Abstract
Cardiovascular pathology is the main cause of morbidity among patients with diabetes mellitus. The development of a specific therapy aimed at either blunting the protein signals involved in pathological cardiomyocyte hypertrophy or upregulating the expression of cardioprotective pathways can support new strategies for treating diabetes-induced cardiac dysfunctions. The aim of the work was to study the impact of intranasal insulin administration (IIA) on the expression of genes encoding insulin-dependent signaling proteins and components of the Ca2+-transporting system, as well as on the activity of Na+/K+-ATPase in cardiomyocytes on the model of experimental type 1 diabetes mellitus (DM1) in rats. It was shown that IIA eliminates the uncoupling of molecular mechanisms involved in electromechanical coupling in rat cardiomyocytes that occurs under the conditions of mild DM1. This allowed us to recommend IIA as a therapeutic approach to the prevention and treatment of structural and functional myocardial disorders caused by diabetes.
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