The novel mechanisms underlying these cardioprotective effects included the following: VD/VDR (1) regulated the expression of Sirt3 to suppress LCAD, (2) indirectly induced mitochondria complex expression via SIRT3 to prevent oxidative damage, (3) regulated transcriptional activity by binding to the VDRE within the Sirt3 promoter, (4) upregulated glucose transport, and (5) suppressed mitochondrial fatty acid utilization to balance energy substrates. The gene discussed is VDR; the disease is long chain acyl-CoA dehydrogenase deficiency.