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Research Article Free access | 10.1172/JCI115077

Differential regulation of adipose tissue glucose transporters in genetic obesity (fatty rat). Selective increase in the adipose cell/muscle glucose transporter (GLUT 4) expression.

I Hainault, M Guerre-Millo, C Guichard, and M Lavau

INSERM U 177, Institut Biomédical des Cordeliers, 75006 Paris, France.

Find articles by Hainault, I. in: PubMed | Google Scholar

INSERM U 177, Institut Biomédical des Cordeliers, 75006 Paris, France.

Find articles by Guerre-Millo, M. in: PubMed | Google Scholar

INSERM U 177, Institut Biomédical des Cordeliers, 75006 Paris, France.

Find articles by Guichard, C. in: PubMed | Google Scholar

INSERM U 177, Institut Biomédical des Cordeliers, 75006 Paris, France.

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Published March 1, 1991 - More info

Published in Volume 87, Issue 3 on March 1, 1991
J Clin Invest. 1991;87(3):1127–1131. https://doi.org/10.1172/JCI115077.
© 1991 The American Society for Clinical Investigation
Published March 1, 1991 - Version history
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Abstract

Adipocytes from young obese Zucker rats exhibit a hyperresponsive insulin-mediated glucose transport, together with a marked increase in cytochalasin B binding as compared with lean rat adipocytes. Here, we examined in these cells the expression of two isoforms of glucose transporter, the erythroid (GLUT 1) and the adipose cell/muscle (GLUT 4) types, in rats aged 16 or 30 d, i.e., before and after the emergence of hyperinsulinemia. GLUT 1 protein and mRNA levels were identical in the two genotypes at both ages. In contrast, the levels of GLUT 4 protein in obese rat adipocytes were 2.4- and 4.5-fold those of lean littermates at 16 and 30 d of age, respectively, in perfect agreement with the genotype effect on insulin-stimulated glucose transport activity. The levels of GLUT 4 mRNA per fat pad were increased 2.3- and 6.2-fold in obese vs. lean rats 16- and 30-d-old, indicating a pretranslational level of regulation. The obese phenotype was not associated with overexpression of GLUT 4 mRNA in gastrocnemius muscle. This work indicates that the fa gene exerts a differential control on the expression of GLUT 1 and GLUT 4 in adipose tissue and provides evidence that independent of hyperinsulinemia, genotype is a major regulatory factor of GLUT 4 expression in this tissue.

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