GLUT5 _ SLC2A5
- Known as:
- GLUT5 _ SLC2A5
- Catalog number:
- Y214336
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- GLUT5 _ SLC2A5
Related genes to: GLUT5 _ SLC2A5
- Gene:
- SLC2A5 NIH gene
- Name:
- solute carrier family 2 member 5
- Previous symbol:
- GLUT5
- Synonyms:
- -
- Chromosome:
- 1p36.23
- Locus Type:
- gene with protein product
- Date approved:
- 1994-05-25
- Date modifiied:
- 2016-10-05
Related products to: GLUT5 _ SLC2A5
anti-Glucose Transporter 5 GLUT5anti-Glucose Transporter 5 GLUT5Anti-Glucose Transporter 5 GLUT5 AntibodyAnti-Glucose Transporter 5 GLUT5 Antibodyanti-Glucose Transporter 5 GLUT5 type: Primary antibodies host: Mouseanti-GLUT5anti-SLC2A5 / GLUT5 (C-Terminus)Anti-SLC2A5, Goat Polyclonal to SLC2A5, Isotype , Host GoatBovine solute carrier family 2 (facilitated glucose_fructose transporter), member 5 (SLC2A5) ELISA kit, Species Bovine, Sample Type serum, plasmaBovine Solute carrier family 2, facilitated glucose transporter member 5(SLC2A5) ELISA kitBovine Solute carrier family 2, facilitated glucose transporter member 5(SLC2A5) ELISA kit SpeciesBovineELISA Kit FOR Solute carrier family 2, facilitated glucose transporter member 5; organism: Mouse; gene name: Slc2a5ELISA Kit FOR Solute carrier family 2, facilitated glucose transporter member 5; organism: Rat; gene name: Slc2a5Glucose Transporter 5 (GLUT5)ELISA kit, HumanGlucose Transporter GLUT5 Lysate Related articles to: GLUT5 _ SLC2A5
- Glioblastoma (GBM) remains one of the most aggressive and treatment-resistant brain tumors in adults. Its immune microenvironment is dominated by tumor-associated macrophages, including both infiltrating monocytes and brain-resident microglia. While metabolic rewiring of infiltrating myeloid cells has been shown to support tumor progression, the role of microglial metabolism in GBM remains incompletely understood. Here, we demonstrate that microglia uniquely express the fructose transporter GLUT5 and are the only immune cells in the GBM microenvironment capable of metabolizing fructose. Using murine orthotopic glioma and Replication-Competent Avian sarcoma leuko virus Splice acceptor (RCAS)-derived tumor models, we show that global deletion of GLUT5 confers profound resistance to tumor growth. This effect is driven by loss of fructose metabolism in microglia and occurs independently of contributions from peripheral immune compartments. In GLUT5-deficient mice, tumors exhibit increased infiltration and activation of both innate and adaptive immunity, including enhanced antigen presentation, clonal expansion of CD8+ T cells, and increased cytokine production. Depletion of B-cells or CD8+ T cells abrogated survival phenotypes in knockout mice, demonstrating that GLUT5 suppresses adaptive immunity. These findings identify microglial fructose metabolism as a critical regulator of immune suppression in GBM and suggest that targeting this pathway may improve immunotherapeutic responses. - Source: PubMed
Publication date: 2026/03/17
Billingham Leah KDeLay Susan LEshac YasminaChia Tzu-YiTripathi ShashwatOlson Ian EZilinger KayleeSubbiah JayWang ZhaoquanSadagopan Nishanth SNajem HindaCognet GuillaumeKatz Joshua LDu RuochenNandoliya Khizar RBoland Lauren KIgnacio Vázquez-Cervantes GustavoWang SiWan HanxiaoLipshutz Allie BMurphy Alina RDuffy JosephBalyasnikova Irina VZhang PengHeiland Dieter HenrikAhmed Atique ULee-Chang CatalinaHeimberger Amy BPerry Justin S AMuir AlexanderChandel Navdeep SMiska Jason - Fructose is an abundant monosaccharide in the human diet and an important source of energy in the human body. GLUT5, a member of facilitative glucose transporter family, is the only membrane transporter that specifically transports fructose in the human body, and plays an important role in dietary fructose uptake and metabolism. Previous studies have shown that medium-chain fatty acids (MCFAs) can regulate glucose metabolism via modulating glucose transporters. However, it has not been addressed if MCFAs can regulate GLUT5-mediated fructose metabolism. In the present study, we demonstrated for the first time that MCFAs but not short chain or long chain fatty acids are able to promote fructose uptake in both IEC-18 rat intestinal epithelial cells and human MDA-MB-231 breast cancer cells (a commonly used cell line for fructose metabolism-related study) measured by 1-NBD-Fructose-based assay, which are well correlated with the activation of GLUT5-KHK axis. Moreover, the activation of GLUT5-ketohexokinase (KHK) axis was also achieved in vivo by the treatment with tricapylin, a precursor of octanoic acid (OA), leading to the improvement in fructose-based energy recovery after fasting. The findings of the present study not only provide novel mechanistic support for MCFAs as regulator of carbohydrate metabolism, but also denote that MCFAs could be useable for managing fructose-associated metabolic diseases or as an enhancer for energy recovery after fasting or exercise. - Source: PubMed
