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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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

A sustained K(+) current (I(ss)) is attenuated in ventricular cells from streptozotocin (STZ)-induced diabetic rats. The in vitro addition of insulin to isolated cells augments I(ss) 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. I(ss) is also augmented by insulin in control cells in a cytoskeleton-dependent manner. However, in contrast to diabetic cells, cytoskeleton-dependent augmentation of I(ss) 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.[1]


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