## 3 Results
### Heart Hypertrophy and Myocardial Remodeling  
Cardiac hypertrophy was observed in the Ang II-treated control and Ang II-treated db/db mice compared to the control and db/db animals, as revealed by evaluation of the heart weight to tibial length ratio (Figure 3A). In the same groups, the cardiomyocyte diameters in the LV significantly increased, as revealed by morphometric measurements (Figure 3B). Moreover, the distances between the cardiomyocyte borders and the external blood endothelial cells (BEC) of the capillary walls were increased in the myocardium of the hearts of mice from all three experimental groups compared to the control, but especially in both groups of mice treated with Ang II (Figure 3C). Of note, histopathological analysis indicated signs of cardiomyocyte injury visible as scattered clumps of eosinophil material within the cytoplasm (Figure 4B) and the focal infiltration of inflammatory cells in the Ang II-treated animals (Figure 4B,C,G,H compared to Figure 4A,E). Remarkably, in areas devoid of granulation tissue and/or scars, macrophages of CD45\({}^{+}\)/CD68\({}^{+}\) phenotype were less numerous in the LV of the db/db mice compared to the macrophage density in the Ang II-treated db/db mice (Figure 5), whereas the total number of CD45\({}^{+}\) inflammatory cells (of CD45\({}^{+}\)/CD68\({}^{+}\) and CD45\({}^{+}\)/CD68\({}^{-}\) phenotypes) was diminished in the db/db compared to the number in the Ang II-treated control mice (Figure 5). The density of macrophages (CD45\({}^{+}\)/CD68\({}^{+}\)) and other inflammatory cells (CD45\({}^{+}\)) was measured in areas devoid of scars and areas adjacent to coronary arteries. Figure 2: Box-plot graphs presenting the obesity-associated symptoms in the experimental groups vs. control at 19 weeks: (**A**) body weight; (**B**) blood glucose levels, (**C**) triglyceride serum levels, (**D**) blood pressure. Statistical analyses were performed with an unpaired Student’s \(t\)-test followed by Mann–Whitney correction (**A**), one-way ANOVA test (**B–D**); * \(p\) < 0.05, **\(p\) < 0.002, ***\(p\) < 0.0002; number of animals in (**A,B,D**), as in the Materials and Methods section; number of samples in (**C**): control n = 14, control + Ang II n = 12, db/db n = 13, db/db + Ang II n = 10. Figure 4: Morphological symptoms of myocardial remodeling in Ang II-treated control (**B**,**F**,**J**), db/db (**C**,**G**,**K**), and Ang II-treated db/db mice (**D**,**H**,**L**) compared with control mice (**A**,**E**,**J**). Hematoxylin–coin-stained histological paraffin sections (**A**–**H**) in small (**A**–**D**) and high (**E**–**H**) magnifications and Picrosirius red-stained sections (**I**–**L**) showing details of myocardial remodeling: cardiomyopathyocyte injury (panels: (**B**), insert and (**G**), black-edged arrows), local accumulation of inflammatory cells ((panels **D**,**G**,**H**), black-edged arrows); (panel **G**) shows the boxed area in (**C**). Areas of collagen deposits shown in Picrosirius red-stained sections: (panels **J**,**L**)—located perivascularly, marked with black-edged arrows; (panel **K**)—interstitial collagen deposits, marked with blue-edged arrows; (panel **L**)—located in scar tissue, marked with yellow-edged arrows. Scale bars: (**A**–**D**)—250 \(\mu\)m; (**E**–**L**)—100 \(\mu\)m. Number of samples—tissue sections (n = 3) for each H&E and Picrosirius red staining from each study group. Figure 3: Myocardial remodeling: comparison of the heart weight (**A**), cardiomyocyte diameter (**B**), and myocardial edema (**C**) presented in box-plot graphs. Cardiac hypertrophy as assessed by the heart weight to tibia length ratio (**A**); cardiomyocyte hypertrophy evaluated by the cardiac cell diameters on cross-sectioned paraffin sections stained with H&E (**B**); myocardial edema measured as the distances between microapillary BEC borders and adjacent cardiomyocyte borders on electron micrographs with cross-sectioned microcapillaries (**C**).