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Last update 08 May 2025

GLUT5

Last update 08 May 2025

Basic Info

Synonyms

Fructose transporter, Glucose transporter type 5, small intestine, GLUT-5

+ [5]

Introduction

Functions as a fructose transporter that has only low activity with other monosaccharides (PubMed:16186102, PubMed:17710649, PubMed:28083649, PubMed:29548810, PubMed:8333543). Can mediate the uptake of 2-deoxyglucose, but with low efficiency (PubMed:1695905). Essential for fructose uptake in the small intestine (By similarity). Plays a role in the regulation of salt uptake and blood pressure in response to dietary fructose (By similarity). Required for the development of high blood pressure in response to high dietary fructose intake (By similarity).

Drugs associated with GLUT5

S-700

Target

GLUT5

Mechanism

GLUT5 blockers

Active Org.

SCOHIA PHARMA, Inc.

Originator Org.

SCOHIA PHARMA, Inc.

Active Indication

Metabolic Diseases

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with GLUT5

100 Translational Medicine associated with GLUT5

0 Patents (Medical) associated with GLUT5

669

Literatures (Medical) associated with GLUT5

01 Apr 2025·Journal of Neuroimmunology

Sugar utilization by microglia in Alzheimer's disease

Article

Author: Shippy, Daniel C ; Ulland, Tyler K ; Marino, Kaitlyn M

Diabetes is a major risk factor for Alzheimer's disease (AD), yet the effect of specific carbohydrate sources in the diet on AD pathology remains unclear. The primary neuroimmune cell, microglia, undergo a metabolic shift during neuroinflammation associated with AD pathology. We utilized existing gene expression data and identified changes in sugar transporters (increased Slc2a1 (glucose) and decreased Slc2a5 (fructose) expression). To examine gene expression with respect to primary sugar source, N9 cells, a mouse microglia cell line, were cultured in glucose or fructose supplemented media and stimulated with lipopolysaccharide (LPS). RNA-sequencing analyses indicated significant changes between control and sugar supplemented media and several differentially expressed genes between glucose and fructose media. Concurrently, 5XFAD mice received equicaloric diets with specific carbohydrate sources: dextrose or fructose. Regardless of diet, sex, or genotype, all mice developed high blood sugar levels; confocal microscopy analyses indicated similar amyloid plaque burden and microglial response relative to the control diet, but there was a change in the microglial response between dextrose and fructose fed mice. Overall, these data indicate microglia preferentially express sugar transporters and sugar source may influence microglial reactivity in response to plaque pathology.

01 Mar 2025·Cancer Cell

Metabolic engineering to facilitate anti-tumor immunity

Article

Author: Pierpont, Kaitlyn ; Chirayil, Rachel ; Schild, Tanya ; Nunes-Violante, Sara ; Chen, Kevin ; Thompson, Craig B ; Wang, Ya-Ting ; Haughton, Lyric ; Scheinberg, David A ; de Stanchina, Elisa ; Perry, Justin S A ; Wallisch, Patrick ; Keshari, Kayvan R ; Cross, Justin ; Zhao, Yixuan

Fructose consumption is elevated in western diets, but its impact on anti-tumor immunity is unclear. Fructose is metabolized in the liver and small intestine, where fructose transporters are highly expressed. Most tumors are unable to drive glycolytic flux using fructose, enriching fructose in the tumor microenvironment (TME). Excess fructose in the TME may be utilized by immune cells to enhance effector functions if engineered to express the fructose-specific transporter GLUT5. Here, we show that GLUT5-expressing CD8⁺ T cells, macrophages, and chimeric antigen receptor (CAR) T cells all demonstrate improved effector functions in glucose-limited conditions in vitro. GLUT5-expressing T cells show high fructolytic activity in vitro and higher anti-tumor efficacy in murine syngeneic and human xenograft models in vivo, especially following fructose supplementation. Together, our data demonstrates that metabolic engineering through GLUT5 enables immune cells to efficiently utilize fructose and boosts anti-tumor immunity in the glucose-limited TME.

01 Mar 2025·Hypertension Research

Possible involvement of up-regulated salt-dependent glucose transporter-5 (SGLT5) in high-fructose diet-induced hypertension

Article

Author: Shimizu, Taisuke ; Hasegawa, Hajime ; Ikari, Akira ; Maeshima, Akito ; Iwashita, Takatsugu ; Takayanagi, Kaori ; Hara, Hiroaki

Excessive fructose intake causes a variety of adverse conditions (e.g., obesity, hepatic steatosis, insulin resistance and uric acid overproduction). High fructose-induced hypertension is a particularly common and pathologically significant condition induced by excess fructose, but its underlying mechanisms remain unknown. We investigated these mechanisms in 7-week-old male Sprague-Dawley rats fed normal rat food or a diet containing 60% glucose (GLU group) or 60% fructose (FRU group) for 3, 6, or 12 weeks. Daily food consumption was measured to avoid between-group discrepancies in caloric/salt intake, adjusting for feeding amounts. The mean blood pressure of FRU rats was significantly higher (12 weeks GLU: 94.8 ± 3.4 mmHg vs. 12 weeks FRU: 103.7 ± 1.2 mmHg), and fractional sodium excretion was significantly lower (12 weeks GLU: 0.084 ± 0.011% vs. 12 weeks FRU: 0.059 ± 0.08%), indicating that the high-fructose diet caused salt retention. The kidney weight and glomerular surface area were greater in FRU rats (12 weeks GLU: 7495 ± 181 vs. 12 weeks FRU: 9831 ± 164 μm²), suggesting that the high-fructose diet induced an increase in extracellular fluid volume. The expressions of GLUT5 and ketohexokinase, an enzyme required for fructose metabolism, were up-regulated in the FRU group rats (GLUT5 12 weeks GLU: 104.7 ± 15.4% vs. 12 weeks FLU: 309.0 ± 99.9%, ketohexokinase 12 weeks GLU: 129.6 ± 3.5% vs. 12 weeks FLU: 163.9 ± 13.0%). Cortical ATP levels were significantly lower in FRU rats (12 weeks GLU: 9.82 ± 1.26 nmol/mg protein vs. 12 weeks FRU: 7.59 ± 1.68 nmol/mg protein), possibly indicating ATP consumption due to fructose metabolism. Unlike in previous reports the high-fructose diet did not affect NHE3 expression (12 weeks GLU: 166.1 ± 6.3% vs. 12 weeks FLU: 142.0 ± 5.9%). A gene chip analysis conducted to identify susceptible molecules revealed that only Slc5a10 (corresponding to SGLT5) showed >two-fold up-regulation in FRU versus GLU rats. RT-PCR and in situ hybridization confirmed the SGLT5 up-regulation (12 weeks GLU: 75.0 ± 5.8% vs. 12 weeks FLU: 230.1 ± 16.0%). Our findings may indicate that the high-fructose diet increased sodium reabsorption principally through up-regulated SGLT5, finally causing salt-sensitive hypertension.

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GLUT5

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