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Glucose Transporter Proteins in Human Insulinoma

Guenther Boden, MD; Erik Murer, MD; and Maria Mozzoli, BS
[+] Article and Author Information

From Temple University Hospital, Philadelphia, Pennsylvania. Requests for Reprints: Guenther Boden, MD, Temple University Hospital, 3401 North Broad Street, Philadelphia, PA 19140. Acknowledgments: The authors thank Michael A. Gyda, MA, and Karen Davis, BS, for providing technical assistance; Ms. Constance Harris for typing the manuscript; the nurses of the General Clinical Research Center for taking care of the patients during their hospitalization; Dr. S.W. Cushman, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland, for providing Glut 1 antiserum (RAB 379); and Dr. L. Slieker from the Eli Lilly Corporation, Indianapolis, Indiana for providing Glut 2 antiserum. Grant Support: By U.S. Public Health Service Grants R01 AG-07988 and RR-00349.


Copyright ©2004 by the American College of Physicians


Ann Intern Med. 1994;121(2):109-112. doi:10.7326/0003-4819-121-2-199407150-00005
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Objective: To determine the reason patients with insulinoma are unable to cease insulin secretion during hypoglycemia.

Patients: Five patients with insulinoma.

Design: All patients fasted for up to 25 hours, during which blood was obtained serially for determination of glucose and insulin concentrations. Insulinomas were surgically removed from all patients and Glut 1 and Glut 2 transporter proteins were measured in solubilized tumor membranes by immune blotting.

Results: In all patients, serum insulin concentrations failed to decrease to less than 30.0 pmol/L (<5.0 µU/mL) and C-peptide concentrations to less than 0.08 nmol/L during hypoglycemia (glucose concentration, <2.2 mmol/L) that was induced by fasting. The islet cell tumors from all five patients contained Glut 1, a low-Km glucose transporter protein, which is not normally present in β-cells. Glut 2, a high-Km glucose transporter protein, which is normally prevalent in β-cells, was undetectable in one patient and was present in what appeared to be low concentrations in the remaining four patients.

Conclusions: Our data are compatible with the concept that continued glucose transport, mediated by the low-Km Glut 1 glucose transporter, was responsible for continued insulin release during hypoglycemia in these patients.

Figures

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Figure 1.
Serum insulin concentrations at various plasma glucose concentrations observed during fasting in four patients with insulinoma.

Hypoglycemia (glucose concentrations, 2.2 mmol/L or less) developed in all four patients but failed to suppress serum insulin concentrations to less than 30.0 pmol/L.

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Figure 2.
Glucose transporter protein concentrations in tumor membranes from four patients with insulinoma and in liver membranes from one healthy person.

The normal liver membrane contained only Glut 2 protein but no Glut 1 protein. The four insulinoma tumor membranes all contained Glut 1 and either no Glut 2 protein (patient 1) or relatively little Glut 2 protein.

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