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The glucose transporter families SGLT and GLUT: molecular basis of normal and aberrant function
Abstract
Glucose enters eucaryotic cells via 2 different types of membrane associated carrier proteins, the Na+‐coupled glucose transporters (SGLT) and glucose transporter facilitators (GLUT). Three members of the SGLT family function as sugar transporters (SGLT1 and SGLT2) or sensors (SGLT3). The human GLUT family consists of 14 members, of which 11 have been shown to catalyze sugar transport. The individual isotypes exhibit different substrate specificity, kinetic characteristics, and expression profiles, thereby allowing a tissue‐specific adaptation of glucose uptake through regulation of their gene expression. Furthermore, some transporters (eg, GLUT4 and GLUT8) are regulated by their subcellular distribution. In addition to catalyzing glucose entry into cells, some isotypes (eg, GLUT2) seem to be involved in the mechanisms of glucosensing of pancreatic beta‐cells, neuronal, or other cells, thereby playing a major role in the hormonal and neural control. Targeted disruption in mice has helped to elucidate the physiologic function of some isotypes (GLUT1, GLUT2, GLUT4). Furthermore, several congenital defects of sugar metabolism are caused by aberrant transporter genes (eg, the glucose‐galactose malabsorption syndrome, SGLT1; the glucose transporter 1 deficiency syndrome; and the Fanconi‐Bickel syndrome, GLUT2). In addition, a malfunction of glucose transporter expression or regulation (GLUT4) appears to contribute to the insulin resistance syndrome.
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“a process that is amplified by the translocation of GLUTs from intracellular pools to the cell membrane following insulin stimulation ( 26, 27 ).”
From Dynamic modulation of glucose utilisation by glucocorticoid rhythms in health and disease (2020) · cites this paper as [26]
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Metadata
- Authors
- Scheepers, A., Joost, H., & Schurmann, A.
- Affiliations
- German Institute of Human Nutrition (DE)
- Venue
- Journal of Parenteral and Enteral Nutrition
- Publisher
- Wiley
- Published
- 2004-09
- Volume
- 28
- Issue
- 5
- Pages
- 364-371
- ISSN
- 0148-6071 (ISSN-L)
- 1941-2444
- OpenAlex
- W1993812967
- Cited by
- 476
- References
- 0
- Citations by year
- 2026: 7 · 2025: 17 · 2024: 16 · 2023: 16 · 2022: 27 · 2021: 26 · 2020: 27 · 2019: 24 · 2018: 29 · 2017: 22 · 2016: 23 · 2015: 29 · 2014: 34 · 2013: 28 · 2012: 28
- FWCI
- 3.76
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Parenteral and Enteral Nutrition (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Keywords
- glucose transporters, GLUT family, SGLT1, SGLT2, GLUT1, GLUT2, GLUT4, GLUT8, glucose transport, sugar transporters, glucose detection, pancreatic beta cells, GLUT1 deficiency syndrome, Fanconi-Bickel syndrome, insulin resistance, gene expression regulation
- MeSH terms
- Animals, Biological Transport, Active, Gene Expression Regulation, Glucose, Humans, Monosaccharide Transport Proteins, Signal Transduction, Protein Isoforms, Mice
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