Figure 2.

Inhibition of β-oxidation activates pyruvate dehydrogenase and increases CoASH and acetyl-CoA content in the heart. Male C57BL/6N mice received an intraperitoneal injection of saline or oxfenicine (0.15 mg/g) at 12 PM. Hearts were excised 30 min post-injection, homogenized, and mitochondria were isolated (+DCA and NaF). A, PDH activity was measured spectrophotometrically. B, E1α subunit content and phosphorylation status of Ser²³² on the PDH E1α subunit were measured by Western blot followed by densitometric analysis. Cardiac tissue excised and frozen 30 min post-oxfenicine injection was extracted, metabolites resolved by reverse phase HPLC and (C) malonyl-CoA, (D) acetyl-CoA, and (E) CoASH quantified by UV/Vis spectroscopy. Values are presented as the mean ± SD (n = 5–9) where significant differences (2-tailed t test) are indicated by ∗p < 0.05, ∗∗p < 0.01, and ∗∗∗p < 0.001. Each data point indicates a separate animal.