodium-dependent glucose transport activity. Furthermore, MFSD4B is involved in the repair of plasma membrane integrity and tight junction integrity injured by heat stress and can reduce peroxynitrite and cell injury caused by cisplatin in renal tubular epithelial cells. Last but not the least, MFSD4B provides protection against damage induced by TLR ligands, in intestinal epithelial cells and in a murine model of septic shock. Thus, activated MFSD4B may be a promising target for inhibition of bacterial-induced inflammatory processes and life-saving treatments.
Fig.1 In the distal lung epithelium, glucose uptake across the apical membrane is through sodium-coupled glucose transporter SGLT1 and the basolateral membrane through GLUTs. (Garnett, 2012)
Application of MFSD4B Membrane Protein in Literature
This article finds that the different clinical features of a dual inhibitor of SGLT1 and SGLT2 may have clinical implications for the use of canagliflozin in the treatment of both type 1 and type 2 diabetes.
This article shows that high levels of SGLT1 in the brush border membrane of intestinal epithelial cells, and saponins have the potential for inhibiting glucose uptake in the gastrointestinal tract.
This article indicates that peroxynitrite is the main mediator of nephrotoxicity caused by high-dose cisplatin, and SGLT1 endogenously exerts cytoprotective effects by reducing the production of peroxynitrite.
This article proposes that activated SGLT-1, apart from its classical metabolic function, may be a promising target for inhibition of bacteria-induced inflammatory processes and life-saving treatments, assuming a novel role as an immunological player.
This article reveals the possibility that over-expressed SGLT1 in cardiomyocytes may represent a potential pharmacological target for cardioprotection.
MFSD4B Preparation Options
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All listed customized services & products are for research use only, not intended for pharmaceutical, diagnostic, therapeutic or any in vivo human use.