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Fig. 3 | Cardiovascular Diabetology

Fig. 3

From: Deletion of Tbc1d4/As160 abrogates cardiac glucose uptake and increases myocardial damage after ischemia/reperfusion

Fig. 3

Tbc1d4-ko and HFD impair heart function and morphology following I/R with unaffected reduced GLUT4 content. Echocardiographic assessment of cardiac A end-systolic and B end-diastolic volume over a time course of 3 weeks (n = 6). C R-wave amplitude at basal state, during ischemia and acute reperfusion phase, normalized to the basal state. Histomorphometrical analysis of WT and Tbc1d4-deficient hearts 3 weeks post-I/R (closed chest) in terms of: D left ventricular wall thickness, E left ventricular lumen, and F infarct size (n = 3). G, H, I Cardiac protein content of H GLUT1 and I GLUT4 three weeks after reperfusion (open chest; n = 6–7). Data presented as mean ± SEM. Statistical analysis was performed using unpaired two-tailed student’s t-Test (A, B, D-F, H, I; WT vs. D4KO: *p < 0.05) or two-way ANOVA with Bonferroni’s multiple comparison test (C; Isch or Rep vs. basal: *p < 0.05, **p < 0.01; WT vs. D4KO: #p < 0.05) (Male mice, 36 weeks of age). WT wild type, D4KO Tbc1d4-knockout, Isch ischemia, Rep Reperfusion

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