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Insulin resistance and altered glucose transporter 4 expression in experimental uremia

Aksentijević, Dunja; Bhandari, Sunil; Seymour, Anne Marie L


Dunja Aksentijević

Sunil Bhandari

Anne Marie L Seymour


Progressive ventricular hypertrophy can lead to the development of insulin resistance, a feature of both chronic kidney disease and heart failure. Here we induced uremia in adult male Sprague-Dawley rats using a remnant kidney model and studied the expression of glucose transporters. As expected, the reduction of nephron mass resulted in impaired renal function, cardiac hypertrophy, glucose intolerance, hyperinsulinemia, anemia, and hypertension. Insulin sensitivity was significantly reduced in the uremic animals as determined by oral glucose tolerance tests. After six weeks of uremia, at a point when cardiac hypertrophy had been established, left ventricle tissue had a marked increase in the expression of GLUT4 (insulin-dependent glucose transporter 4), consistent with hypertrophic remodeling, but not GLUT1 (insulin-independent glucose transporter 1). However, although uremic animals had systemic insulin resistance and glucose intolerance, there was no evidence of impaired GLUT4 translocation in the heart at 6 weeks of uremia, suggesting that other mechanisms may underpin insulin resistance in the uremic heart.


Aksentijević, D., Bhandari, S., & Seymour, A. M. L. (2009). Insulin resistance and altered glucose transporter 4 expression in experimental uremia. Kidney International, 75(7), (711-718). doi:10.1038/ki.2008.691. ISSN 0085-2538

Journal Article Type Article
Publication Date 2009-04
Deposit Date Nov 13, 2014
Journal Kidney International
Print ISSN 0085-2538
Electronic ISSN 1523-1755
Publisher Elsevier
Peer Reviewed Peer Reviewed
Volume 75
Issue 7
Pages 711-718
Keywords Nephrology
Public URL