Diabetic Hyperglycemia: Link to Impaired Glucose Transport in Pancreatic β Cells

Unger, Roger H.

doi:10.1126/science.2006409

Cited by 263Pancreatic function and diabetesDiabetes and associated disordersDiabetes Treatment and Management

Diabetic Hyperglycemia: Link to Impaired Glucose Transport in Pancreatic β Cells

Unger, Roger H.·1991·Science

DOI 10.1126/science.2006409

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Abstract

Glucose uptake into pancreatic β cells by means of the glucose transporter GLUT-2, which has a high Michaelis constant, is essential for the normal insulin secretory response to hyperglycemia. In both autoimmune and nonautoimmune diabetes, this glucose transport is reduced as a consequence of down-regulation of the normal β-cell transporter. In autoimmune diabetes, circulating immunoglobulins can further impair this glucose transport by inhibiting functionally intact transporters. Insights into mechanisms of the unresponsiveness of β cells to hyperglycemia may improve the management and prevention of diabetes.

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GLUTs are involved in glucose sensing in pancreatic beta cells, and the GLUT isoforms in these insulin-secreting cells have a different glucose sensitivity threshold than those in fat and muscle cells.
“GLUTs are also involved in glucose sensing in pancreatic beta cells, with the caveat that the GLUT isoforms present in these insulin-secreting cells possess a different glucose sensitivity threshold than those in fat and muscle cells ( 28-31 ).”
From Dynamic modulation of glucose utilisation by glucocorticoid rhythms in health and disease (2020) · cites this paper as [31]
Parameters associated with glucose uptake in peripheral cells and maximum rates of production and utilisation were estimated from prior data.
“the parameters associated to glucose uptake in peripheral cells, as well as maximum rates of production and utilisation, were estimated from ( 31, 43, 44 ).”
From Dynamic modulation of glucose utilisation by glucocorticoid rhythms in health and disease (2020) · cites this paper as [31]
In pancreatic beta cells, GLUT1, GLUT2 and GLUT3 are involved in glucose sensing and possess different affinities for extracellular glucose compared to those in fat and muscle cells.
“In pancreatic beta cells, GLUT1, GLUT2 and GLUT3 are involved in glucose sensing and possess different affinities for extracellular glucose compared to those in fat and muscle cells (26, 28).”
From The progression of secondary diabetes: A review of modeling studies (2022) · cites this paper as [28]

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Self-citation
Underexpression of β Cell High K m Glucose Transporters in Noninsulin-Dependent Diabetes
Johnson, J. H., Ogawa, A., Chen, L., Orci, L., Newgard, C. B., Alam, T., & Unger, R. H. (1990) · Science · doi:10.1126/science.2237405 · Cited by 201 · see citing works
Self-citation
Reduced beta-cell glucose transporter in new onset diabetic BB rats.
Orci, L., Unger, R. H., Ravazzola, M., Ogawa, A., Komiya, I., Baetens, D., Lodish, H. F., & Thorens, B. (1990) · Journal of Clinical Investigation · doi:10.1172/jci114883 · Cited by 96 · see citing works
Self-citation
Pancreatic β-cells express a low affinity glucose transporter: functional consequences in normal and diabetic states
Marshall, M. O., THOMAS, H. M., Seatter, M. J., Greer, K. R., Wood, P. J., & Gould, G. W. (1993) · Biochemical Society Transactions · doi:10.1042/bst0210164 · Cited by 4 · see citing works

Authors: Unger, R. H.
Affiliations: Center for Diabetes Research, Gifford Laboratories, Dallas, TX.
Corresponding author: Unger, Roger H.
Venue: Science
Publisher: American Association for the Advancement of Science (AAAS)
Published: 1991-03-08
Volume: 251
Issue: 4998
Pages: 1200-1205
ISSN: 0036-8075 (ISSN-L)
1095-9203
DOI: 10.1126/science.2006409
OpenAlex: W2075542857
Cited by: 263
References: 71
Citations by year: 2025: 1 · 2024: 1 · 2022: 3 · 2021: 3 · 2020: 6 · 2019: 3 · 2018: 6 · 2017: 6 · 2016: 3 · 2015: 6 · 2014: 5 · 2013: 4 · 2012: 6
FWCI: 9.74
Type: journal article
Language: en
Open access: closed
Locations: Science (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health (5r37dk002700-34, 5p01dk042582-04)
National Institute of Diabetes and Digestive and Kidney Diseases (1-PO1-DK42582-01, 5-R37-DK02700-31)
Topics: Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
Keywords: diabetic hyperglycemia, pancreatic beta cells, glucose transport, GLUT2, insulin secretion, autoimmune diabetes, transporter downregulation, immunoglobulins
MeSH terms: Adult, Aged, Child, Diabetes Mellitus, Diabetes Mellitus, Type 1, Diabetes Mellitus, Type 2, Glucose, Humans, Hyperglycemia, Islets of Langerhans, Middle Aged, Models, Biological, Monosaccharide Transport Proteins

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Diabetic Hyperglycemia: Link to Impaired Glucose Transport in Pancreatic β Cells

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