Figure 5.

Triglyceride content, oxygen consumption and cardiac function in Atg/KO mice treated with PPAR-α agonists. (a) Cardiac and hepatic triglyceride content in 6-week-old female Atg/KO mice on chow diet with or without 0.1% Wy14643 for 3 weeks (n = 5). (b) Cardiac and hepatic triglyceride content in 6-week-old female Atg/KO mice on chow diet with or without 0.2% fenofibrate for 10 weeks (n = 4–5). (c) mRNA expression levels of PPAR-α and PPAR-δ target genes and genes encoding PGC-1α and PGC-1β in cardiac muscle of female wild-type and AtglKO mice fed a chow diet with or without 0.1% Wy14643 for 3 weeks (n = 5). (d) Oxygen consumption in cardiac muscle preparations under both basal conditions and succinate-stimulated conditions of 9-week-old male wild-type, Atg/KO mice and Atg/KO mice fed a chow diet with 0.1% (wt/wt) Wy14643 for 3 weeks (n = 5). (e) Representative echocardiographic images (M- and B-Mode) of a 9-week-old female wild-type and Atg/KO mouse on chow diet and a 9-week-old female Atg/KO mouse fed a chow diet containing 0.1% (wt/wt) Wy14643 for 3 weeks. We measured interventricular septum (IVS) and posterior wall (PW) thickness from original tracings. We measured left ventricular end-systolic dimensions (ESD) and left ventricular end-diastolic dimensions (EDD) from original tracings according to the leading edge convention of the American Society of Echocardiography. (f,g) Left ventricular fractional shortening (LVFS) (f) and left ventricular (LV) mass (g), calculated from the echocardiographic tracings as previously described⁵⁴ (n = 5). Error bars show means ± s.d. *P < 0.05, **P < 0.01 and ***P < 0.001.