ArticleThe Journal of biological chemistry2013
Mutations in SLC2A2 gene reveal hGLUT2 function in pancreatic β cell development.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 27 citations in OpenAlex.
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- Progress in Understanding the Regulation of Glucose and Fructose Metabolism.Annual review of nutrition · 2025Review
- The glucose transporter 2 regulates CD8Nature metabolism · 2023Article
- Pax4-Ghrelin mediates the conversion of pancreatic ε-cells to β-cells after extreme β-cell loss in zebrafish.Development (Cambridge, England) · 2023Article
- Evidence-Based Anti-Diabetic Properties of Plant from the Occitan Valleys of the Piedmont Alps.Pharmaceutics · 2022Review
- Ambush predation and the origin of euprimates.Science advances · 2022Article
- Decreased GLUT2 and glucose uptake contribute to insulin secretion defects in MODY3/HNF1A hiPSC-derived mutant β cells.Nature communications · 2021Article
- Fanconi-Bickel Syndrome: A Review of the Mechanisms That Lead to Dysglycaemia.International journal of molecular sciences · 2020Review
- Review
- Functional and structural analysis of rare SLC2A2 variants associated with Fanconi-Bickel syndrome and metabolic traits.Human mutation · 2019Article
- Genetic Analysis of Signal Generation by the Rgt2 Glucose Sensor ofG3 (Bethesda, Md.) · 2018Article
- Cholesterol trafficking and raft-like membrane domain composition mediate scavenger receptor class B type 1-dependent lipid sensing in intestinal epithelial cells.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2018Article
- Multiple Transceptors for Macro- and Micro-Nutrients Control Diverse Cellular Properties Through the PKA Pathway in Yeast: A Paradigm for the Rapidly Expanding World of Eukaryotic Nutrient Transceptors Up to Those in Human Cells.Frontiers in pharmacology · 2018Review
- 20-HETE attenuates the response of glucose-stimulated insulin secretion through the AKT/GSK-3β/Glut2 pathway.Endocrine · 2016Article
- Monogenic Diabetes: What It Teaches Us on the Common Forms of Type 1 and Type 2 Diabetes.Endocrine reviews · 2016Review
- Isoform-selective inhibition of facilitative glucose transporters: elucidation of the molecular mechanism of HIV protease inhibitor binding.The Journal of biological chemistry · 2014Article
- Management of Dysglycemia in a Pregnancy Complicated by Fanconi-Bickel Syndrome.AACE clinical case reportsArticle
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Authors and funding
15 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The structure-function relationships of sugar transporter-receptor hGLUT2 coded by SLC2A2 and their impact on insulin secretion and β cell differentiation were investigated through the detailed characterization of a panel of mutations along the protein. We studied naturally occurring SLC2A2 variants or mutants: two single-nucleotide polymorphisms and four proposed inactivating mutations associated to Fanconi-Bickel syndrome. We also engineered mutations based on sequence alignment and conserved amino acids in selected domains. The single-nucleotide polymorphisms P68L and T110I did not impact on sugar transport as assayed in Xenopus oocytes. All the Fanconi-Bickel syndrome-associated mutations invalidated glucose transport by hGLUT2 either through absence of protein at the plasma membrane (G20D and S242R) or through loss of transport capacity despite membrane targeting (P417L and W444R), pointing out crucial amino acids for hGLUT2 transport function. In contrast, engineered mutants were located at the plasma membrane and able to transport sugar, albeit with modified kinetic parameters. Notably, these mutations resulted in gain of function. G20S and L368P mutations increased insulin secretion in the absence of glucose. In addition, these mutants increased insulin-positive cell differentiation when expressed in cultured rat embryonic pancreas. F295Y mutation induced β cell differentiation even in the absence of glucose, suggesting that mutated GLUT2, as a sugar receptor, triggers a signaling pathway independently of glucose transport and metabolism. Our results describe the first gain of function mutations for hGLUT2, revealing the importance of its receptor versus transporter function in pancreatic β cell development and insulin secretion.
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