The dairy cow experiences an abrupt surge in energy demand at the onset of lactation, as glucose is prioritised to the mammary gland for milk production. This is exacerbated by a pronounced decline in feed intake around parturition. Like all organisms when energy economics shift either locally or systemically there are consequences for other processes. The intense reallocation of energy to meet milk requirements often results in metabolic disorders, excessive fatty acid mobilisation, fatty liver and a diminished immune response. Similarly, humans experience metabolic disease when energy utilization becomes dysregulated. The mitochondrion is central to the conversion of nutrients to energy and has an ability to adapt to different fuel sources. Mitochondrial adaptation has shown to be pivotal in many metabolic, lipid and immune disorders in humans and other species. Moreover, the communication between the mitochondrion and nuclear DNA is increasingly being recognised as important in epigenetic control, thus influencing metabolic functionality.
The aim of this project is to explore how the mitochondrion adapts to energy demands in the dairy cow, with the aim to identify areas of intervention; nutritional, management or genetic strategies which would reduce the burden of metabolic disease and improve welfare and performance.