Fig. 1

HFD-induced cardiac remodeling is blunted by ASMase inhibitor. C57B/L6 mice were treated with high fat-diet for 6 weeks and then were given imipramine, an ASMase inhibitor for 4 weeks. a Glucose tolerance test was performed by intraperitoneal injection of glucose. b–d Fasting blood glucose levels, total triglyceride levels and cholesterol levels were detected by biochemical methods. e–p Echocardiographic parameters were recorded. In order, they are heart rate, ejection fraction(EF %), fraction shortening(FS %), cardiac output, left ventricular anterior wall thickness at systole (LVAW; s), left ventricular anterior wall thickness at diastole (LVAW; d), left ventricular posterior wall thickness at systole (LVPW; s), left ventricular posterior wall thickness at diastole (LVPW; d), left ventricular volume at systole(Volume; s), left ventricular volume at diastole (Volume; d), left ventricular internal dimension at systole (LVID; s); left ventricular internal dimension at diastole (LVID; d). q The heart weight to body weight was calculated. r Echocardiography images. s Myocardial hypertrophy and fibrosis were assessed by H&E, MASSON trichrome and Sirius Red staining (Scale bar:100 μm). Data were presented as Mean ± SEM. n = 5. ^*P < 0.05, ^**P < 0.01, ^***P < 0.001, ^****P < 0.0001