Restricted expression of the erythroid/brain glucose transporter isoform to perivenous hepatocytes in rats. Modulation by glucose.

M Tal; D L Schneider; B Thorens; H F Lodish

doi:10.1172/JCI114801

Whitehead Institute For Biomedical Research, Cambridge, Massachusetts 02142.

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Whitehead Institute For Biomedical Research, Cambridge, Massachusetts 02142.

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Whitehead Institute For Biomedical Research, Cambridge, Massachusetts 02142.

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Whitehead Institute For Biomedical Research, Cambridge, Massachusetts 02142.

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Published in Volume 86, Issue 3 on September 1, 1990
J Clin Invest. 1990;86(3):986–992. https://doi.org/10.1172/JCI114801.
© 1990 The American Society for Clinical Investigation

Published September 1, 1990 - Version history

The "erythroid/brain" glucose transporter (GT) isoform is expressed only in a subset of hepatocytes, those forming the first row around the terminal hepatic venules, while the "liver" GT is expressed in all hepatocytes. After 3 d of starvation, a three- to fourfold elevation of expression of the erythroid/brain GT mRNA and protein is detected in the liver as a whole; this correlates with the expression of this GT in more hepatocytes, those forming the first three to four rows around the hepatic venules. Starvation-dependent expression of the erythroid/brain GT on the plasma membrane of these additional hepatocytes is lost within 3 h of glucose refeeding; however, by immunoblotting we show that the protein is still present. Its loss from the surface is possibly explained by internalization.

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