Dunja Aksentijevi?
Insulin resistance and altered glucose transporter 4 expression in experimental uremia
Aksentijevi?, Dunja; Bhandari, Sunil; Seymour, Anne Marie L
Authors
Sunil Bhandari
Anne Marie L Seymour
Abstract
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.
Citation
Aksentijevi?, 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 |
DOI | https://doi.org/10.1038/ki.2008.691 |
Keywords | Nephrology |
Public URL | https://hull-repository.worktribe.com/output/461305 |
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