Abstract <p>Heart failure of various etiologies, including diabetic cardiomyopathy(DCM), is a global problem. However, the features of DCM pathogenesis,including the role of the T-tubular system in this process, arenot fully understood. The available literature data on T-systemremodeling in diabetic rodent models are contradictory, with changesin this system being demonstrated in some of them already at the prediabeticstage. So, this work was aimed to assess changes in the T-systemin a rat model of metabolic syndrome (MS) that precedes type 2 diabetesmellitus. MS was induced in Wistar rats by a high-carbohydrate (HC)and a combined high-carbohydrate high-fat (HCHF) diets for 10 weeks.The parameters to be finally estimated were body, abdominal fat,and heart weights, as well as fasting plasma glucose levels measuredby a glucose tolerance test (GTT). The structure of the T-systemwas examined via confocal microscopy in isolated hearts stainedwith DI-8-ANEPPS. HCHF-fed rats developed more severe MS since theirbody and abdominal fat weights, as well as fasting plasma glucoselevels, were significantly higher compared to the controls; moreover,GTT revealed the signs of glucose tolerance. HC-fed rats were characterizedby a moderate MS, as manifested only in an increase in abdominalfat weight. The structural correlates of T-system remodeling werealso found in HCHF-fed rats only, as manifested in a significantincrease in the average interval between the rows of T-tubules.These findings differ from our results obtained in a model of type1 prediabetes and diabetes. Thus, T-system remodeling in rat cardiomyocytesbegins already at the stage of HCHF-induced MS and proceeds similarlyto that described for type 2 diabetes, but differs from that intype 1 prediabetes and diabetes, suggesting different pathways ofDCM pathogenesis in different diabetic types.</p>