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Expression of the Low Km GLUT-1 Glucose Transporter Is Turned on in Perivenous Hepatocytes of Insulin- Deficient Diabetic Rats^*

MICHAEL TAL, BARBARA B. KAHN and HARVEY F. LODISH

Whitehead Institute for Biomedical Research (M.T., H.F.LJ Cambridge, Massachusetts 02142
the Department of Biology, Massachusetts Institute of Technology (H.F.LJ Cambridge, Massachusetts 02139
the Charles A. Dana Research Institute and Harvard-Thorndike Laboratory of Beth Israel Hospital, Department of Medicine, Beth Israel Hospital and Harvard Medical School (B.B.K.) Boston, Massachusetts 02215

Address all correspondence and requests for reprints to: Dr. Michael Tal, Whitehead Institute for Biomedical Research, 9 Cambridge Center, Cambridge, Massachusetts 02142.

Abstract

In normal fed rats the low K. glucose transporter GLUT-1 is expressed only in one row of hepatocytes immediately surrounding a terminal hepatic venule, while the high K_m GLUT-2 is expressed in every hepatocyte. Previously, we showed that additional perivenous hepatocytes express GLUT-1 in fasting animals. In diabetes, as in starvation, the liver functions to release glucose into the circulation, but unlike starvation, circulating extracellular glucose is high in diabetes. By immunofluorescence and Western blotting we studied whether glucose or insulin is the primary extracellular signal for inducing GLUT-1 expression in hepatocytes. We observed that streptozocin-induced diabetes causes induction of GLUT-1 expression in the plasma membrane of hepatocytes within four cell rows of a terminal hepatic venule; GLUT-2 expression is unaltered. Chronic insulin treatment of diabetic rats reduces the number of rows of hepatocytes expressing GLUT-1 from—four to -two. In contrast, chronic insulin infusion into nondiabetic rats does not affect the number of hepatocytes expressing GLUT-1. Thus, both fasting and diabetes induce GLUT-1 expression in specific hepatocytes that normally do not express this gene. This induction correlates with low insulin levels in the blood, and not with circulating glucose levels.(Endocrinology 129: 1933–1941,1991)

Footnotes

^* This work was supported by NIH Grants GM-40916 and HL-41484(to H.F.L.) and NIH Physician Scientist Award AG-00294 and Juvenile Diabetes Foundation Grant 189833 (to B.B.K.).

Supported by a fellowship from the European Molecular Biology Organization.

Received April 16, 1991.

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