Cited by 425Pancreatic function and diabetesDiabetes Treatment and ManagementMetabolism, Diabetes, and Cancer

Human and rat beta cells differ in glucose transporter but not in glucokinase gene expression.

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De Vos, A, Heimberg, H, Quartier, E, Huypens, P, Bouwens, L, Pipeleers, D, Schuit, F·1995·Journal of Clinical Investigation

Abstract

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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  • Glucose transport via GLUT1 is not rate limiting in these cases, and the sensing is explained by the presence of the high Km glucokinase.

    “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).”

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Research works printed but not linked: 2

  1. [9]9. Efrat, S., M. Leiser, Y. J. Wu, D. Fusco-DeMane, O. A. Emran, M. Surana, T. L. Jetton, M. A. Magnuson, G. Weir, and N. Fleischer. 1994. Ribozymemudao ss suss ss eunc mice results in impaired glucose-induced insulin secretion. Proc. Natl. Acad. Sci. USA. 91:2051–2055.
  2. [17]17. Pipeleers, D. 1994. Treatment of diabetes by islet cell transplantation. In Biomedical and Health Research. Vol. 3, Advances in Medical Biology. C. Baya, editor. IOS Press, Amsterdam. 185–197.

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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)
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
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 › Surgery › 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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