The usefulness of short-term high-fat/high salt diet as a model of metabolic syndrome in mice.

Diabetic cardiomyopathy (DC) describes diabetes-associated changes in the structure and function of myocardium that are not directly linked to other factors such as hypertension. Currently there are some models of DC; however, they take a large time period to mimic key features. In the present study, we investigated the effects of a short-term high-fat/high salt diet (HFHS) treatment on myocardial function and structure, and vascular reactivity in C57BL/6 male mice. After 14 weeks HFHS induced hypertension (MAP = 144.95 ±â€¯16.13 vs 92.90 ±â€¯18.95 mm Hg), low glucose tolerance (AUC = 1049.01 ±â€¯74.79 vs 710.50 ±â€¯52.57 a.u.), decreased insulin sensitivity (AUC = 429.83 ±â€¯35.22 vs 313.67 ±â€¯19.55 a.u.) and increased adiposity (epididymal fat weight 0.96 ±â€¯0.10 vs 0.59 ±â€¯0.06 OW/BW × 102), aspects present in metabolic syndrome. Cardiac evaluation showed diastolic dysfunction (E/A ratio = 1.20 vs 1.90 u.a.) and cardiomyocyte hypertrophy (cardiomyocyte area = 502.82 ±â€¯31.46 vs 385.58 ±â€¯22.11 µm2). Lastly, vascular reactivity was impaired with higher contractile response (136.10 ±â€¯3.49 vs 120.37 ±â€¯5.43%) and lower response to endothelium-dependent vasorelaxation (74.01 ±â€¯4.35 vs 104.84 ±â€¯3.57%). In addition, the diet was able to induce an inward coronary remodeling (vascular total area: SCNS 6185 ±â€¯800.6 vs HFHS 4085 ±â€¯213.7 µm2). Therefore, we conclude that HFHS short-term treatment was able to induce metabolic syndrome-like state, cardiomyopathy and vascular injury working as an important tool to study cardiometabolic diseases.