Indeed, PPAR-α expression and activity are diminished in cardiac tissue of pressure overload–induced hypertrophy murine model [145], in hypertrophic heart of spontaneously hypertensive stroke-prone rats [146] and in hypoxic cardiomyocytes [147] leading to a reduction in the capacity for fatty acid oxidation and increased rates of glucose utilization. The gene discussed is PPARA; the disease is stroke disorder.