GLUT2

Last update 08 May 2025

Basic Info

Synonyms

Glucose transporter type 2, liver, GLUT-2, GLUT2

+ [4]

Introduction

Facilitative hexose transporter that mediates the transport of glucose, fructose and galactose (PubMed:16186102, PubMed:23396969, PubMed:28083649, PubMed:8027028, PubMed:8457197). Likely mediates the bidirectional transfer of glucose across the plasma membrane of hepatocytes and is responsible for uptake of glucose by the beta cells; may comprise part of the glucose-sensing mechanism of the beta cell (PubMed:8027028). May also participate with the Na(+)/glucose cotransporter in the transcellular transport of glucose in the small intestine and kidney (PubMed:3399500). Also able to mediate the transport of dehydroascorbate (PubMed:23396969).

100 Clinical Results associated with GLUT2

100 Translational Medicine associated with GLUT2

0 Patents (Medical) associated with GLUT2

2,609

Literatures (Medical) associated with GLUT2

01 Dec 2025·Molecular Biology Reports

Do human adipose stem cell-derived artificial insulin-producing cells develop tumorigenic characteristics throughout differentiation?

Article

Author: Forouzanfar, Mohsen ; Jafarinia, Mojtaba ; Salehi Babadi, Parastoo ; Dayer, Dian

BACKGROUNDArtificial insulin-producing cells (IPCs) used to treat diabetes mellitus type 1 (DMT1) are naturally hampered by their carcinogenicity. This in vitro study aimed to examine the carcinogenic potential of IPCs produced by the differentiation of human adipose tissue-derived mesenchymal stem cells (hADSCs).METHODS AND RESULTShADSCs were transformed into IPCs by administering insulin-transferrin, selenium (ITS), and nicotinamide in a 14-day differentiation protocol. The cells were transfected with 20 μg of pure Pdx1-pIRES recombinant vector on the tenth day of differentiation. The successful transfection was confirmed by Pdx1 overexpression and GFP fluorescence activity. The differentiated cells' capacity to release insulin and glucose-dependent C-peptide was used to evaluate their functionality. Gene expression was assessed using real-time PCR. Meanwhile, protein expression was investigated using western blotting. The transfected cells exhibited fluorescence activity and Pdx1 overexpression. The differentiated IPCs were able to secrete C-peptide and insulin. The artificial IPCs showed significantly reduced Oct4 and Nanog expression. However, the differentiation process induced a noticeable elevation in tPA expression. The artificial IPCs expressed much lower c-MYC expression compared to undifferentiated hADSCs. The differentiated cells exhibited a significant elevation in Glut2, MMP-2, CD24, P16, and P21 expression.CONCLUSIONSThe differentiation technique used in this work produced functional beta-like cells devoid of typical markers of stem cells. The synthetic IPCs displayed characteristics of newly generated β-like cells. The artificial IPCs showed no signs of expressing tumor-associated markers. The findings imply that the artificial IPC cells lack tumor characteristics in vitro.

01 Jul 2025·Food and Chemical Toxicology

Glyphosate exposure impairs glucose and lipid metabolism by disturbing the circadian clock system in mice liver

Article

Author: Jin, Yaping ; Chen, Huatao ; Xiao, Bonan ; Wang, Aihua ; Jiang, Haizhen ; Li, Chao ; Dong, Hao ; Zhang, Haisen ; Gao, Dengke

Glyphosate, the most extensively applied organophosphonate herbicide, poses risks to aquatic ecosystems and potentially compromises human health via dietary exposure. Although toxicological assessments have confirmed glyphosate-induced hepatotoxicity in mammalian systems, the cellular pathogenesis involving metabolic disruption warrants further mechanistic investigation. This study aimed to elucidate the effect of glyphosate exposure on hepatic glucose/lipid metabolism and its association with circadian clock disruption using murine hepatocytes (AML12) and mice models. Time-course analysis revealed that glyphosate exposure significantly suppressed core circadian and metabolic transcripts in AML12 hepatocytes, with corresponding reduction in NR1D1 protein level. Longitudinal locomotor activity monitoring revealed that glyphosate exposure caused photophase-specific hyperlocomotion and circadian period elongation in mice. Glyphosate exposure elicited marked depletion of hepatic glycogen reserves and serum total cholesterol concentrations. Notably, glyphosate also disrupted the expression of hepatic metabolic genes, paralleled by alterations of circadian clock genes expression at both mRNA and protein levels in mice. Additionally, Hmgcr and Glut2 mRNA levels were significantly decreased in Bmal1^-/- AML12 cells compared to their control groups, no further significant reduction was detected in Bmal1^-/- AML12 cells with glyphosate exposure. Collectively, the current study demonstrated that glyphosate exposure impairs glucose and lipid metabolism by disturbing the circadian clock system.

01 Jun 2025·Pediatric Nephrology

Etiology, clinical characteristics, genetic profile, and outcomes of children with refractory rickets at a referral center in India: a cohort study

Article

Author: Krishnamurthy, Sriram ; Sravani, Madhileti ; Ramprabhu, Gopalan Suresh ; Krishnasamy, Sudarsan ; Deepthi, Bobbity ; Mathew, Varna ; Yadav, Prabhaker ; Mandal, Kausik ; Bhatt, Girish Chandra

BACKGROUNDLimited research exists regarding the genetic profile, clinical characteristics, and outcomes of refractory rickets in children from India.METHODSPatients with refractory rickets aged ≤ 18 years were enrolled. Data regarding clinical features, etiology, genotype-phenotype correlation, and estimated glomerular filtration rate (eGFR) were recorded.RESULTSSeventy-two patients with refractory rickets (non-nutritional, with normal kidney function at presentation) from 65 families attending the pediatric nephrology clinic from 2005-2024 were included. Median (IQR) age at first presentation was 2 (1, 4) years. Clinical features included failure-to-thrive (49 [68.1%]), polyuria (37 [51.4%]), nephrocalcinosis (33 [45.8%]), fractures (10 [13.9%]), and hypokalemic paralysis (4 [5.6%]). Major etiologies included distal renal tubular acidosis (dRTA) [34(47.2%)], hereditary hypophosphatemic rickets (11 [15.3%]), cystinosis (9 [12.5%]), Lowe syndrome (3 [4.2%]), vitamin D-dependent rickets (4 [5.5%]), and Fanconi-Bickel syndrome (3 [4.2%]). Next-generation sequencing identified 61 variants among 71 children tested (85.9%), of which 56 variants (among 55 children) were pathogenic (P)/likely-pathogenic (LP) (77.5% diagnostic-yield). P/LP variants included SLC4A1 (n = 14), CTNS (n = 9), PHEX (n = 8), WDR72 (n = 5), OCRL (n = 2), SLC2A2 (n = 3), ATP6V0A4 (n = 4), VDR (n = 3), CLDN16 (n = 2), ATP6V1B1 (n = 1), SLC12A1 (n = 1), CLCN5 (n = 1), SLC34A3 (n = 1), ATP7B (n = 1), and KCNJ1 (n = 1). Fifteen novel P/LP variants and five novel variants-of-uncertain-significance (VUS) were identified. c.2573C > A in exon 19 among SLC4A1-dRTA (n = 14) was a recurrent mutation. Five patients with cystinosis, two patients with SLC4A1-dRTA, two with WDR72-dRTA, and two with Bartter syndrome showed progression to CKD stage 2 or greater during follow-up.CONCLUSIONSdRTA, X-linked hypophosphatemic rickets, and cystinosis were common causes of refractory rickets. The c.2573C > A variant in exon 19 was a recurrent mutation in SLC4A1-dRTA.

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GLUT2

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