Skip to main content
. 2003 Jan 27;100(3):1226–1231. doi: 10.1073/pnas.0336724100

Figure 4.

Figure 4

Diet-induced cardiac lipotoxicity depends upon fatty acid chain length but does not require increased flux of fatty acids through mitochondrial pathways. (a) MCT diet rescues cardiac dysfunction in MHC-PPAR mice. Bars represent mean echocardiographic-determined LV fractional shortening of NTG and MHC-PPAR mice (404-3 line; n ≥ 5 for each group) 8 weeks after initiation of control, LCT, or MCT diet administration. *, P < 0.05 vs. NTG mice. **, P < 0.05 vs. NTG mice and MHC-PPAR mice on control or MCT chows. NS = nonsignificant. (b) LCT but not MCT HF diet increases myocardial TAG levels. Bars represent mean levels of TAG-associated fatty acids with chain length of 16:0, 18:1, and 18:2 in MHC-PPAR mouse ventricles after 8 weeks of control, LCT, or MCT diet administration. *, P < 0.05 vs. MHC-PPAR mice fed control or MCT chow. (c) Inhibition of mitochondrial fatty acid import exacerbates cardiac dysfunction in MHC-PPAR mice. Fractional shortening of MHC-PPAR mice (404-4 line; n ≥ 5 for each group) after 3 weeks of daily injections of etomoxir sodium (25 ng/kg/day) while receiving control or HF chow. *, P < 0.05 vs. MHC-PPAR mice on control chow. **, P < 0.05 vs. MHC-PPAR mice on control chow and saline-treated HF mice.