T-system remodeling of rat cardiomyocytes in metabolic syndrome

Heart failure of various etiologies, including diabetic cardiomyopathy (DCM), is a worldwide problem. However, the features of DCM pathogenesis, including the role of t-tubules in this process, are not fully understood. Available literature data on T-system remodeling in diabetes models are sometimes contradictory, and t-tubule changes in some of them have been shown already at the prediabetes stage. So, the aim of this work was to evaluate changes in the t-tubule system in a model of metabolic syndrome (MS), preceding the development of type II diabetes mellitus, in rats on high-carbohydrate and high-carbohydrate and high-fat diets. The experiments were performed on male Wistar rats. MS induction in the animals of the experimental groups was carried out using high-carbohydrate (HC) and combined high-carbohydrate and high-fat (HCHF) diets for 10 weeks. The weight of the animals, of the abdominal fat, and of the heart were also assessed, and a glucose tolerance test (GTT) was also performed. The structure of the T-system was studied using confocal microscopy on isolated hearts stained with DI-8-ANEPPS. Rats on the HCHF diet developed more severe MS: body weight, abdominal fat mass, and fasting blood glucose level were significantly higher in these animals than in the controls. Signs of glucose tolerance in the GTT were also revealed. Rats on the HC diet were characterized by the development of moderate MS, manifested only in an increase in abdominal fat mass. Signs of t-tubule system remodeling were also revealed only in the HCHF diet group: they were manifested by a reliable increase in the average interval between t-tubule rows. This differs from the results obtained in the model of type I diabetes and prediabetes. Thus, it can be concluded that changes in the T-system in rat cardiomyocytes appear already at the stage of MS induced by the HCHF diet and are similar to the changes described for type II diabetes, but differ from the changes in type I diabetes and prediabetes, which may indicate different pathogenesis pathways of DCM in different types of diabetes.