Publication date: 2026/01/27
Hou JiruLi JiaxuanZhao ChongYin ShutaoHu Hongbo - Excessive saccharide intake contributes to type 2 diabetes development. Polyphenols may decrease saccharide absorption in the small intestine. We investigated the potential of curcuminoids to modulate glucose and fructose absorption and expression of saccharide transporters SGLT1 and GLUT5 in differentiated Caco-2 cells. We also examined the impact of glucose-to-fructose ratios on curcumin's ability to inhibit saccharide absorption. Caco-2 cells were pre-exposed to 1 mM phloretin, 500 μM phlorizin, 400 μM dibenzoylmethane, 200 μM curcumin, or 200 μM bisdemethoxycurcumin for 4 h followed by a 30-min exposure to different glucose-to-fructose ratios. Basolateral glucose and NBD-fructose levels were measured, along with SGLT1, GLUT5, and MLCK1 expression. FITC-dextran absorption was assessed to evaluate paracellular fructose absorption. All reported changes were statistically significant (p < 0.05). Dibenzoylmethane reduced glucose absorption by 50 % and SGLT1 expression by 45 %. Curcumin decreased glucose absorption by 72 % and SGLT1 expression by 25 %. Bisdemethoxycurcumin led to a 37 % reduction in glucose absorption and an 80 % decrease in SGLT1 expression. Interestingly, curcumin and bisdemethoxycurcumin increased basolateral NBD-fructose concentrations by 170 % and 105 %, respectively, without any changes in GLUT5 expression. Higher glucose-to-fructose ratios reduced curcumin's inhibitory effect on glucose absorption by 15 %, but did not affect fructose absorption stimulation. Lower fructose eliminated curcumin's fructose absorption stimulation. Curcumin increased FITC-dextran permeation by 20 % across ratios, suggesting increased paracellular permeability. In contrast, MLCK1 expression decreased by 30 %. In conclusion, dibenzoylmethane demonstrated potent inhibition of glucose absorption and SGLT1 expression, while curcumin and bisdemethoxycurcumin decreased glucose absorption and enhanced fructose absorption in differentiated Caco-2 cells. - Source: PubMed
Publication date: 2025/07/31
Dohmen C G MTroost F JMuijsenberg ASthijns M M J P E - Pheochromocytomas and paragangliomas (PPGLs) with SDHB mutations frequently develop metastases, but the molecular mechanisms driving this progression remain unclear. Here we show that SDHB-mutant metastatic PPGLs display an amplified hypermethylation signature, particularly in genes involved in neuronal differentiation, building on previous findings in SDHx-mutated tumors. This epigenetic shift is already detectable in benign SDHB-mutant tumors, suggesting early priming toward a less differentiated state. In parallel, we identify hypomethylation of genes linked to carbohydrate metabolism, notably the fructose transporter SLC2A5. Functional assays reveal that SDHB loss, hypoxia, exogenous succinate, and fructose availability promote tumor cell growth and induce cell-type-restricted, SDHB-dependent, induction of SLC2A5 expression. These findings highlight the dual role of SDHB mutations in driving epigenetic reprogramming and metabolic adaptation, promoting tumor cell plasticity and survival under metabolic stress. By uncovering a fructose-driven metabolic vulnerability, our study provides insights into the molecular mechanisms underlying metastatic PPGLs and identifies potential therapeutic targets at the intersection of epigenetic and metabolic regulation. - Source: PubMed
Publication date: 2026/01/15
Cubiella TamaraAlba-Linares Juan JoséSan-Juan-Guardado JaimeSuarez-Priede AlvaroGómez-Suárez NereaTous MariaBancos IrinaVillabona CarlesSerrano TeresaTena IsabelDel Olmo MaribelForga LluisValdés NuriaFraga Mario FChiara María-Dolores - L-Glucose is an enantiomer of D-glucose. It is controversial whether intestinal absorption of L-glucose is mediated by sodium/glucose cotransporter 1 (Sglt1). We examined whether L-glucose is absorbed via Sglt1 using KGA-2727, an Sglt1-specific inhibitor, and via glucose transporter (Glut5), a fructose transporter, using fructose-fed rats as well. KGA-2727 significantly blocked the increase of plasma L-glucose levels and lowered the C and AUC values. Feeding the high-fructose diet induced significantly higher intestinal Glut5 mRNA expression and higher absorption of orally administered D-fructose, but did not affect L-glucose levels and pharmacokinetic parameters. The results suggest that L-glucose is likely transported via Sglt1 in rat small intestine. - Source: PubMed
Kishida KunihiroToyoda YukiyasuTsuzuki Takamasa