The DOI matches its Crossref record; 44 of the 44 references it cites were found in a registry or an index.
Human and rat beta cells differ in glucose transporter but not in glucokinase gene expression.
Open accessAbstract
Glucose homeostasis is controlled by a glucose sensor in pancreatic beta-cells. Studies on rodent beta-cells have suggested a role for GLUT2 and glucokinase in this control function and in mechanisms leading to diabetes. Little direct evidence exists so far to implicate these two proteins in glucose recognition by human beta-cells. The present in vitro study investigates the role of glucose transport and phosphorylation in beta-cell preparations from nondiabetic human pancreata. Human beta-cells differ from rodent beta-cells in glucose transporter gene expression (predominantly GLUT1 instead of GLUT2), explaining their low Km (3 mmol/liter) and low VMAX (3 mmol/min per liter) for 3-O-methyl glucose transport. The 100-fold lower GLUT2 abundance in human versus rat beta-cells is associated with a 10-fold slower uptake of alloxan, explaining their resistance to this rodent diabetogenic agent. Human and rat beta-cells exhibit comparable glucokinase expression with similar flux-generating influence on total glucose utilization. These data underline the importance of glucokinase but not of GLUT2 in the glucose sensor of human beta-cells.
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“Apparently glucose transport via GLUT1 is not rate limiting in these cases, and the sensing is explained by the presence of the high K m glucokinase (39,40).”
From Paradoxical Stimulation of Glucagon Secretion by High Glucose Concentrations (2006) · cites this paper as [39]
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Cites
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Efeyan, A., Comb, W. C., & Sabatini, D. M. (2015) · Nature · doi:10.1038/nature14190 · Cited by 1,110
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Metadata
- Authors
- De Vos, A., Heimberg, H., Quartier, E., Huypens, P., Bouwens, L., Pipeleers, D., & Schuit, F.
- Venue
- Journal of Clinical Investigation
- Published
- 1995-11-01
- Volume
- 96
- Issue
- 5
- Pages
- 2489-2495
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC185903
- OpenAlex
- W2015001567
- Cited by
- 425
- References
- 40
- Citations by year
- 2026: 3 · 2025: 13 · 2024: 16 · 2023: 16 · 2022: 15 · 2021: 23 · 2020: 14 · 2019: 15 · 2018: 12 · 2017: 17 · 2016: 27 · 2015: 21 · 2014: 23 · 2013: 23 · 2012: 21
- FWCI
- 11.19
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Eli Lilly and Company
- Universitaire Stichting
- Université de Genève
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- pancreatic beta cells, GLUT2, GLUT1, glucokinase, glucose transporter gene expression, glucose detection, glucose homeostasis, alloxan, glucose phosphorylation, diabetes mellitus
- MeSH terms
- Animals, Cells, Cultured, Glucokinase, Glucose, Humans, Islets of Langerhans, Monosaccharide Transport Proteins, Phosphorylation, Gene Expression, Glucose Transporter Type 1, Glucose Transporter Type 2, Rats
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