Metabolic state during oogenesis and embryogenesis is so tightly regulated with dynamic changes in metabolic substrates and pathways, that its dysregulation causes detrimental effects on oocytes and preimplantation embryos, and may further affect postnatal physiological states and/ or susceptibility to adult metabolic diseases. It is well known that mitochondria, as major sites of energy production and reactive oxygen species, a by-product of oxidative phosphorylation, are much responsible for metabolism. Recently, it has been revealed that quite a lot of mitochondrial proteins are acetylated and thereby regulated in their functions. Most of them are involved in many metabolic pathways, suggesting that protein acetylation is also an important modification in embryogenesis. Recent studies have also elucidated that the mitochondrial protein deacetylation process mostly depends on certain members of the sirtuin family, a NAD dependent deacetylase family, that are involved in a variety of (patho) physiological events such as tumorigenesis and metabolic disorders. This article reviews recent and current studies of mitochondrial functions in early embryos and their regulatory mechanisms, focusing on mitochondrial protein deacetylation by the sirtuin family.