SLC2A8 Membrane Protein Introduction

Introduction of SLC2A8

Solute carrier family 2, facilitated glucose transporter member 8 (SLC2A8), also known as Glucose transporter type 8 (GLUT-8) or Glucose transporter type X1, is a protein that in humans is encoded by the SLC2A8 gene. It is the eighth member of the glucose transporter superfamily which is characterized by the presence of two leucine residues in its N-terminal intracellular domain, which influences intracellular trafficking.

Function of SLC2A8 Membrane Protein

Members of the glucose transporter (GLUT) family of facilitative hexose transporters are widely recognized as regulators of whole-body metabolic homeostasis. GLUT8 (SLC2A8), a cytoplasmic glucose transporter, has been shown to be expressed in highly oxidative tissues, including heart, skeletal muscle, fat, and liver. It has been reported that the expression of GLUT8  (SLC2A8) is also found in neuronal cells in several brain areas, such as the cerebral cortex, hippocampus, amygdala, and hypothalamus. Studies in a variety of models indicate that SLC2A8 regulates metabolic homeostasis. Specifically, the hepatic SLC2A8 protein is up-regulated in both streptozotocin-induced and GLUT4-haploinsufficient diabetic models. Recently, a study showed that immunoreactivity for GLUT8, but not GLUT7, GLUT11, or GLUT12, is located in epithelial cells of the choroid plexus and in the ependymal cells, suggesting the contribution of SLC2A8 to the transport of intravascular fructose into the brain.

Fig.1 Trehalose docks in the inward open glucose binding pore of GLUT8. (Mayer, 2016)

Application SLC2A8 of Membrane Protein in Literature

1. Mayer A.L., et al. Enhanced Hepatic PPAR α Activity Links GLUT8 Deficiency to Augmented Peripheral Fasting Responses in Male Mice. Endocrinology. 2018, 159(5):2110-26. PubMed ID: 29596655
   
   

   This article suggests that hepatocyte GLUT8 regulates adaptive fasting in part through regulation of the PPARα signaling cascade. Moreover, the ketotic and thermic responses to fasting are differentially encoded within the GLUT8-PPARα communication axis. GLUT8, therefore, represents a therapeutic target that can be leveraged against cardiometabolic disease.

2. Banerjee A., et al. Testicular glucose and its transporter GLUT8 as a marker of age-dependent variation and its role in steroidogenesis in mice. Journal of Experimental Zoology Part A: Ecological Genetics and Physiology. 2014, 321(9):490-502. PubMed ID: 25078271
   
   

   This article suggests that there is a significant correlation between changes in GLUT8 and glucose levels with changes in StAR level in the testis and circulating testosterone level in the mice from birth to senescence. It indicates that the changes in glucose level either directly or indirectly lead to changes in testicular steroidogenesis during aging.

3. DeBosch B.J., et al. Glucose transporter 8 (GLUT8) mediates fructose-induced de novo lipogenesis and macrosteatosis. Journal of Biological Chemistry. 2014, 289(16):10989-98. PubMed ID: 24519932
   
   

   This article suggests that GLUT8 is essential for hepatocyte fructose transport and fructose-induced macrosteatosis. Fructose delivery across the hepatocyte membrane is thus a proximal, modifiable disease mechanism that may be exploited to prevent NAFLD.

4. DeBosch B.J., et al. Glucose transporter-8 (GLUT8) mediates glucose intolerance and dyslipidemia in high-fructose diet-fed male mice. Molecular endocrinology. 2013, 27(11):1887-96. PubMed ID: 24030250
   
   

   This article suggests that GLUT8 blockade prevents fructose-induced metabolic dysregulation, potentially by enhancing hepatic fatty acid metabolism through PPARγ and its downstream targets. It indicates that GLUT8 could use as a promising target in the prevention of diet-induced obesity, metabolic syndrome, and type 2 diabetes mellitus in males.

5. DeBosch B.J., et al. Glucose transporter 8 (GLUT8) regulates enterocyte fructose transport and global mammalian fructose utilization. Endocrinology. 2012, 153(9):4181-91. PubMed ID: 22822162
   
   

   This article suggests that GLUT8 could regulate enterocyte fructose transport by regulating GLUT12 and that disrupted GLUT8 function has deleterious long-term metabolic sequelae. GLUT8 may thus represent a modifiable target in the prevention and treatment of malnutrition or the metabolic syndrome.

SLC2A8 Preparation Options

To provide high-quality products, we have developed an advanced Magic™ membrane protein production platform. Aided by our versatile Magic™ anti-membrane protein antibody discovery platform, we also provide customized anti-SLC2A8 antibody development services.

• Magic™ Membrane Protein Production Platform
• Magic™ Anti-Membrane Protein Antibody Discovery Platform

With extensive experience and professional scientists, Creative Biolabs is dedicated to promoting global customers’ programs. Except for SLC2A8 membrane protein products, we also provide other membrane protein preparation services to meet every client’s specific requirements. To learn more information, please feel free to contact us for more information.

Reference

1. Mayer, et al. (2016). SLC2A8 (GLUT8) is a mammalian trehalose transporter required for trehalose-induced autophagy. Scientific Reports. 6: 38586.

All listed services and products are For Research Use Only. Do Not use in any diagnostic or therapeutic applications.