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Am J Physiol Endocrinol Metab 281: E575-E585, 2001;
0193-1849/01 $5.00
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Vol. 281, Issue 3, E575-E585, September 2001

Type 1 diabetes leads to cytoskeleton changes that are reflected in insulin action on rat cardiac K+ currents

Y. Shimoni1 and J. B. Rattner2

Departments of 1 Physiology and Biophysics and 2 Anatomy and Cell Biology, University of Calgary Health Sciences Centre, Calgary, Alberta, Canada T2N 4N1

A sustained K+ current (Iss) is attenuated in ventricular cells from streptozotocin (STZ)-induced diabetic rats. The in vitro addition of insulin to isolated cells augments Iss in a process that is blocked by disrupting either actin microfilaments (with cytochalasin D) or microtubules (with colchicine). When these agents are added at progressively later times, the effect of insulin becomes evident in a time-dependent manner. Iss is also augmented by insulin in control cells in a cytoskeleton-dependent manner. However, in contrast to diabetic cells, cytoskeleton-dependent augmentation of Iss by insulin occurs at a considerably faster rate in control cells. Immunofluorescent labeling shows a reduced density of beta -tubulin in diabetic cells, particularly in perinuclear regions. In vitro insulin replacement or in vivo insulin injections given to STZ-treated rats enhances beta -tubulin density. These results suggest an impairment of cytoskeleton function and structure under insulin-deficient conditions, which may have implications for cardiac function.

cardiac potassium channels; microtubules; actin microfilaments


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