GLUT2 underexpression has been reported in the +-cells of Zucker diabetic fatty rats and db/db mice, models of spontaneously occurring NIDDM with antecedent obesity. To determine whether the +-cells of a nonobese rodent model of NIDDM exhibit the same abnormalities in GLUT2, we studied Goto-Kakizaki rats. In these mildly diabetic animals glucose-stimulated insulin secretion was reduced at all ages examined from 8 to 48 wk. In normal control Wistar rats, immunostainable GLUT2 was present on all insulin-positive cells in the pancreatic islets. Only 85% of +-cells were GLUT2-positive in GK rats at 12 wk of age, and only 34% were positive at 48 wk of age. GLUT2 mRNA was 50% of normal in 12-wk-old GK rats. In the latter age-group, glucose-stimulated insulin secretion was only 28% of normal at a time when 85% of +-cells were GLUT2-positive and initial 3-O-methyl-D-glucose transport rate was 77% of the control value. We conclude that although GLUT2 is underexpressed, neither the magnitude of the underexpression of GLUT2 nor of the reduction in GLUT2 transport function in islets of GK rats is sufficient by itself to explain the profound reduction in glucose-stimulated insulin secretion.
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Original Articles|
July 01 1993
GLUT2 Expression and Function in β-cells of GK rats with NIDDM: Dissociation Between Reductions in Glucose Transport and Glucose-Stimulated Insulin Secretion
Makoto Ohneda;
Makoto Ohneda
Center for Diabetes Research and Gifford Laboratories, University of Texas Southwestern Medical Center
Dallas
Department of Veterans Affairs Medical Center Dallas
Texas
Institute of Histology and Embryology, Center Medical Universitaire
Geneva, Switzerland
Department of Internal Medicine, Tohoku University, School of Medicine
Sendai, Japan
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John H Johnson;
John H Johnson
Center for Diabetes Research and Gifford Laboratories, University of Texas Southwestern Medical Center
Dallas
Department of Veterans Affairs Medical Center Dallas
Texas
Institute of Histology and Embryology, Center Medical Universitaire
Geneva, Switzerland
Department of Internal Medicine, Tohoku University, School of Medicine
Sendai, Japan
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Lindsey R Inman;
Lindsey R Inman
Center for Diabetes Research and Gifford Laboratories, University of Texas Southwestern Medical Center
Dallas
Department of Veterans Affairs Medical Center Dallas
Texas
Institute of Histology and Embryology, Center Medical Universitaire
Geneva, Switzerland
Department of Internal Medicine, Tohoku University, School of Medicine
Sendai, Japan
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Ling Chen;
Ling Chen
Center for Diabetes Research and Gifford Laboratories, University of Texas Southwestern Medical Center
Dallas
Department of Veterans Affairs Medical Center Dallas
Texas
Institute of Histology and Embryology, Center Medical Universitaire
Geneva, Switzerland
Department of Internal Medicine, Tohoku University, School of Medicine
Sendai, Japan
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Ken-Ichi Suzuki;
Ken-Ichi Suzuki
Center for Diabetes Research and Gifford Laboratories, University of Texas Southwestern Medical Center
Dallas
Department of Veterans Affairs Medical Center Dallas
Texas
Institute of Histology and Embryology, Center Medical Universitaire
Geneva, Switzerland
Department of Internal Medicine, Tohoku University, School of Medicine
Sendai, Japan
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Yoshio Goto;
Yoshio Goto
Center for Diabetes Research and Gifford Laboratories, University of Texas Southwestern Medical Center
Dallas
Department of Veterans Affairs Medical Center Dallas
Texas
Institute of Histology and Embryology, Center Medical Universitaire
Geneva, Switzerland
Department of Internal Medicine, Tohoku University, School of Medicine
Sendai, Japan
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Tausif Alam;
Tausif Alam
Center for Diabetes Research and Gifford Laboratories, University of Texas Southwestern Medical Center
Dallas
Department of Veterans Affairs Medical Center Dallas
Texas
Institute of Histology and Embryology, Center Medical Universitaire
Geneva, Switzerland
Department of Internal Medicine, Tohoku University, School of Medicine
Sendai, Japan
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Mariella Ravazzola;
Mariella Ravazzola
Center for Diabetes Research and Gifford Laboratories, University of Texas Southwestern Medical Center
Dallas
Department of Veterans Affairs Medical Center Dallas
Texas
Institute of Histology and Embryology, Center Medical Universitaire
Geneva, Switzerland
Department of Internal Medicine, Tohoku University, School of Medicine
Sendai, Japan
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Lelio Orci;
Lelio Orci
Center for Diabetes Research and Gifford Laboratories, University of Texas Southwestern Medical Center
Dallas
Department of Veterans Affairs Medical Center Dallas
Texas
Institute of Histology and Embryology, Center Medical Universitaire
Geneva, Switzerland
Department of Internal Medicine, Tohoku University, School of Medicine
Sendai, Japan
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Roger H Unger
Roger H Unger
Center for Diabetes Research and Gifford Laboratories, University of Texas Southwestern Medical Center
Dallas
Department of Veterans Affairs Medical Center Dallas
Texas
Institute of Histology and Embryology, Center Medical Universitaire
Geneva, Switzerland
Department of Internal Medicine, Tohoku University, School of Medicine
Sendai, Japan
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Address correspondence and reprint requests to Dr. Roger H. Unger, Department of Veterans Affairs Medical Center, 4500 South Lancaster Road, Dallas, TX 75216.
Diabetes 1993;42(7):1065–1072
Article history
Received:
March 19 1992
Revision Received:
February 26 1993
Accepted:
February 26 1993
PubMed:
8513973
Citation
Makoto Ohneda, John H Johnson, Lindsey R Inman, Ling Chen, Ken-Ichi Suzuki, Yoshio Goto, Tausif Alam, Mariella Ravazzola, Lelio Orci, Roger H Unger; GLUT2 Expression and Function in β-cells of GK rats with NIDDM: Dissociation Between Reductions in Glucose Transport and Glucose-Stimulated Insulin Secretion. Diabetes 1 July 1993; 42 (7): 1065–1072. https://doi.org/10.2337/diab.42.7.1065
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