Figure 2. Inability to oxidize 3OHB in the heart results in worsened pathologic cardiac remodeling in the context of pressure overload/ischemic stress.

Echocardiographic data collected 4 weeks following sham or TAC/MI surgeries in Bdh1^fl/flCre– (control) and csBDH1^–/– male mice aged 8–11 weeks at time of surgery. (A) EF graphed as percent, (B) EDV (left), and ESV (right) graphed as volume (µl). Bars represent mean ± SEM (Sham, n = 5; TAC/MI, n = 8–9); *P < 0.05 TAC/MI control vs. TAC/MI csBDH1^–/–, using unpaired, 2-tailed t test. EF, ejection fraction; TAC/MI, transverse aortic constriction with myocardial infarction; EDV, end-diastolic volume; ESV, end-systolic volume, csBDH1^–/–, cardiac-specific β-hydroxybutyrate dehydrogenase–deficient.